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All BIL 268 Notes

by: Sydney Marie

All BIL 268 Notes BIL268

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Sydney Marie
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All notes from every class for the semester.
Dr. Lu
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This 50 page Bundle was uploaded by Sydney Marie on Wednesday September 21, 2016. The Bundle belongs to BIL268 at University of Miami taught by Dr. Lu in Fall. Since its upload, it has received 17 views. For similar materials see Neurobiology in Biology at University of Miami.

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Date Created: 09/21/16
Audition III •Encoding of sound intensity -Firing rate (number of action potentials): nervous system can tell the intensity of the stimulus -Firing rate increases (almost linearly) with decibel increase, but levels off at saturation level -After the saturation level, the firing rate cannot increase anymore -Threshold and saturation level can vary between certain types of neurons -Number of active neurons -Weak sound will displace the basilar membrane slightly, while strong sounds will displace the membrane a lot •Neural encoding of sound frequency -Place theory (tonotopy): high frequency will generate maximum displacement at the base, while low frequency will generate maximum displacement at the apex -Tuning curve: Threshold (dB) vs frequency (Hz) -Characteristic frequency: frequency at best sensitivity -Best sensitivity: lowest threshold -Tuning: parameter that represents the sharpness of tuning: CF/FBW -To find bandwidth, go 10 dB up from the threshold, and measure the width of the curve -Neurons are selectively tuned to certain frequencies -If you graph individual neuron response, you just take the lowest thresholds and make a graph (behavioral audiogram) -Phase locking (Volley theory): pure tones -Neurons will fire at the same phase of each period (some at 90 degrees, some at 180 degrees, etc) -Brain measures interspike interval (the time between action potentials) to determine frequency -It is much harder to determine high frequencies because the refractory period is around 1 ms. Theoretically, brain can only detect up to 1000 Hz -To detect higher frequencies, the brain measures the interspike interval over DIFFERENT neurons -If there is a peak, then the neuron is phase locked. If firing is random, it is not •Sound localization -In the horizontal plane -Interaural time differenceL for low frequency (20-2000 Hz) -Interaural intensity differences: sound shadow, for high frequency (2000-20000 Hz) -Neural circuits in the superior olive -MSO: encoding of ITD •Echolocation -Daniel Kish: echolocation using clicks to recognize objects •Auditory Cortex: Primary auditory cortex (temporal lobe) -Six layers: -Binaural interaction: stimulation of one ear results in stimulation of the other ear -Characteristic frequency map -Tonotopy -Isofrequency bands: organized by frequency into bands •Disorders: threshold is shifted up more than 15 dB (hearing loss), more than 90 dB is profound hearing loss -Three types of deafness: -Conductive deafness: ear infection (middle ear filled with fluid) -Sensorineural deafness: Spiroganglion cells (loss of hair cells or spiroganglion cells) hair cells sensitive to antibiotics -Central deafness: central auditory pathways (tumor in cochlea) Action Potential •Properties of action potential: change of membrane potential in a short period of time -To measure action potential: one electrode in the cell, one outside of the cell, a ground electrode, an amplifier, and an oscilloscope display -Membrane potential starts around -65mV, increases to about 35 mV, and then falls back down to the undershoot during an action potential -Rising phase, overshoot, falling phase, undershoot -Generation of action potential -Threshold: lowest membrane potential at which an action potential can be generated -Membrane must be depolarized to the threshold to generate an action potential -As the firing rate increases, the depolarizing current rate increases -Refractory period -After the onset of action potential, another stimulus cannot generate another action potential no matter how strong the stimulus is -The closer a stimulus is to another action potential, the stronger it must be to generate another action potential -Absolute refractory period is from the threshold to the falling phase: another action potential CANNOT be generated •Mechanisms of action potential -Depolarization: influx of Na+ -Repolarization: efflux of K+ -Hyperpolarization: refractory period -Voltage clamp used (Kenneth Cole) to study ionic movement across the cell membrane used on giant squid axon -TTX from pufferfish blocks inward current of sodium ions -Likewise, TEA from poisonous mushroom blocks potassium efflux -Sodium rushes in during rising phase, and then potassium rushes out during falling phase (Huxley and ??) -Patch clamp invented by Sakmann and Neher generates negative pressure to suck up cell membrane and take piece away for experimentation -Noticed that at depolarization, sodium ion channels open -Voltage-gated ion channels -Sodium channels -When membrane reaches threshold, sodium channels open -4 subunits, 6 alpha helices/subunit, four pore loops (ion selectivity) -Hydrated sodium ions smaller than hydrated potassium ions, so potassium cannot pass through these channels -Open with little delay (open extremely quickly after depolarization) -Stay open for about 1 ms -Cannot be opened again by depolarization until Vm reaches threshold -TTX blocks voltage gated sodium channels -Brevetoxin-3 is a sodium ion gate activator, and causes hearing