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BROWN U / Neuroscience / NEUR 0010 / What are the different parts of neurons?

What are the different parts of neurons?

What are the different parts of neurons?

Description

School: Brown University
Department: Neuroscience
Course: Intro to Neuroscience
Professor: Michael paradiso
Term: Fall 2016
Tags: intro, to, and neuroscience
Cost: 50
Name: Neuro 1 Final Exam
Description: Neurons, Synapses, Vision, Audition, Anatomy, Somatosensory
Uploaded: 12/12/2016
60 Pages 53 Views 1 Unlocks
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Neurons and the Resting Potential 


What are the different parts of neurons?



Topics: 

 Neurons- parts and diease

 Axoplasmic Transport

o Disease

 Glia

 Membrane Potential

 Ions+ Pumps

 Diffusion and Electrical Forces

Neuron Parts 

-

Dendrites 

- Most synapses end on dendrites


What is the meaning of dendrites in neurons?



- Special receptor protein on cell membrane bind a NT

- Shape + density of spines determines strength of interaction - Spines change with brain development and learning

- Extent of spine abnormality correlates with intellectual impairment o Ex. 1 General intellectual impairment (dendrites are long, spindly and sparse)

o Ex. 2 Fragile X syndrome (long, dense spines)

If you want to learn more check out What is the meaning of the southern manifesto in history?

Key Functions of Organelles in Soma 


What is the meaning of fragile x syndrome?



2 Key Functions 

 1. Protein Synthesis 

DNA (in nucleus within soma) -- (transcription)----> mRNA – (translation)---> protein 

- Ribosomes (protein factories)

- Rough ER and Golgi  

Apparatus involved

- Energy

- Currency= ATP

- Krebs cycle in mitochondria  

produces adenosine  

triphosphate (ATP)- 3  

phosphate groups, when you  

have a chemical reaction  

where you lose one, you  

release energy (conversion to

ADP releases energy)If you want to learn more check out What are the characteristics of the watson and crick dna structure?
Don't forget about the age old question of When jj thomson discovered the electron, what physical property of the electron did he measure?

Neuron Cytoskeleton 

- Scaffolding proteins affect neuron shape and function - microfilaments

- neurofilaments

- microtubules

-  If you want to learn more check out What are some of the models used to explain psychological disorders?

- Microtubule Associated Proteins (MAPs)

- regulate assembly and function of microtubules

- e.g. tau proteins- links microtubules (like pearls on a string)  Alzheimer’s Disease

- cognitive loss- memory loss. Confusion, cognitive decline - macro brain – cells die, sulci expand, gyri shrink

Amyloid Protein is normal in many cells.  

Error leads to beta-amyloid or BA. Which is abnormal

Signs:  

 - Amyloid plaques 

 - Neurofibrillary tangles Don't forget about the age old question of What does the frog of the foot do?

Alzheimer’s Disease Progression- B amyloid hypothesis

- BA clumping because- beta amyloids are sticky, make others stick to  them, toxic to neurons

- BA clump into plaques

- BA triggers formation of tangles If you want to learn more check out What is the difference between depth and width?

- Something about Tau interaction with BA changes the shape of the Tau  protein (hyper-phosphorylation)  

- Changes shape + changes function -> can’t hold microtubules  together, pearls fall apart -> neurons dies

- Leftover Tau = tangle = neuron gravestone

- Distorted Tau affects other neurons

- Mad Cow disease

Axons

- No ribosomes

- No protein synthesis

Axoplasmic transport 

- most protein synthesizes in soma and is shipped to axon Anterograde- toward terminal – controlled by kinesin

Retrograde- away from terminal- controlled by dynein proteins

Disease and axoplasmic transport 

Cold sores- HSV-1 (herpes simplex virus 1) 

1. virus enters nerve terminal

2. retrograde to soma

3. replication

4. STRESS= anterograde back to axon terminal

Disease -> rabies

- Animal bite- saliva infection

1. Retrograde to Soma

2. Replication

3. Cell Death

4. Virus infects other cells

5. Death- days to weeks

Glia- 50-100 Billion 

- not just glue

- electrically insulate cells

- protect

- nourish cells metabolically

- perhaps involved in brain computations (signaling information)

Astrocytes- most common glia 

- Fills spaces between neurons, “glue” function

- Regulates ion concentration around neurons

- Guide neurons in development (make sure they end up in the right  place)

- Protect by taking up toxins

Oligodendroglia and Schwann Cells 

- electrically insulate cell with myelin

- increase speed of electrical conduction down axons

- Oligo (CNS)- one cell body myelinates multiple axons - Schwann (PNS)- myelinates one axon

CNS tumors

- Most not neuron tumor, glial tumor

- Astrocytoma

- Oligodendroglioma

(Glial cells multiply throughout life)

Resting Potential and Action Potential 

The Neuronal Membrane at Rest

- no AP

- Potential difference- energy to push electrons through wire (voltage= potential difference)

* Potential difference- energy to drive ions (an ion is a molecule that has  an electrical charge) across cell membrane

Inside of a typical neuron is 65 mV more negative than outside

Vm= membrane voltage or membrane potential

At rest Vm= -65 mV

Vm is determined by distribution of ions (inside vs. outside of cell)

ION CONCENTRATIONS

ION

Inside  

(Axoplas

mic)

Outside  

(Extracellu lar)

Potassiu

m (K+)

100 (a lot  inside)

5

Sodium  

(Na+)

15

150

Chloride  (Cl-)

13

150

Calcium  (Ca++)

.0002

2

ACTION POTENTIAL

- Action potential (AP) conveys info over distances in the nervous  system.  

- AP- for an instant, inside cell positively charged compared to outside. - AP code frequency and pattern

- AT rest, neuronal membrane steady potential difference of about  -65mV

AT REST: cytosol in neuron NEGATIVELY charge with respect to extracellular  fluid (potential difference of about -65mV)

ACTION POTENTIAL: cytosol in neuron POSTIVELY charged with respect to  extracellular fluid

Frequency and pattern of AP= neuron’s code to transfer information

STEPS

1. Rest

2. Depolarization beyond threshold, RISING PHASE (Na+ channels open,  Na+ in, depolarize)

3. Overshoot- Vm reaches peak of around 40 mV- inside of neuron +  charged with respect to outside

4. Falling phase- K+ out (delayed rectifier- potassium gates open 1 msec  after), Na+ no longer coming in, hyperpolarize

5. Undershoot

6. Absolute Refractory Period

7. Relative Refractory Period

Firing Frequency of AP reflects magnitude of depolarization current. Max frequency is about 1000 Hz

Sodium Channel 

When membrane = depolarized to threshold, the molecules twists into a  configuration that allows the passage of Na+ through the pore.