loss of fish when injected at a sublethal dose -Potassium channels -Open with 1 ms delay -TEA channel blocker -Structure similar to sodium channels -1) Sodium channels open during rising phase 2) Sodium rushes in and causes depolarization 3) Falling phase: Na channels inactivate and K channels open, causing K to rush out and depolarization 4) Undershoot: channels working too well, too much K rushes out causing hyper polarization towards Ek (all sodium channels closed) 5) Absolute refractory period: Na channels inactivate, cannot generate AP 6) Relative refractory period: difficult to generate AP -Sodium/potassium pump reestablishes the concentration gradient after the action potential is generate -If there was a drug that blocked the sodium/potassium pump, the gradient would not exist and thus action potentials would be impossible (resting membrane potential would be 0) •Action potential conduction -Moves about unmyelinated axon relatively slowly, but the myelin sheath speeds it up -Potential does not travel back to the cell body because of the absolute refractory period -The larger the diameter, the less resistance, and faster the action potential -Spike initiation zones: axon hillock and sensory neuron Brain Control of Movement •Descending pathways -Two pathways: lateral and ventromedial (dependent on location of the fiber tract) -Lateral pathway: corticospinal tract and rubrospinal tract (gray matter on the lateral side of the spinal cord) -Ventromedical: medullary reticulospinal tract, pontine reticulospinal tract, vestibulospinal tract, tectospinal tract -Lateral pathway: voluntary movement that originates in the motor cortex -Descends contralaterally -Rubrospinal tract: evolutionarily old, red nucleus receives input from ipsilateral side -Corticospinal tract (pyramidal): large pyramidal cells -Lesions in corticospinal lesions -Deficit in fractionated movement of arms and hands due to damage -If it is completely cut, then paralysis on contralateral side -Recovery if the rubrospinal tract remains intact -Rubrospinal lesion reverses recovery -Ventromedial pathway -Posture and balance; originates in brainstem -Vestibulospinal tract: bilateral innervation down spinal cord, head balance and head turning -Tectospinal tract: orienting response originating in the superior colliculus -Pontine and medullary reticulospinal tract (ipsilateral descent) -Pontine: enhances antigravity reflexes (supporting of the body) -Medullary: liberates antigravity muscles from reflex •Motor cortex -Area 4 (M1) and Area 6 (SMA & PMA): M1 is posterior to the central sulcus -Area 6 is anterior to Area 4 -2 subparts to Area 6: SMA (distal motor units) and PMA (proximal motor units) -Coding of movement -Monkeys could control a robotic arm with their brains -Direction vector: amplitude and direction -Sum of direction vector is the population vector PV=(X1+X2), (Y1+Y2) -You can predict movement by adding the vectors from each neuron •Basal Ganglia -Know individual nuclei in basal ganglia -Basal ganglia have inhibitory effects -In order to have normal movement, there must be a balance of excitatory stimuli and inhibitory stimuli -Basal ganglia nuclei -Striatum: composed of putamen and caudate nucleus, target of cortical input to the basal ganglia -Globus pallidus: source of output to the thalamus -Subthalamic nucleus -Substantia nigra -The motor loop -Excitatory connection from cortex to putamen -Cortical activation excites putamen and inhibits globus pallidus (spontaneous) -Release VL from inhibition -Activity in VL influences activity in SMA -Basal ganglia disorders -Parkinson's disease: trouble initiating willed movements due to increase inhibition of the thalamus by basal ganglia -Symptoms: bradykinesia, akinesia, rigidity, and tremors of hand and jaw -Less dopamine neurotransmitters -Dopa treatment: facilitates production of dopamine to increase SMA activity -Huntington's disease: due to gene mutation -Symptoms: hyperkinesia, dyskinesia, dementia, personality disorders -Loss of neurons in basal ganglia -Hemiballismus •Cerebellum -Can be divided into 10 lobules, in the middle is called the vermis -Lies on top of the 4th ventricle -Function: sequence of muscle contractions -Cerebellar lesions -Ataxia: uncoordinated and inaccurate movements -Dyssyngergia: Decomposition of synergistic multipoint movements -Dysmetria: overshoot or undershoot target Brain Rhythms •Electronenchepalogram (EEG, recording of cortex) and Auditory Evoked Potential (AEP/ABR, recording of brainstem) -7 unique peaks and troughs that correspond to 7 different nuclei in the brain -EEG >> 1 microvolt AEP<<1 microvolt -EEG 1) brain activity recorded from scalp (connected to an amplifier) 2) EEG results from synaptic excitation in the cerebral cortex 3) Synchronous activity of many pyramidal neurons -Depending on where the electrode is placed, artifacts can be detected (such as blinking, vibration of the ground, etc) -How are synchronous EEG waves generated? Two hypotheses 1) Pacemaker: one neuron, the "pacemaker", releases a neurotransmitter that affects many other neurons 2) Mutual excitation and inhibition: requires only two neurons (one inhibitory and the other excitatory) with a physical synapse between them -EEG waves 1) Beta, fastest, >14 Hz, activated cortex 2) Alpha: 8-13 Hz, waking states 3) Theta: 4-7 Hz, sleep states 4) Delta: <4 Hz, deep sleep, large amplitude -Functions of brain rhythms: three hypotheses 1) Disconnect the cortex from sensory input (to allow you to rest) 2) Coordinate activity between regions of NS 3) No function, perhaps just byproduct of neuronal activity -Seizures and epilepsy -Seizures result from extremely synchronous brain