Potassium Channel 

- Does not open immediately =, delayed rectifier

- When the memebrane is depolarized, the subunits are believed to twist into a shaoe that allows K+ to pass through

- TTX- clogs Na+ permeable pore by binding tightly to a specific site on  the outside of the channel (blocks all sodium dependent APs)

AP propagate in one direction, because the membrane just behind it is  refractory due to inactivation of the sodium channels.

AP can be generated by depolarization at either end of the axon, can  propagate in either direction.

AP Paths 

1. Down axon

2. Across axon diameter

∙ The greater the axon diameter, the greater the velocity (Here’s why:  https://www.khanacademy.org/science/health-and-medicine/nervous system-and-sensory-infor/neuron-membrane-potentials-2014-03- 27T17:58:17.207Z/v/effects-of-axon-diameter-and-myelination)

∙ An axon with a larger diameter offers less resistance to the movement  of ions down the axon, causing them to move faster through axon. - Smaller axons require greater depolarization to reach AP threshold and  are more sensitive to being blocked by local anesthetics.

Why? With smaller axons, more of the voltage sodium channels must  function to ensure AP doesn’t fizzle out.

Myelin + Saltatory Conduction 

- APs jump from node to node= saltatory conduction

Nodes of Ranvier- voltage gated Na+ channels concentrated in membrane of nodes  

Synapses 

Electrical- two cells come very close together, connexons come together,  become gap junctions (used by glial cells)

Electrical and Chemical Communication 

Types of Synapses 

a Between axon and dendrites- AXODENDRITIC

b Between axon and cell body- AXOSOMATIC

c Between axon and axon- AXOAXONIC

d Between motor neuron and muscle cell- NMJ Neuromuscular junction

What happens at the synapse? 

Signal Conversion

Electrical signal (AP)  Chemical Signal (NT)  Electrical Signal  (de/hyperpolarization)

4 Stages 

1. Synthesis and Packaging

2. Release of NT

3. Action in postsynaptic cell

4. Termination of signal

NT Synthesis  

Terminal bouton materials - into vesicles

Amino Acids Transmitters 

- Glutamate

- Glycine

- GABA

Catecholamine Transmitters 

- Dopamine

- Norepinephrine (NE)

- Epinephrine (Adrenaline)

Requirements to be considered a NT… 

Monoamines 

- Serotonin (5-HT) - Acetylcholine

Peptide NT 

- Endorphins

- Substance P

- Neuropeptide Y

 1) NT is synthesized by a biochemical process and stored in vesicles  2) Electron Stimulation causes release 

 3) Elicits effect 

 4) Method of termination 

Amino Acids are basis for all NT 

NT are either…

1. Amino Acids themselves

2. Amino Acid derivatives

3. Peptides- strings of Amino Acids

Examples (from Simplest to more  

Complex)

1. Glutamate ------(glutamic acid

decarboxylase enzyme) --

GABA

a. 1 ezyme converts 1  

substance into another

b. 1 precursor, 1 product

2.

3. 7.

8.

9. Acetyl CoA + Choline --- ( choline (ChAT)  

acetyltranferase) - Ach  +CoA

a. 1 enzyme converts 2  substances into  

another product

12.

13. Tryptophan ---- (Tryptophan hydroxylase) - 5-HTP --- (5 HTP  

decarboxylase) - 5-HT  Serotonin

a. Multi-enzymatic  

processes

b. More than 1 enzyme  involved

16.

17.

18.

4.

5.

6.

10.

11. 14.

15. 19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

 43. Tyrosine ---(Tyrosine   Hydroxylase) -  DOPA --- 

(Dopa decarboxylase) -  

Dopamine ----(Dopamine B   hydroxylase) --  

Norepinephrine---- 

(Phentolamine N-  

 methyltranferase) --  

Epinephrine 

 44. (4 Enzymes involved, 3  NT made along the way) 

45.  46. 47. 48.

49. In the above cases, everything needed for synthesis is found in  terminal bouton BUT Peptide ( string of amino acids) NT synthesis  different

50.

 51. Where are proteins made? Nucleus of cell 

52. DNA(coded in genome) –(transcribed into mRNA) RNA – (translated into a protein by ribosomes) protein

53. Peptide bonds attach amino acids together

54.

 55. How are NT packaged 

56. Energy needed to push NT into vesicles against concentration  gradient.

57.

58. Proton Gradient- NT transporter uses protein gradient to drive  concentration of GABA into vesicle

59.

60.

 61. Dale’s Principle

62. 1 neuron = 1 NT

63. any given neuron will only make 1 NT

64. But what about catecholamines?

65. Along pathway of neurosynthesis there are 3 (dopamine, NE,  Epinephrine)

66. If cell is genetically programmed to be dopaminergic, it won’t  make NE and Epinephrine. Pathway stops at dopamine.

67.

68. So Dale’s principal holds to an extent based on genetic  programming

69.

 70. Tight Regulation 

71. Norepinephrine Terminal Bouton

72. End Product Inhibition (Feedback Inhibition)

73. Think of Catecholamine synthesis/pathway as assembly line. 74. Rate of production is dependent on slowest person in the lin.  75. Slowest person = rate-limiting

76. You can control how much and how fast you make your product  by controlling the action of the rate-limiting enzyme, usually the first  enzyme.

77.

78. Excess NT (Norepinephrine in this case) leaks out and feeds back and inhibits the enzyme telling system not to make any more NT, there is NE production stops

79.

 80. How are peptides packaged?  

1. DNA in nucleus mRNA is sent out into cytoplasm

2. mRNA grabbed onto by ribosome

3. Precursor peptide (large protein, not yet NT) is synthesized in rough ER (ribosome makes the protein)

4. Protein moves to loomin of ER, buds off into Golgi apparatus 5. In Golgi Apparatus peptide NT can be chopped up into smaller active  pieces

6. Packaged into secretory granules

7. Transported down axon by axoplasmic flow

8. Once it ends up in terminal bouton it matures in synaptic vesicles 9. Synaptic vesicles stored in terminal bouton

81.

82.  

83.

84. Peptide NT have much higher molecular weight  dense core  vesicles

85.

 86. Release of NT 

87. Otto Loewi

88. 2 Frog Hearts

89. Vagus nerve goes into heart- If stimulated, beating slows down 90. Vaggusstoff  Acetylcholine

91. Accelerancestoff  Epinephrine

92. (balance between acetylcholine and epinephrine controls heart  rate)

93.

94. When AP arrives at Terminal Bouton, vesicles close to membrane  FUSE with itand release contents into synaptic cleft

95.

 96. There are proteins involved in this process 

 97. SNARE proteins- trap and hold the vesicle 

 98. Types 

a. V-snares- found on the vesicle

b. T-snares (target snares) found on inner leaflet

99.

 100. Synaptotagmin- calcium sensing protein

1. When AP arrives at Terminal Bouon, there are voltage gated Ca++  channels that pop open

2. Calcium rushes into the cell, binds to synaptotagmin

3. Vesicle slams down onto the membrane of the terminal buton and  fuses with iy

4. NT released into terminal bouton

101.

 102. Release of Peptides 

103. Voltage- gated calcium channels and vesicles

104. In case of peptide NT, calcium channels are farther away from  where vesicles are anchored

105. More electrical stimulation required.  

106.

 107. Action on Post-Synaptic Cell 

108. Receptor molecules on Post-synaptic cell recognize very  specifically their individual NT (lock and key)

109. Chemical Signal interaction with post-synaptic cell ultimately  alters post0synaptic ell to change membrane potential

110.

 111. How rapidly membrane potential changes in post synaptic cell… 112. Fast-milliseconds

113. Intermediate- seconds

114. Slow- seconds to minutes

115. *depends on mechanisms of receptive signaling 116.

 117. Which direction? 

118. (Hyper/Depolarize?)

119. Depends on the ion whose permeability hs changed (Na+-  depolarize, K+ hyperpolarize, l- hyperpolarize, Ca++ depolarize) 120.

121. Fastest- Ligand (NT) gated ion channel

122. - NT binds in synaptic cleft, changes confirmation (shape) so hole in the middle opens

123. Depending on ion selectivity of hole it will let ion flow 124.

 125. Acetylcholine will usually gate Na+ 

 126. Glutamate will usually gate Na+ or Ca++  127. GABA will usually gate Cl- 

 128. Glycine will usually gate Cl

129.

 130. Many Ligand-Gated Receptors have subtypes 

131. Glutamate (has 3 different subtypes)

1. AMPA receptor

2. NMDA receptor

3. Kainate receptor

 132. G-protein coupled receptors (GPCRs) 

- Single polypeptide chain

- Go through membrane 7 times

133.

 - NT related substances- Major NT that will activate / act through GPCR

 o Acetylcholin e 

 o Glutamate  o GABA 

 o Serotonin  o Dopamine  o Norepinephr ine 

 o Enkephalin  o Cannabinoid 

 - Guanine-Nucleotides 134.

136.

137. *GDP attached to Alpha

subunit

138.

139.

140.

141.

142.

1. NT released into cleft, bind to receptor

2. Changes shape of receptor, gains affinity  

for subunits

3. GTP _> GDP exchange reaction

4. GDP pops off and is replaced by GTP

143.

144.

145.

146.

5. Beta and Gamma always stay together  

6. Activated GTP- bound G-protein splits

7. GTP-ase converts GTP  GDP by removing  

one of the phosphate groups

8. GDP then inactivates alpha subunit

9. Re-associates beta gamma

147. 10. Turns of activation

148.

149.

150.

 151.  

135.  

152. 153.

154.

 155. Two things can happen that will alter the activity of the post synaptic cell 

- Direct effect

- G-protein alpha subunits acts through enzyme  enzyme makes  other chemical messengers in the cell

156.

157.

 158. Direct G-protein signaling 

 159. Muscarinic/ Acetylcholine Receptor

160.  

1. Beta-Gamma floats of and interacts with potassium channel,  2. opens it,  

3. potassium flows out of cell,  

4. membrane potential hyperpolarizes

5. (Acetylcholine chemical signal converted into electrical signal) 161. Takes seconds vs. milliseconds of ligand-gated receptors 162.

163.

164.

165.

166.

167.

168.

 169. Second Messenger Cascade 

170.

171.  172.

1. NT binds to receptor

2. GTp- GDP exchange

3. Alpha-subunit buds off

4. Alpha subunit interacts with enzyme

5. Enzyme produces intermediate chemical second messengers 173.

 174. EX. Adenylyl cyclase system 

175.

176.  

177.

178.

 179. Protein Kinases 

- Protein kinase takes ATP, removes terminal phosphate from ATP (A-P-P P  A-P-P)

- Places terminal phosphate on the protein, changing its activity  (activate it, inhibit it, activate it, close it, etc)

- Process is called phosphorylation

- Phosphatase reverses this process

180.

 181. Cyclic AMP Signaling System 

182.  183.

 184. Receptor- G- protein - coupled receptor (GPCR) 1. G-protein

o Gs (or Gi) alpha I inhibits adenylyl cyclase 2. Effector Enzyme

o Adenylyl Cyclase (AC)

3. Substrate of effector enzyme

o Adenosine triphosphate (ATP)

4. Second Messenger

o Cyclic AMP (cAMP)

o Protein Kinase

o cAMP- dependent protein kinase (PKA)

185.

186.

187.  

188.

 189. Phosphoinositide Signaling Team 

 190. Receptor- GPCR

 191. G- protein- Gq

 192. Effector Enzyme: Phospholipase C (PLC)

193. Substrate o Effector Enzyme: (PIP)

 194. Second Messengers: DAG, IP3, Ca2++

 195. Intermediaries: IP3 receptor, ER (endoplasmic reticulum)  Calmodulin (CaM)

 196. Protein Kinases: PKC, PKA (calcium/calmodulin- dependent  protein kinase)

197.

198. Opening a sodium channel or calcium channel results in a small  depolarization of the cell. These small depolarizations are… 199.

 200. EPSP’s (excitatory post-synaptic potentials) 

- Opening a channel for chloride or potassium results in a small  hyperpolarization

 201. IPSP’s (inhibitory post-synaptic potentials) 

202.

 203. Synaptic Integration  

204. Cell has to collect all of its input in its dendritic tree and send  that message to the spike initiation zone.  

205.

206. Integrate all input and make a determination

207.

 208. Synaptic NTransmission  Quantal 

209. Each packet of NT released from a vesicle is able to depolarize  the post-synapses membrane by some fixed amount – Mini’s add up! 210.

211.

212.

213.

214.

215.

 216. Types of Integration

217.  

218.

 219. Length Constant- a measure of how far depolarization will spread 220.

 221. Increasing the Length Constant 

222.  223.

224.

 225. Passive vs. Excitable 

226. With an excitable membrane, voltage gated sodium channels  spread depolarization further

227.  

228.

229. An inhibitory synapse can cancel out excitatory synapse, the AP  never reaches hillock because negated.  

230.

 231. Terminaton of Singaling 

232. NT removal from synapse

233.  1. Diffusion (not very efficient)- used by peptides

2. Degradation- chemically degrade the NT so no longer active 3. Reuptake- take NT back up to terminal bouton, NT repackaged, very  little is wasted

234.