activity, too many neurons firing simultaneously -Generalized/partial seizure: blackout for a couple seconds -Epilepsy: repeated seizures •Sleep -Universal among higher vertebrates: in dolphins, evidence shows that they shut off opposite sides of their brain. This is their sleep -Sleep deprivation: a human can last 3 days without sleep, any longer will cause neuron damage -One-third of our lives in the sleep state -"Sleep is a readily reversible state of reduce responsiveness to, and interaction with, the environment." -Not much neuronal activity -Do fish sleep? -Sleep deprivation by electrical shock or constant light -Hypocretin -Two states of sleep -REM & nonREM -Somnambulism -PET scans: measurement of 2-DG (deoxyglucose) in the brain via fluorodeoxyglucose -Sleep cycle -Stage 1: non-REM, Theta Stage 2: non-REM, spindle and K complex Stage 3: non-REM, Delta Stage 4: non-REM, Delta Stage 5: REM, Beta Repeat every 90 min -Why do we sleep? 1) Restoration 2) Adaptation -Mechanisms underlying sleeo -Sleep is an active process -DMS (diffuse modular system) --> thalamus ---> control EEG and block sensory input -REM-on cells: ACh in pons -REM-off cells: NE and serotonin in locks coeruleus and raphe nucei •Circadian Rhythms -Chronobiology -Ultradian rhythms: <24 h, sleep cycle, heartbeat -Circadian rhythms: 24 h, sleep-wake cycle -Infradian rhythms: >24 hours, menstrual cycles -Circadian: rhythms with a period of one day -Zeitgebers: environmental time cues -Primary zeitgeber: light-dark cycle -Sleep cycle controlled by internal factors (25 h clock) and environmental factors (light-dark cycle) -Internal biological clocks -Suprahiasmatic nuclei (SCN) in hypothalamus: luminance -NT: GABA -Light sensors (retinal GCs) --> clocks --> output -Benson and colleagues: Discovered specialized type of ganglion cell in retina -Photoreceptors, but not rods or cones -contain melanopsin, slowly excited by light -Synapses directly onto SCN neurons -Molecular clocks similar in humans, mice, flies, mold -Clock genes: Period (per), Timeless (Tim), Clock, know flow chart below per mRNA PER protein tim mRNA TIM protein increase in [PER/TIM dimers] dissociated PER transported into nucleus PER binding to CLK/CYC transcription factor removal of CLK/CYC from promoter of per & tim turn off per & tim Audition 1 •Properties of sound -Frequency (period): pitch, cycles/sec (Hz), F=1/T -Amplitude: loudness, decibel (dB), SPL=20(log(P/Pref)) -T=sec -Pref=0.0002 dynes/cm^2 -P=F/A -You cannot compare sound unless they have the same reference level -Starting phase: -Pure tone 1000 Hz: not in the natural world -Fourier's theory: a complex sound is equal to a sum of simple sounds. Convert time-domain to frequency-domain -Audible range: 20-20000 Hz, hearing loss is loss of high frequency hearing -Anything below the green line, we cannot hear -In a workplace, if an employee must work in 85 dB conditions for more than 8 hours, they must provide hearing protection -Higher than 20,000 Hz= ultrasound, below 20 Hz=infrasound •The ear -Structure and function -Pinna=earlobe -Outer, middle, and inner ear -Antibiotics can kill auditory receptor cells -Three pairs of tiny bones (ossicles) -Middle ear: change air to fluid -Tympanic membrane and 3 ossicles -Outer ear: pinna, auditory canal -Catch and funnel sound -Inner ear: cochlea, 2 otolithic organs (saccule, utricle), 3 semi-circular canals with ampullae -Balance -Auditory pathway stages: sound waves, tympanic membrane, ossicles, oval window, cochlear fluid, sensory neuron response via auditory vestibular nerve -The middle ear: impedance matching Pt(At)=Po(Ao) -Amplifier -Eustachian tube connects our ear to our mouths -The attenuation reflex -Response where onset of loud sound causes tensor tympani and stapedius muscle contraction -Function: adapt ear to loud sounds, understand speech better -Three canals of cochlea: scala vestibule, scala tympani, and one that contains endolymph. Scala vestibule and scala tympani filled with perilymph -In perilymph, sodium content is high and potassium content low -In endolymph, sodium content is low and potassium content high -Stria vascularis absorbs sodium -Organ of Corti: sits on top of basilar membrane (very flexible to allow vibration) -Inner hair cells and outer hair cells: humans have more outer hair cells -Tectorial membrane on top of Organ of Corti, which bends hair cells upon vibration to activate them -Hair cells innervated by spiral ganglion cells -Rods of Corti separate inner hair cells and outer hair cells: on the top, called the reticular lamina -Outer hair cells serve as acoustic amplifiers -Two types of spiral ganglion cells -Type I: large, 95%. Innervate inner hair cells, one IHC to many SGCs -Type II: small, 5%, OHCs, many OHCs to one SGC Audition II •Efferent fibers: fibers that send messages from the brain to regulate auditory receptor cells -The basilar membrane -Base: narrow, stiff, high freq. -Apex: wide, floppy, low freq. -Labyrinth=bony structure outside the cochlea -Vibration of the oval window will vibrate the scala vestibuli -von Bekesy's traveling wave model -Hole in cochlea called helicotrema -Hair cells (Ciliary bundles) -Shape of hair bundles can be w or v -Hairs are tiered, so when the are moved from short hair bundles to high hair bundles, they are innervated. The other way around inhibits -Auditory and vestibular hair cells -Gap in W called stereo cilia or kinocilium -Vestibular hair cells: you can find kinocilium for each hair cell -Hair cells: mechanically gated ion channels (NOT voltage gated) -K+o>K+i -Ends of hairs are connected via tip links -you can find mechanically gated ion channels in the lower end of the tip links (NOT higher