 235. Calcium- How to Get Rid of It 

236. ATP-ase in ER membrane hydrolyzes ATP to drive it back into the  ER (storage depot for calcium)

237. There are also ATP-ases in plasma membrane where calcium can  be pumped out of the cell

- Also requires ATP hydrolysis

238.

 239. Phosphorylated Proteins 

- Protein phosphatases come in and remove a phosphate group from  proteins

240.

241.

242.

 243. Brain Anatomy 

244.

245. Spinal Cord- grey matter- mostly neuron cell bodies 246. White matter- mostly axons, outside in the spinal cord 247.

248.  

249.

 250. Meninges 

- Structural support and protection of brain

- Brain is floating in a bag of fluid

- Cerebrospinal fluid- fluid that inflates the bag

- Ventricles- generate cerebrospinal fluid

251.

252.   253. Development of Nervous System 

 - We all start from single cell, a fertilized egg 

 - Cell multiply in numbers 

 - Subdivide labor- Differentiation 

254.

 255. Neural Plate 

 - Primary Layers 

 o Mesoderm- on inside 

 o Endoderm- inside wall 

 o Ectoderm- on outside- skin and nervous system develop from this 256.

257.  

258.

259. * Ectoderm pinched off in (d) is the neural tube that will form  spinal cord and brain

260. Neural crest will form peripheral system that’s outside of bone. 261.

262.

263.

264.  

- If neural tube is not zipped up/fused properly in caudal direction it can  lead to spina bifida, some or more of spinal cord exposed in back - If brain doesn’t zip up in rostral direction- brain will not develop anencephaly (no brain) FATAL

265.

266. 267.

 268. Forebrain  

(Prosencephalon) 

269. Diencephalon (Thalamus,  

hypothalamus)

270. Telencephalon (cortex,  

basal ganglia)

271.

 272. Midbrain  

(Mesencephalon) 

273. Tectum- dorsal- roof  

(contains colliculi, hills)

274. Tegmentum- ventral- floor

275.

 276. Hindbrain  

(Rhombencephalon) 

277. Rostral- cerebellum

278. Caudal- Medulla

279.

280.

281.

282.

 283. Cell proliferation and Migration 

284.

285. Where are these cells coming from?

286. Neurons are born from stem cells.  

287. Stem cells are localized around ventricles.  

288. The original ventricle was in the neural tube.

289. The tube pinched off from ectoderm and there was a fluid filled  space down the middle of the tube.  

290. At that zone, more and more neurons are added.  291. They develop, differentiate and crawl away to their final location  (migrate)

292. Most cells born between 5th weeks and 5th month of gestation  and aggressively pruned away.  

293. Apoptosis- Programmed Cell Death

294. Are new neurons born in adults?

295. Mew research says, YES.

296.

297. Experiment to show elderly constantly generate new neurons  throughout life.  

1. Dividing cells need to be labeled

2. DNA in nucleus has to be copied to divide

3. In animal studies, a compound (BrdU) (a version of uridine that is  incorporated in DNA that is being replicated.  

4. Any daughter cell will forever have this compound in DNA 298. *Glial cells- this compound was expected in glial cells because  they are always dividing. Most cancers in brain are gliomas or glial cells  that divide out of control but they also found neurons!

299. 5. Subjects were people who were terminally ill. 300.

301. There were a few hotspots in the brain where neuron generation  was happening

- Hippocampus

- Part of olfactory system

302. (Both brain areas adjacent to ventricles)

303.

304. There is programmed cell death (Apoptosis) in these areas to  keep brain volume within tolerable range.  

305.

306. How do you increase neurogenesis?

- Physical exercise (shown with rats on a treadmill)

- Learning (rats given novel stimulus)

- Death of existing neurons (MS, Alzheimer’s, Huntington’s, Stroke)

o Not nearly enough to keep up with the amount of cell loss - Human study: Neurons positive for cell proliferation marker Beta III tubulin seen in brain area surrounding stroke.

307.

308.

309. Locating Major Structures in Simplified Version of NS 310.

311. ALL IN ONE!

312.

313.

314.

315.

316.

317.

318. MIDBRAIN

319.

320. Fluid in 3rd ventricle funnels into cerebral aqueduct and empties  out into 4th ventricle.

321.

322.

323.

324.

325. Vision: In a nutshell

326. Reception of light by retina in each eye.

327. Processing of information by retina.

328. Optic nerve transmits information to a relay station called the  thalamus 

329. Thalamus inputs sorted.

330. Thalamus inputs begin to be processed

331. Information flows to visual cortex 

332. Visual cortex extracts features from scene: shape, color, distance,  motion

333.

334. Information flow in cortex is both sequential and parallel 335.

336.

337. Light:

338. Electromagnetic radiation 

339. Light lies on spectrum

340.

341.

342. You can characterize different points along the spectrum by the length  of the waves at the point.  

343.

344. Light- longer than x-ray but shorter than microwaves

345. Infrared- can't be detected by eyes (used by TV remotes to send  signals)

346. Ultraviolet- UV, eyes not sensitive to this

347. Visible light- part of spectrum our eye can actually see 348.

349. Photons- particles, minimum unit of light

350.

351. The Eye

352. Light collected by lens, changes its shape to focus the light by the  action of ciliary muscles 

353. Light recorded on retina by photoreceptors 

354. Photoreceptors convert light energy into neuronal activity 355. Transmits image signal down optic nerve 

356. Eyeball pivots by action of oculomotor muscles 

357. Eye adjusts to differences in illumination by controlling pupil diameter 358.

359. Photoreceptors

Tightly packed at the center- fovea (higher resolution at center) 360.

361.

362. Retinal Layers

363.

364.

365. Three Main Functional Stages, Two Synaptic Layers 1 Photoreception (deeper layer, farthest from where the light enters) 2 Internal Transmission

3 Output

366.

367. Light detection occurs in photoreceptors

368. Light signal transmitted synaptically and processed by a series of  interneurons

∙ Bipolar cells 

∙ Retinal Ganglion Cells 

369.

370. At each stage there are laterally connecting cells

∙ Horizontal and amacrine cells (allow synchronization and integration of  input)

371.

372. Axons of retinal ganglion cells bundled into optic nerve which  distributes visual information in the form of parallel action potentials that code  for each visual feature detected

373.

374. Sent on to deep brain regions.

375.

376.

377.

378.

379. Photoreceptors

380. Rods and Cones 

381.

382. Both have inner segment, synaptic terminal, outer segment 383.

384. Rods- low light levels

385.

386. Cones- higher light levels and detection of color

387.

388. Photo- Transduction 

389. Conversion of Electromagnetic energy --> To Chemical --> To  Electrical

390. 1 Photons enter the eye

2 Fall onto retina

3 Photons absorbed by photoreceptor cells in the outer segment 4 Photons transduced into chemical energy

5 Chemical signal to an electrical signal through change in membrane  potential in the outer segment

6 Electrical to chemical at synaptic terminal

391.

392. Rods outnumber cones in retina by about 20 to 1

393.

394. Photo-transduction converts light energy into changes in membrane  potential in the photoreceptor cells

395.

396. Photoreceptors, rather than reacting to a chemical ligand, react to  electromagnetic energy in the form of photons

397.

398. Certain molecules can absorb photons at particular at particular  wavelengths and this causes the molecule to change shape.

399.

400. Rods- conversion of light to chemical signal- protein called rhodopsin 401. Rhodopsin= G-protein coupled receptor = opsin, ligand = retinal 1 Binding of a ligand to a receptor

2 activates G-proteins in the membrane,

3 stimulates generation of cytoplasmic second messenger molecules 4 Second messenger molecules change the conductance of ion channels, 1 changing neuronal membrane potential

1 Rhodopsin- unlike other GPCR's, its ligand retinal is already tightly bound to  the GPCR protein backbone, opsin

2 When photon is absorbed by retinal, the shape of retinal changes, 1 change in opsin backbone 

1 Causes activation of G-protein transducin,

2 changes in cytoplasmic concentration of second messenger molecules cyclic GMP by action of enzyme cGMP phosphodiesterase 3 Leads to modulation of cGMP- gated ion channels and changes in  membrane potential

402.

403. In the dark, cGMP opens sodium and calcium ion channels in  outer segment- depolarizing cell after sodium influx

404. Release NT in dark

405.

406. In light, cGMP depleted, closing ion channels, hyperpolarizing the cell

407. Stop releasing NT in light

408.

409.

410. Amplification- each activated rhodopsin can activate hundreds of G proteins, can activate many phosphodiesterase's, generate thousands of  cGMP molecules

411. This means visual system can detect as little as a single photon 412.

413.

414. Color Vision

415. Cones- can perceive finer detail and more rapid changes 416.

417. Each type of cone has a different visual pigment able to sense different wavelengths of the light spectrum

418.

A S- cones (short wave cones)- detect blue light

B M-cones (middle- wave cones)- detect green light

C L- cones (long wave cones)- detect red light

419.

420. Spectral sensitivity and difference in the signals received from the  three cone types allows the brain to perceive a continuous range of colors 421.

422. Cone receptors- all contain a GPCR protein called photopsin/ cone  opsin

423. Photopsin- able to transduce light  

424.

425. Photopsin portein differs by a few amino acids for each cone type color sensitivity

426.

427. Representing a range of colors- spectral sensitivity curves overlap 428. Different wavelengths of light elicit different levels of responses 429.

430. Tri-chromat- three color vision

431.

432. The color we perceive depends on the overlap of the spectum of the  light with the absorption of the cones across all three cone types 433. Metamers- different patterns that elicit the same percept 434.

435.

436.

437. Deuteranopia: red- green color blindness, individuals lack M-type cones and and green are perceived the same way because they excite thr remaining  cones identically

438.

439. Night vision= scotopic vision- rods far more active than cones 440. Day vision- photopic vision

441.

442.

443. How does retina generate a visual image  

444.

445.

446. Three main specialized cellular layers:

447.

448. Outer nuclear layer- contains rods and cones- Photoreception 449. Inner- nuclear layer- contains interneurons (bipolar, horizontal,  amarcine cells)- Internal Transmission

450. Ganglion layer- contains ganglion cells- Output neurons that generate  action potentials, transmitted via optic nerve to the brain  

451.

452. Ganglion cells- only cells in the retina capable of generating action  potentials

453. All other cells (except amacrine cell types)- respond to stimulation with graded changes in their membrane potential

454. Detection of graded changes in membrane potential harder to record  and study.

455.

456. Kuffler experiements- used cats, able to map region of the screen that  affected the activity of the neurons he was recording from- neuron receptive  field

457.

458. Receptive field- the region of visual space that when stimulated,  evokes a response in the cell

459. For retinal ganglion cells, Kuffler was able to show that the receptive  field was organized in a center surround organization

460.

461. In some cells- response recorded when center of the receptive field  was illuminated

462. Response stopped when part or all of the surround was illuminated as  well

463.

464. Work in the reciprocate- off center-surround organization 465.

466.

467.

468. ON Center

469. Cells -  

470. OFF Center

471. Cells

472. Ganglion cell responses are built from the interactions of the upstream  bipolar and horizontal cells.

473.

474. Each photoreceptor and interneuron can be part of the center and  surround of a receptive field of different retinal ganglion cells

475.

476. Most retinal ganglion cells respond better to small spot of light than to  diffused light because center surround flied enhances sensitivity to edges and contrast  

477.

478.

479. Retinal Circuit

480. Direct pathway of information- input photoreceptor cell through a  bipolar cell to an output retinal ganglion cell,  

481. Lateral pathway- in each synaptic connection btwn cell layers, the  neuronal responses are modulated by the lateral connections of horizontal  and amacrine cells.  

482.

483. Information flow from photoreceptors to bipolar cells 1 Photoreceptors release NT when depolarized (main NT is amino acid  glutamate)

2 Photoreceptors are depolarized in the dark and hyperpolarized in the light 3 Direct Pathway 

a Based on responses to glutamate released by photoreceptors, bipolar  classified as ON or OFF cells

i In OFF bipolar cells- glutamate- gated cation channels mediate a  depolarizing EPSP aafter sodium influx

ii In ON bipolar cells- G-protein coupled receptors respond to glutamate released by photoreceptors via hyperpolarization

∙ (ON or OFF for bipolar cells means cells depolarize in  response to light off (more glutamate) or light on (less  

glutamate)

iii Each bipolar cell receives direct synaptic input from a cluster of  photoreceptors

iv Each bipolar cell also connected via horizontal cells to a ring of  photoreceptors that surround the central direct cluster

v The receptive field to which these cells respond consists of two parts ∙ Circular central area of retina providing direct input from the  photorecptorsm and a surrounding area of retina providing  

indirect input via horizontal cells  

484. Retinal ganglion cell output to optic nerve

485.

486. Things to Know

487.

488. LGN- passes information about color, contrast, shape, and movement  on to the visual cortices

489. Superior colliculus- controlling the movement and orientation of the  eyeball itself , an example of retinotopy because the arrangement of cells in  the colliculus is identical to that of the corresponding cells in the retina 490. Pretectum- controlling the size of the pupil

491.