end) -TRPA1 channel has nothing to do with hearing (correct the book) -Channels open and potassium rushes in -Some tip links cause tenting due to the high pressure -TMC 1 and TMC2: connected to ion channels? -Hypotheses: connected to the MGCs or are they the MCGs? •Ear can generate sound as well as receive sound -Otoacoustic emission -Electromotility of OHCs -Motor protiens--> length change of OHC--> cochlear amplifier -Prestin: Peter Dallos' Lab: HC gene -Prestin is protein underlying electromotility •Central auditory pathways •Spiral ganglion connected to cochlea •Medulla: cochlear nucleus, superior olivary complex, inferior colliculus, MGN, auditory cortex (ascending input) Chemical Control of the Brain and Behavior •Hormones are chemicals released into the blood, and via the blood will reach its target structure •Neural hormones are released by the hypothalamus •The hypothalamus -General function: homeostasis; maintenance of a constant internal environment (temperature, blood pressure, salinity, and more) -Underneath the dorsal thalamus and posterior to the optic chiasm, also in the anterior wall of the third ventricle -Hypothalamus controls chemicals released by the pituitary gland -Can be divided into three layers: lateral, medial, periventricular -Pathways to the pituitary 1) Hypothalamic control (periventricular) of the posterior pituitary: magnocellular neurosecretory cells --> neurohormone --> blood capillaries -Oxytocin: ejection of milk -Baby cry --> Mom's auditory system --> hypothalamus --> magnocellular neurosecretory cells --> oxytocin --> blood --> breasts --> milk (the hormone is released into the posterior pituitary gland) -Loss of blood --> blood pressure low or no water --> blood salt concentration high --> hypothalamus --> magnocellular neurosecretory cells --> vasopressin--> blood --> kidney --> reduce urine --> water retention -In the pituitary: posterior pituitary is an extension of the brain (nerve tissue), where the anterior lobe of the pituitary is not part of the brain (only secretory tissue) 2)Hypothalamic control of the anterior pituitary gland: parvocellular neurosecretory cells--> hypophysiotropic hormone release --> blood --> hormone secreting cells in anterior pituitary --> hormones --> blood --> action of various organs -Stress --> Hypothalamus --> Corticotropin releasing H (CRH) --> Blood --> H. secretory cells in anterior pituitary --> Adrenocorticotropin (ACTH) --> Blood --> Adrenal gland (cortex) --> Cortisol --> Blood --> mobilize energy reserve and suppress immune system -Adenohypophosis is another name for the anterior pituitary •Autonomic Nervous System - ANS (visceral NS): PNS innervating internal organs, blood vessels, and glands, not under voluntary control -Central control: hypothalamus and solitary nucleus: sensory input --> solitary nucleus --> hypothalamus --> preganglionic neurons -Sympathetic and Parasympathetic 1) Sympathetic: thoracic and lumbar, fight or flight, short preganglionic fibers (closer to the spinal cord), preganglionic release: ACh and postganglionic release: NE 2) Parasympathetic: brain stem and sacral, normal conditions, long preganglionic fibers, ACh -All release ACh from preganglionic neurons -All are ACh nicotinic receptors, except for the parasympathetic synapse at the smooth muscle and cardiac muscle (muscarinic) -Muscarinic: G-protein coupled -Nicotinic: ion channel •Diffuse Modulatory Systems: each neuron in the brain is sending out many branches of axons that innervate target structures (hundreds of thousands of synapses) 1)Norepinephrine system -Locus coeruleus in the pons -Regulation of attention, arousal, sleep-wake cycle, learning and memory, anxiety and pain, mood, and brain metabolism 2) Serotonin system -Raphe nucleus in the brainstem -Control of sleep-wake cycle, mood, and emotion, REM -4 pairs of Raphe nuclei in the brain -LSD is the agonist of serotonin 3) Dopamine system -Substantia nigra and ventral segmental area in the midbrain -Initiation of motor responses and pleasurable sensation -Cocaine and amphetamines block uptake of dopamine (creates excessive dopamine and excessive excitation) 4) ACh system -Basal forebrain complex in the telencephalon (learning and memory) -Pontomesencephalotegmental cholinergic complex: regulates excitability of sensory relay nuclei -Alzheimer's disease: degeneration of cholinergic neurons in the basal nucleus of Meynert Final Exam Review •52 multiple choice questions, 104 possible points •Spinal Cord Control of Behavior -Know different types of lower motor neurons and their differences: alpha, gamma -Slow and fast motor neurons, what is a motor unit? -Mechanisms underlying muscle excitation, relaxation and contraction -Four reflexes -Myotatic reflex vs reverse myotatic reflex -Cross extensor reflex -Two types of sensors in the skeletal muscle: muscle spindle and Golgi tendon -Muscle fibers: introfusal (innervated by gamma neurons) and extrafusal -1A is sensory fiber -Compare Golgi tendon and muscle spindle -Spindle: muscle stretch -Tendon: tension -Function of gamma motor loop -Central pattern generator •Brain control of movement -Lateral descending pathways and ventromedial descending pathways -Know general function of each descending pathway -Motor cortex: primary motor cortex (M1) (where is it?), Area 6, PMA & SMA -Basal ganglia (structure and function) -Neural coding of movement: direction vector, population vector -Somatotopic map of motor cortex: three primary characteristics -Motor homunculus •Chemical control of brain and behavior -Hypothalamus and pituitary gland -ANS: Sympathetic and Parasympathetic 1)Length of axons 2)Neurotransmitters 3)Location of nuclei 4)Chemical