492. Two major visual pathways

1 Retina to optic nerve to brainstem

2 Retina to optic nerve to lateral geniculate nucleus of thalamus to primary  visual cortex (area 17) to temporal and parietal cortices

493.

494. Decussation- some axons from optic nerves cross over to the other  side of the brain: half of each retina's visual field is represented on each side  of the brain

495.

496.

497. ipRGCs- contain melanopsin (photosensitive), send information to  suprachiasmatic nucleus of hypothalamus, detect overalllight sensitivity,  regulate circadium rhythms

498.

499. Lateral geniculate nucleus organization- keeps visual info separate  based on which eye it is from

500. Magnocellular layers in the lateral geniculate nucleus are in the bottom two layers and receive input from the M-type ganglion cells.  

501.

502. Parvocellular layers of the lateral geniculate nucleus are the top four  layers and receive input from the P-type ganglion cells

503.

504. Koniocellular cells in the lateral geniculate nucleus are in between  layers and receive input from the non-M/non-P ganglion cells.  

505.

506. Corticofugal pathway- from the primary visual cortex to the LGN 507.

508. Primary visual cortex is in the occipital lobe.

509.

510. Spiny stellate cells of the visual cortex- in layer IV

511.

512. Pyramidal cells of the primary visual cortex- are in all layers,  connecting to other brain regions

513.

514.

515. What are sounds?

516. We live surrounded by air, atmosphere is pressing on you, 100,000  newtons for square meter, keeping you from exploding

517.

518.

519. Pressure: force per unit area, pascal

520. Molecules in the air moving around with energies associated with  temperature of the room

521.

522. When an object moves in the air, it pushes on the molecules of air and  creates a wave of molecules that move away from the pushing, when it  retreats, the molecules are sucked back, near field- actual flow of the  molecules

523.

524. If you get much further away, the air molecules are no longer moving  in a flow, movement makes a transition to become pressure changes, no net  flow of molecules, molecules are instead condensing and expanding, far field compressions and rarefactions  

525.

526. Compression- air pressure higher from average pressure in room 527. Rarefied- a short distance away or short time away- atmospheric  pressure lower than average

528. Space-time distribution of changes in density of air molecules

529.

530. Aneroid barometer- reference pressure inside of it, measures  atmospheric pressure

531. Weather fronts and temperature influence pressure.

532. Also measures pressure in relation to altitude

533. Aneroid altimeter- for airplane, on basis of air pressure, tells you how  far you are from ground, as you go up, decrease in air pressure

534.

535.

536. Birds have lagena, organ in inner ear, sealed pressure chamber with a  membrane over it and hair cells for measuring air pressure changes as  manifested in movement of membrane. The lagena is an aneroid altimeter  and barometer for the bird. Bird know its altitude as reflected by excitation of  the nerve fibers that come fro the lagena.  

537.

538. Homing pigeon, not only aware of air pressure in terms of height above the ground, but also air pressure of relatively low frequency propagated  pressure changes that can come from long distances. Thunder is a very  strong, low frequency signal, a homing pigeon can determine a thunderstorm  is approaching. Uses the lagena for navigation. We can't hear such low  frequency sounds, we do not have a lagena.

539.

540. We hear faster fluctuations.

541.

542. A microphone is an air pressure measuring device which measures  high frequency fluctuations of air pressure. It has a small hole in it to prevent  low frequency pressure changes from moving to the microphone diaphragm.  Adjusting the size of hole changes the frequency of sounds you hear.  Principle of Mammalian Inner ear too.  

543.

544. Hertz pressure changes over time,  

545. We normally hear sounds between 20 hertz, 20,000 hertz  546.

547. As sound pressure fluctuations move the diaphragm, voltage changes  come out in the microphone and into a recorder. SUMMARY: Similarly, when  sound pressure pushes ear drum in, a linkage of bones causes fluid to flow  inside the inner ear and you get an electrical response, triggering the  occurance of nerve spikes. Below average air pressure pushes ear drum out  and pulls the bone linkages the other way, alters the flow of fluid inside the  cochlea and the voltage that causes nerve spikes goes down and nerve  spikes stop.

548.

549. Sound Pressure

550. Sound Pressure Changes have two dimensions to them. 551. Intensity- amplitude of the sound pressure waves

552. Amplitude changes in pascals.

553.

554.

555. For higher frequency sounds, you are changing the number of cycles  per second, number of events per second

556. Period- time interval between successive cycles

557. Amplitude- sound pressure change

558.

559. No air= no sound waves

560.

561. Recap: Atmospheric Pressure

562. Air Molecules are compressed and rarefied at source 563. Waves travel from source to ear drum

564. Ear drum moves back ad forth in synch

565.

566. Sound is dissipated as it travels through the air by a molecular process  described as friction. As the sound moves through the air, it warms the air  because some of the energy in the sound is being transferred through the air  thermally.  

567.

568. Under auditory system, we identify different speakers from the  combination of frwequencies present in the sound, pitch of the sound carries  most of the information about vowels,  

569.

570.

571. 20 micropascals- 0.00002- lowest you can hear

572. 10-20 pascals- highest you want to hear

573.

574. In going from pascal scale to dB scale you simplify the representation  of the numbers

575.

576.

577.

578. The Pinna

579. When the sound reaches the external ear, now we are talking about  physiological, biological effects

580.

581. The external ear begins with a horn-shaped pinna, which funnels down  into the ear canal, internal auditory meatus, primary function: having a large  receiving surface, focuses down on a much smaller diameter ear drum,  aperture of the horn, or mouth of horn

582. External ear, the antennae for receiving patterns

583.

584. Relative risk in being able to figure out what's going on in one direction vs not knowing there's a cat coming up behind you in the other direction, a  solution to this illustrated in rabbit or deer, ears are large and can move, we  have smaller external ears and are fixed, but we move our entire head to look at source of sound, automatic reflex steers head

585.

586. Ear drum, tympanic membrane is the end of the external ear, the  inside of the tympanic membrane belongs to the inner ear system. It has a  function related to the movement of sound (vibrations from the air to the  fluids inside the cochlea.  

587. When the sound gets to the bottom of the ear canal it vibrates the  tympanic membranes and that engages the middle ear ossicles (little bones) 588. Ossicles

589. Malleus or hammer, rotates around a center of gravity 590. Incus, anvil, has a curved shape, is attached to malleus, when malleus  moves, so does the incus, the end of the incus is attached to a joint 591. Stapes, stirrup, has a circular footplate, inserts into fluids of inner ear,  fluid travels along spinal cochlea until it finds a place where the freq of the  movement of footplate and stapes matches the properties of basilar  membrane  

592. Basilar membrane varies in stiffness from very stiff at the base of the  cochlea and very unstiff or compliant at spiral tip of cochlea

593.

594.

595.

596.

597.

598.

599. A very stiff structure won't vibrate except at very high frequencies 600.

601. Round window, thin, translucent memebrane, very compliant, when  footplate of the stapes goes in, the round window goes out to releive the  pressure, reciprocal movement by footplate of stapes and round window to  relieve pressure

602.

603.

604.

605.

606. Black arrows above give a sense of the movement of things: the  movement of the tympanic memebrane pushes on the handle of the  hammer, or, the manubrium of the malleus, causing it to rotate  

607.

608. 3 things happening in system to increase sensitivity to hearing 1 Relatively large diameter or the aperture of your external ear compared to the  small diameter at the base of the external ear system (diameter of tympanic  membrane) amplification by 10

2 Tympanic memebrane much larger than the diameter at the footplate of the  stapes, amplification process by gathering energy over the whole tympanic  memebrane and concentrating it (pistum effect, delivering energy to small  surface)

3 Length of handle of hammer and length of incus (a bit shorter) an improvement in force caused by the lever effect of the bones

609.

610.

611. Very dense, inelastic bones, high frequency sounds make it all the way into inner ear

612.

613. Attached to the stapes is a muscle called the stapedius muscle,  attached to the hammer handle is another muscle, the tensor tympani muscle

∙ When these muscles contract, they stiffen the bony structures of the middle  ear system, reducing the sound going into ithe cochlea from the ear drum,  (protective) when you hear a very loud sound, these muscles contract and  

reduce the strength of the sound going into the inner ear, also, when you  vocalize, the sound you are generating is not only going from larynx to the  bone of the cochlea, but from the mouth to the ear,your voice is louder than  you experience it to be because middle ear muscles (stapedius and tensor  tympani muscle) contract (synchronous middle ear muscle contraction)

∙ Middle ear muscle reflex- you hear a loud sound and muscles immediately  contract to impose the protective effect

∙ When footplate of stapes moves in and out, it introduces fluid flow in the fluid inside the vestibular system

614.

615. Spiral Structure of the Cochlea 

616. Human cochlea has about three and a half turns to it 617.

618. Stria Vascularis- privdes ions to operate the inner ear system (battery  to the hir cells)

619. Scala (tube, spiral) vestibuli (up, closer to vestibular organ)- one of two big tubes, the one on top

620. Scala tympani- closer to tympanic memebrane

621. Organ of Corti- assembly of cells, organ for hearing, roughly similar to  eyeball

622. Scala media- middle tube, only place on the body where you can find a strong electrical voltage

623. Perilymph- fills both scalas (vestibuli and tympani) surrounds the organ of corti

624. Reissner's membrane- separates fluid from both scalas 625. Endolymph- fills scala media

626. Tectorial membrane- network roof that reaches over the top of organ of corti, doesn't contain cells

627.

628. Somatic Sensory System

629. Tuesday, October 25, 2016

630. 12:59 PM

1 Exteroception- something from outside world impacting the individual, using  somatesensory system to analyze what is going on

a Mechanoreception (touch)

b Thermoreception (temperature)

c Nociception (pain)

631. *Intimate sensation

1 Proprioception (position)- Where am I in space? Important for planning  movements

2 Enteroception (visceral sensory) (is my stomach full or empty, is my blood  pressure rising?) Focused on what's going on within body)

632.

Outline for SS system 

633. Several sub modalities within somatic sensation

634. Those sub-modalities can be divided into:

a Protopathic (pain and temperature and itch) and  

b Epicritic (touch and vibration)

635.

636. Transduction Pathway- In order to be sensitive to something you have  to transduce physical stimulus out in the periphery first and convert in into a  change of membrane potential. (In visual system, more or less light going into  the eye caused more or less depolarization of those photoreceptors)(In  

auditory system, sound waves moves hair cells, opening and closing potassium channels)

637.

638. Again… THE BASICS

1 Transduce physical stimulus out in the periphery

2 Send info into the CNS

3 Works way up into the thalamus

4 Relayed up into the cortex

5 Perception happens

639.

640. Receptor subtypes (and receptive fields)

641. Receptor density and acuity- relationship between the two ∙ In visual system we saw the fovea has greater density of photoreceptors,  larger number of ganglion cells, better acuity

∙ Auditory system- not as big a difference

∙ Lips or fingertips magnified in central maps, more acuity

642.

o Sensory density and acuity

o Sensory fiber types and central projections

o Topographic mapping in the CNS

o Damage and disease of the SS system

o Nociception vs. Pain

643.

∙ In visual system you have a 2D sensory surface looking out at the world, if  you just map the machinery in retina, to areas in the brain and keep the  register, you'll keep that 2D representation in the map  

∙ In auditory system, map for tone, but no 2D surface sensing auditory  stimulus, it was computed

∙ Somatosensory system, back to 2D surface, surface of the skin, axons from  finger go to one area of brain, axons from wrist go to neighboring area of brain, good topographic mapping

644.

645. Receptor Density and Cortical Magnification

∙ Does density determine cortical magnification (how exaggerated the  representation of that body part is demonstrated in the brain) and acuity (i.e.  central vision highly exaggerated in visual cortex compared to peripheral visual space)?

∙ What other factors may play a role?

646.

647. Are Cortical Maps "Hardwired"

∙ Evidence from training

∙ Evidence from amputation

∙ Phantom limb sensations

648.

649. Is Sensory Processing always bottom up?  

650. Bottom Up is basically- From periphery, to central, to cortex, ultimately  you are conscious of it

651.

i.e.

652. Some stimulus is applied to the surface of the skin,  causes a change in membrane potential of sensory fibers in  my finger, a change in the frequency of action potentials going into my spinal cord up to my brain stem, that gets relayed to  neurons in the thalamus, then primary sensory cortex (S1) ,  then consciousness

653. If you inactivate that relay in thalamus, something could be pressing  on finger and you could be unaware

654. Skin--- brain stem--- thalamus ---S1--- consciousness 655.

656. Top-Down would be anything that comes from the brain and influences  the information as it attempts to go from the bottom up to your cortex (in  visual system thalamic relay neurons, projections backwards from visual  cortex)

657.

658. Two types of skin 

∙ Hairy skin

∙ Glaborous skin- lack of hair (lips, fingertips)

659.

660. Hair cells very sensitive- Axon, hair follicle receptor wrapped around  hairs follicles, stimulus stretches axons and causes action potentials 661.

∙ Some of the axon terminals are really close to the surface of the skin, like  Meissner Corpuscles and Merkel's Disks

∙ Some are buried deep underneath like Ruffini's end-organs and the  Pacinian Corpuscles

662.