function -Diffuse modulatory system: definition, four subsystems -DA, 5-HT, ACh, NE -Neural hormones and examples •Emotion -Cannon-Bard and James-Lange -Brain structures underlying emotion -Limbic system, Papez circuit -Fear and aggression -Experiments and conclusion -Kluber-Bucy syndrome -What experimental evidence shows amygdala is related to fear? -Neural circuit of learned fear -Types of aggression and brain structures for each, hormones and neurotransmitters -Pleasure and displeasure centers: which neurotransmitter is involved in pleasure center? •Brain Rhythms -EEG -How to record EEG -How compared to ABR -Different types of EEG waveforms: DTAB -Seizures and epilepsy -Why do we sleep? -Sleep cycle -Circadian rhythm -Primary zeitgeiber -Brain clock, where to find -Which genes? PER and TIM •Language and Attention -Which cerebral hemisphere is dominant in language processing for most people? -Two important language areas and where are they located -THree different types of aphasia -Two hypotheses of processing spoken language -Split brain cases -Which experiment supports that right hemisphere can read but not speak? Setup and conclusion -Attention can shorten reaction time -Attention can increase neural responses -Three common techniques used in research language processes -What is neglect syndrome •Wiring the Brain -3 steps of the genesis of neurons: proliferation, differentiation, migration -Development of the cortical layers is inside out -3 phases of the genesis of neuronal connection -What is the growth cone? -Synaptic formation is bidirectional -Chemoattractants and chemorepellants -Hebbian modification -Critical period -Apoptosis -Synaptic plasticity •Learning and Memory -Different types of memory -Two different types of amnesia -What is the engram, physical location of memory -What brain structures are related to memory -Hippocampus -Procedural learning: non associative learning -Lowry -Animal model -What behavior? -Molecular basis -Habituation -LTP: long term potentiation and depression -Which brain tissues? -Brain GPS: place neurons Exam 1 Review -50 MC questions evenly distributed -Bring calculator for Nerst's equations: must make sure the membrane is permeable to that type of ion - Eion= 2.303 (RT/zF) log 1([iono]/[ioni]) -Remember that Z=charge of ion and the rest are constant -Answer will be in V -At that voltage, the membrane will be completely permeable to that ion -To calculate the real membrane potential -Vm-Eion -Sample Qs 1) Water make an effective solvent of other polar molecules because a) the hydrogen atom has a greater affinity for electrons b) the oxygen atom acquires a positive charge c) of the electrical polarity d) of the electrical charge 2) What would happen if all impermeable anions within a neuron suddenly became permeable? a)the membrane potential would remain unchanged b) the cell would be slightly depolarized c) the cell would be greatly depolarized: because of the efflux of anions in the cell, membrane potential travels toward 0 d) the cell would be slightly hyperpolarized e) the cell would be greatly hyperpolarized 3) The equilibrium potential of an ion is the point at which there is: a) no concentration gradient driving the ion b) no electrical gradient driving the ion c) no movement of the ion across the membrane d) no net movement of the ion across the membrane 4) Temperature is a factor when figuring the equilibrium potential of an ion? a) true b) false 5) What is the approximate concentration of Na+ outside the neuronal membrane? a) 100 mM b) 150 mM c) .0002 mM d) .0005 mM • To figure out the direction of an ion, figure out equilibrium potential to see if there is a driving force, and then look at the membrane potential to figure out which direction the ions will move to bring it back to equilibrium potential -Depolarization: becoming more positive -Hyperpolarization: becoming more negative •Know all names of ion channels •Don't worry about the history of neuroscience •Chapter 2: Know major people and their discoveries -Reticular theory, neuron doctrine •Major properties of actions potentials: all or none theory Exam II Review 1) The structure of the eye that is responsible for converting light energy into neural activity is called the a) cornea b) sclera c) retina d) lens 2)Why is the organization of the eye considered imperfect? a) Light must be refracted multiple times before reaching the retina, distorting it b) The black color of the pupil absorbs a percentage of light, allowing less overall light to reach the retina c) The pupil is too large to adequately focus light from distant objects d) Light must travel through many retinal cell layers before reaching photoreceptors, distorting the image 3) Opening potassium channels that are exposed to endolymph would cause a hair cell to a) depolarize b) hyperpolarize c) change its membrane potential d) None of the above 4) In what part of the brain is the fundamental auditory processing for localization in the horizontal plane? a) Inferior olive b) Superior olive c) Cochlear nucleus d) MGN 5) The sensory homunculus in the primary somatosensory cortex a) is an example of somatopy b) reflects the variations in innervation density found in the skin of the body c) reflects the amount of use of skin on different parts of the body d) all of the above Chapters: 8, 9, 10, 11, 12, BRING CALCULATOR Equations dB=20log(p/pref) Q10dB= CF/FBW (Q10dB= parameter for tuning curve, no units; if it is large, then it is sharply tuned) BS= best sensitivity, lowest threshold Rate-level function: spike rate vs stimulus level F=1/T /\= C/F (/\=wavelength) Visual Pathway 1) Retinal ganglion cells, depending upon the location, either project to ipsilateral or contralateral side of the brain. -Nasal half, to contralateral side -Temporal half, to ipsilateral side 2) 2 types of ganglion cells: M type and P type -M project to layers 1 and 2 of the LGN -P project to layers 3-6 of the LGN -M type projected to 4CA and then to layer 4B -P type projected to 4CB and then to layers 2 and 3 in V1 3) In LGN: layers 146 from contralateral, 235 from ipsilateral -On bipolar cell definition: depolarized by light -On center ganglion cell: when light is in the middle of concentric receptive field, depolarized -There will be questions on visual field deficits -Retinotopy Auditory Pathway -Dont worry about vestibular system, don't worry about type 1 and type II cells -Primary function of outer hair cells: electromotility and amplification Taste and Smell -Know the flow charts: in particular, whether they use ion channels or g-coupled protein receptors Somatosensation -Different receptors in the skin -2 type of mechanoreceptors -Pathways of each receptor, projection, at what levels do each cross to the contralateral side -Somatic sensation deficits -Gate theory (pain): inhibitory interneuron that controls pain A1: temporal V1: occipital S1: ??? Language and Attention •Language -Language areas in the brain: left cerebral hemisphere 1) Broca's area: frontal lobe 2) Wernicke's area: temporal lobe -Wada procedure -Used to determine hemisphere dominant for speech: anesthetized one side of the brain and saw what happened to speech -Brodmann areas: Korbinian Brodmann -Aphasia 1) Broca's aphasia (expressive/motor), anomia, agrammatism, paraphasic errors 2) Wernicke's aphasia: fluent/sensory, person can talk, but can't comprehend -Hypothesis of language processing -Wernicke-Geschwind model -Spoken word: reaches A1, goes to Wernicke's area, then arcuate fascicles, to Broca's area and then to motor cortex -Written word: V1, angular gyrus, Wernicke's area, Broca's area, motor cortex -Split-brain studies: corpus callosum -Visual stimulation of one hemisphere -Roger Sperry (19050s) -Split-brain procedure -Sever axons making up the corpus callosum -No major deficits -With proper experiments, animals behaved as if they had 2 brains -Left hemisphere language dominance -Right visual field, repeated easily -Left visual field, difficulty verbalizing -Functions of the right hemisphere: read and understand numbers, letters, and short words (nonverbal response) -Baynes, Gazzaniga, and colleagues: right hemisphere able to write, but cannot speak -Asymmetry in the brain: planum temporale in the temporal lobe -In 65% of people, the planum temporale is larger -Three techniques: -electrical stimulation -positron emission tomography (PET) -magnetic resonance imaging (MRI) -Blood-oxygen level dependent contrast •Attention -Consequences: enhances detection and shortens reaction time -Neglect syndrom: an attentional disorder Learning and Memory •Types of memory 1) Declarative and procedural memory a. Declarative: facts and events b. Procedural: skills or behavior 2) Short term and long term memory a. Short-term: temporary, limited capacity b. Long-term: permanent, greater capacity -Short term memory consolidated into long-term memory 3) Amnesia: problems of the memory a. Retrograde: loss of memory of events that occurred before trauma b. Anterograde: cannot learn new things after trauma •Engram -Physical location of memory -Lashley's study: found that all cortical areas contribute equally to learning and memory. In cutting out parts of the rat's brain, more errors occurred in navigating a maze -Hebb's cell assembly: proposed that memory is stored in synapses, and the same neurons for sensation and perception. But this was found incorrect -Eric Kandel: Short-term synaptic changes involve modification of pre-existing proteins, leading to modification of pre- existing synaptic connections -Long-term synaptic changes involve activation of gene expression, new protein synthesis, and the formation of new connections -When a bird expert was shown a picture of birds, they had more brain activity than a car expert. And when shown a picture of a car, the car expert showed more brain activity than the bird expert •The temporal lobe -Declarative memory -Medial-temporal lobectomy: removal of the medial temporal lobe -Structures: hippocampus, amygdala, and other cortical areas -HM Case (because of severe epilepsy): Severe anterograde amnesia and problems with declarative memory and long-term memory -Delayed non-match to sample (DNMS): experiment of brain lesions done with animal model •Procedural learning a. Non-associative (looking at one stimulus): habituation and sensitization b. Associative: classical conditioning (associating a bell with food) and instrumental conditioning c. Alpysia- gill/syphon withdrawal reflex with water, monosynaptic 1)Habituation: presynaptic modification 2)Sensitization: serotonin, G-protein coupled receptors -IN L29: receive sensory input from the head, and synapses on the terminal of the sensory neuron, and modulates the sensory neuron •Procedural learning •Long-term potentiation and depression (LTP & LTD), increase in effectiveness in the synapse. Result of increased calcium, LTP, resulting in low calcium, LTD Introduction to Neurobiology •Animal Welfare: -Animal Welfare Act of 1966: to protect certain animals from inhumane treatment -Inhumane treatment produces unreliable results due to stress on the animal -USDA monitors this, but only defines animals as as warm-blooded species except for rats, mice, birds, and farm animals -Inspects covered species annually -To use any animals in labs, must submit "assurance statement" to OLAW -"The Guide" defines animals as vertebrates