663. Meissner Corpuscles and Merkel's Disks- right underneath  glabrous skin, playing important role in fine discrimination and two point  resolution (differentiating coins in your pockets)

664.

665. Somatosensory system- first system where receptive field described  (multimodal- these cells sensitive to touch/temperature), easier to access and record a nerve extracellularly

666.

667. Vallbo & Johansson

∙ Easy access to somatic sensory system, did many of these experiments on  themselves

∙ Put needles through arm, mapped receptive fields

∙ System where following concept were described first  

o Receptive fields

o Parallel processing

∙ Different receptors

∙ Different conduction velocities

o Topographic mapping

o Cortical Magnification Structures

668.

669.

670.

671.

672.

673.

674.

675.

676.

677.

678.

679.

680.

681.

682.

683.

684.

685.

686.

687.

688.

689. Classes of Mechanoreceptors

690. Mnemonic devices:

691. Small and superficial- German- Meissner and Merkel 692. Pacinian, Ruffini- Italian- Large and deep

693.

694. Property of Adaptation- change in presence of physical stimulus that  is activating the cell the most

695. Pacinian corpuscle, for example, have fast adaptation- Response when  pressure is applied, no response when pressure is constant, response when  pressure is removed- fast adaptation

696. Merkel's and Ruffini's ending- respond all the way through 697. (in visual system phasic responses (turn light on, get big  response initially and then it fades away) vs tonic responses (you turn the light on, it fires fast and then it keeps firing while light is on) 698. Meissner and Pacinian- Respond more when stimulus is changing 699.

700. Adaptations can develop in a number of ways:

∙ Circuits- a network of cells that excite and inhibit each other ∙ Could be built into membrane itself, depolarize the membrane, gets really  excited but then some other current comes in, some molecular process  inside the cell gets turned on, it shuts that down, fires a lot at very  beginning and the slows down a bit.  

∙ Mechanical properties of receptors out in the skin- look at Pacisnian  corpuscles, axon contains stretch activated sodium channels o Surface of skin and axons

o Axon has voltage gated sodium channels in it, ready to go o If membrane potential depolarizes beyond threshold, its going to start  generating action potentials

o There are also mechanically gated sodium channels (like with hair  cells)

o If channel is stretched, sodium channels opening

o Action potential

o Little pressure gives little depolarization

o Pressing harder, fire AP at higher frequency

o Frequency of action potentials carries info of amount of pressure

o More pressure, more stretch, more action potentials because more  sodium channels opening

o What can slow down the firing? Another mechanical process

o Pacinian corpuscles wrapped with layers and layers of gelatinous stuff  on the outside

o If you get rid of the encapsulation, and you poke onto the cell, you'll  see the membrane potential depolarize

o If you maintain pressure, gelatinous layers slide off to the side and  relieve the pressure on the side of the axons

o When you pull it away you get a suction effect that draws the  membrane in the other direction and you get another potential as a  consequence.  

701.

702. Why do we have adaptation?

∙ Physical signal first present, you activate mechanoreceptors, aware, but a  few hours later, no longer aware of watch on wrist

703.

704. Why is vibration important?

705. Pacinian corpuscles  

∙ have a characteristic frequency where most sensitive to stimuli ∙ On Y axis, looking at micrometers

∙ If stimulus frequency is less than 10 hertz, even a one mm poke is not  enough to activate Pascinian corpuscles

∙ But if you are poking the skin in and out 300 times/ second, then one  micrometer is enough

706. Meissner's corpuscles

∙ Different characteristic frequency

∙ 50 hertz

707.

∙ Vibration- gives clues about texture

708.

709. 710.

711. Acuity: two-point discrimination

712. Do you feel one point or two points

713. Acuity on finger 20X better than back

714. Maybe density of receptors 20X higher on finger than back 715. Maybe receptive field size 20X smaller

716. Cortical Magnifier 20X greater

717.

718. If lower density receptors, tend to have larger receptive field 719. If higher density receptors, tend to have smaller receptive fields 720.

721. Primary Afferents

722. Afferent information going into the central nervous system, carried  through a number of  

723. different types of fibers

724.

725.

726.

727.

728.

729.

730.

731.

732.

733.

734.

735.

736.

737.

738.

739.

740.

741.

742.

743.

744.

745.

746.

747. What are the differences?

748. Large diameter, high degree of myelination, fastest conducting 749. C- fibers- slow

750. Different kinds of info travel through different axons, some can afford  fast, some slow

751. Why not make everything fast?

752. There's a cost associated with making everything fast, that doesn't  make it worthwhile.

∙ Too many resources to make a big fat axons, wouldn't have enough space,  cell bodies of axons that are really big are bigger, peripheral nerves would be  huge

∙ Reflexes have to be really fast, but sometimes you can get away with a  slower signal

753.

754.

755. 756.

757.

758.

759.

760.

761.

762.

763.

764.

765.

766.

767.

768.

769.

770.

771.

772.

773.

774.

775.

776.

777.

778.

779.

780.

781.

782.

783.

784. Segmental Organization of the Spinal Cord and Dermatomes 785. Cervical - 8 segments

786. Thoracic- 12 segments

787. Lumbar- 5 segments

788. Sacral- 5 segments

789.

790. Arms- cervical and thoracic

791. Legs- lumbar and sacral

792. There is significant overlap so you would have to cut several spinal  nerves in a row before you'd end up with a dead patch of skin, where you  can't feel anything.

793. A reinfection- affects one of these domains like in chicken pox -->  shingles

794.

795. First pathway

796. Dorsal Column- Medial lemniscal Pathway, carries epicritic information  (touch and vibration)

∙ Comes in from the skin through dorsal root of the spinal cord ∙ Travels up the Dorsal column on the same side that it came in (ipsilateral) ∙ Dorsal column nuclei of medulla, first synapse, on the same side(ipsilateral) ∙ Axons coming out of dorsal column nuclei cross the nervous system  (Decussate) in medulla (contralateral)

∙ Ventral Posterior nucleus (VP) of thalamus (contralateral)

∙ S1 of cortex (contralateral)

797.

798. DCML Pathway- Epicritic, touch vibration

799. Spinal cord coming in, splits into dorsal and ventral (ventral is motor  out, dorsal is sensory in)

800. Cell body sitting in dorsal root ganglion

801. All of primary somatosensory fibers are unipolar neurons, (cell body  with one neurite coming out, the neurite splits, one end is out in periphery  (fingertip) and one in medulla))

802.

803. In spinal cord, information is ipsilateral

804.  

805.

806.

807.

808.

809.

810.

811.

812.

813.

814.

815.

816.

817.

818.

819.

820.

821.

822.

823. 824. 825. 826. 827. 828. 829. 830. 831. 832. 833. 834. 835. 836. 837.

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