and outlines proper care for lab researchers -No specific regulations for invertebrates -IACUC evaluates its facilities and programs at least twice a year -Institutional Animal Care and Use Committee (IACUC) okays research proposals -AAALAC has higher standards and accredited facilities inspected by reps every 3 years -Three R's: -Reduction: use statistics to reduce the number of animals needed to reach research goals -Refinement: finding a better way to achieve research results -Replacement: Replace animals with other techniques or models •Animal Rights: -An increasingly violet position held by a minority who seeks to abolish all animal use in experiments -Animals have the same legal and moral rights as humans -Animal models: c. elegans, insects, squid, zebrafish, rodents, monkeys •General things about animals in research: -The more basic the research question at hand, the more distant the evolutionary relationship can be between the species and humans -Most of the animals used for research are rodents and mice •Nervous System Disorders -Alzheimer's & Parkinson's Disease: progressive degeneration of specific neurons in the brain Neurons and Glia •There are approximately 1 trillion cells in the brain -Neurons and glia -Glial cells outnumber neurons tenfold and their role is to support, nourish, and insulate neurons -Most cannot generate action potentials and do not have axons. They support the extracellular environment -Neurons (the elementary unit of the nervous system) sense changes in the environment, communicate these changes to other neurons and command the body's responses to these changes •The Neuron Doctrine -Neuroscience was impossible before the microscope was invented -In the 19th century, scientists learned how to harden brain tissue without disrupting the structure by soaking tissue in formaldehyde, which allowed them to make thin slices (using a microtome) easy to study with a microscope -Cajal used the Golgi stain to conclude that neurites of different neurons are CONTIGUOUS, not continuous •Histology: the microscopic study of tissues -Electron microscopy limit of 0.1 nm -Following the breakthrough of formaldehyde, the second breakthrough in neurohistology was the staining of certain types of cells -The Nissl stain allows neurologists to see the nuclei and Nissl bodies of the neuron (rough ER), thus distinguishing neurons and glia from one another -The Golgi stain (soaking brain tissue in silver chromate) pigments the neuronal cell body, which revealed that the neuronal cell body was only a small fraction of the structure of the neuron -Also showed that neurons contain a cell nucleus and numerous thin tubes that radiate away from the central region •Neuronal structure -The central region containing the nucleus is called either the soma, perikaryon, or the cell body - Neurites are axons and dendrites -Axons involved with output of a signal, dendrites involved with reception of a signal -Dendrites have spines containing ribosomes, which are the receiving points -Golgi I neurons: long axons Golgi II neurons: local circuit neurons -Structure of the soma: -Salty cytosol with organelles: Golgi, RER, SER, mitochondrion, etc -Nucleus: gene transcription, expression, RNA processing -Ribosome: protein synthesis (RER) and free ribosomes -Mitochondrion: energy -Neuronal membrane consisting of phospholipid bilayer (hydrophobic tail and hydrophilic head) -Cytoskeleton -Microtubules: polymer of tubulin and dynamic, run longitudinally down neurites -MAPs= mictrotubule associate proteins produce neurofibrillary tangles of dead cells (Alzheimer's disease), but also anchor microtubules to one another -Microfilaments: polymer of actin, closely associated with both soma and neurites and play a huge role in muscle contraction -Neurofilaments: intermediate filaments (only neurons) which are spring like and very strong -Axon -Axon hillock (spike triggering zones), efferent/afferent signals, terminal bouton (end of axon, swollen disk) -No ribosomes -Axon collaterals divided into different fibers (branching of the axon) -Axoplasmic transport: anterograde and retrograde -Terminal arbor is the collective term to describe the dendrites or cell bodies that an axon is transmitting a signal to -Synapse: -synaptic transmission by neurotransmitter or just by ion: synaptic vesicles fuse with the presynaptic membrane to release chemicals into the synaptic cleft -neurotransmitter -presynaptic cleft, postsynaptic cell, and receptor -Dendrites: receptors and polyribosomes •Neuron classifications -Based on # of neurites -Unipolar: one neurite -Bipolar: two neurites -Multipolar: three or more neurites -Based on dendrites (smooth or spiny) -Based on connections (sensory, motor, interneurons) -Based on axon length (Golgi type I and Golgi type II) -Based on neurotransmitters (Cholinergic, acetylcholine) •Glial Cells -Astrocytes: Remove neurotransmitters from the synaptic cleft, control extracellular ions, help determine the growth pattern for neurites -Myelinating Glia: oligodendrocytes (CNS, multiple neurons), Schwann cells (peripheral NS, single neurons). Insulation, wrap around neurons -Ensure that the action potential travels solely down the neuron and not anywhere else -Between oligodenroglial cells, there are bits of exposed neuronal membrane called a Node of Ranvier -Other Glia: ependymal cells, microglia •Transport -Since the cytoplasm of axons lacks ribosomes, they must travel from the soma to the end of the axon -Axoplasmic transport is the natural flow of material from the soma through the axon -All movement of material in the direction of the soma to the axon terminal is anterograde transport, facilitated by the protein kinesin -Movement in the direction of axon terminal to soma is retrograde transport, facilitated by the protein dyenin Neurotransmitter Systems •How to identify NTs -Three criteria: 1) Synthesis, in situ hybridization (some are peptides used as antibodies) 2) Release stimulus --> neurotransmitter release 3) Response microionophoresis (can use current to drive out substance out of pipette if electrically charged) -Immunocytochemistry: localize molecules to cells -Different types of antibodies -Epitope= antigen binding site -First, primary antibody binds to protein, and secondary antibody binds to primary antibody -Secondary antibody topped with fluorescent marker -Ensures signal amplification -Fish have a sheet of sensory epithelial receptors on their ear -Marine biological lab, Shimomura, Chalfie, and Tsien discovered GFP by studying jellyfish -Found that other species express the GFP too -Synaptic mimicry -Molecules evoking the same response as neurotransmitters -Microionophoresis: Assesses the postsynaptic actions -Microelectrode: measures effects on membrane potential -Receptors -NT-receptor binding -Receptor subtype: can evoke completely different response with the binding of the same neurotransmitter to a different receptor type -Henry Dale's principle: proposed that a neuron only contains one type of neurotransmitter (incorrect) -Receptor subtypes: -ACh: nicotinic, muscarinic -Nicotinic= ion channel -Muscarinic= G protein coupled receptors -Glutamate: AMPA, NMDA, Kainate -GABA (inhibitory NT): A, B -Nicotinic receptor: Nicotine is the agonist, Curare is antagonist. ACh binds to receptor, opening of cation channel, influx of Na+ and efflux of K+, depolarization of skeletal muscle fibers, muscle contraction. -Muscarinic receptor: Muscarine is the agonist, atropine is the antagonist. ACh binds to receptor, activation of G protein, opening of G protein gated K+ channel, efflux of K+. hyper polarization of cardiac muscle fibers, heartbeat reduction. •NT Chemistry -Cholinergic (ACh Neurons): Acetyl CoA + choline uses the enzyme choline acetyltransferase (ChAT) to produce ACh and CoA -ACh is broken down by AChE (acetylcholinesterase) to produce choline and acetic acid -Catecholaminergic neurons: involved in movement, mood, attention, and visceral functions -Tyrosine: Precursor for three amine NT's that contain catechol group -Dopamine (DA) -Norepinephrine (NE) -Epinephrine (E, adrenaline) -Serotonergic (5-HT) neurons -Amine neurotransmitter, derived from tryptophan -Regulates mood, emotional behavior, sleep -Selective serotonin reuptake inhibitors (SSRIs)= antidepressants -Serotonin is an excitatory neurotransmitter •NT Gated Channels -Basic structure: pentamer (5 subunits) -For ACh, the nicotinic receptor is on the alpha subunit -Amino acid-gated ion channels -Glutamate-gated channels: EPSP, influx of Na+ -NMDA receptor: voltage dependent, blocked by magnesium ion -GABA and glycine gated channels: IPSP, influx of Cl- (modulators, not antagonists/agonists) -Modulators have separate binding site from neurotransmitter, and binding affects the ion channel in some way -G Protein coupled receptors and effectors -Basic structure -Single polypeptide with seven membrane spanning alpha helices -The shortcut pathway: ACh binds to muscarinic receptor, activates g protein, which activates potassium channel -Second messenger cascades: g-protein couples neurotransmitter with downstream enzyme activation, amplification of signal -Phophorylation and dephosphorylation -Protein kinases attach the phosphate group to a protein, and protein phosphatase removes the phosphate group from the protein. These change the structure of the protein. -Divergence and convergence -divergence: one transmitter activates multiple receptor subtypes, greater postsynaptic response -Convergence: Different transmitters converge to affect same effector system The Chemical Senses •Phenylthiocarbamide (PTC) -Arthur Fox from DuPont Co. lab: discovered PTC test when he synthesized it on accident and his friend said it tasted bitter, but he didn't taste anything -Thus the taste gene was discovered: form 1/form 1 (very bitter), form 1/form 2 (slightly bitter), and form 3/form 3 (no taste) •Five basic tastes: saltiness, sourness, sweetness, bitterness, and umami (deliciousness: monosodium glutamate (MSG)) -Sweet: sugars like fructose, sucrose, artificial sweeteners (saccharin and aspartame) -Bitter: K+, Mg, quinine, caffeine •Taste organs -Tip of tongue: sweetness -Back of tongue: bitterness -Sides: saltiness and sourness -The bumps on the tongue are called papillae -Two types of cells in the taste buds: receptor taste cells -Taste cell receptors die within two weeks -Basal cells -Receptor cells detect membrane potential change: can also generate action potentials, but we do NOT call them neurons •Sensory transduction -Transformation of sensory information by receptor cells to electrical information -Different taste receptor cells have a different membrane potential change (graded) with different tastes •Transduction mechanisms - Uses ion channels and g-protein coupled receptors -Saltiness -Sodium ion channels always open, so sodium diffuses into cell membrane and causes depolarization -However, there are also voltage gated sodium ion channels too and calcium ion channels, and influx of calcium will cause neurotransmitter release -Sourness: acidity, low pH -Increase in hydrogen ions move into cell, and cause depolarization and closure of potassium ion channels (additional depolarization) -Voltage gated sodium and calcium channels open, and then influx causes neurotransmitter release -Sweetness, Bitterness, and Umami: G protein coupled receptors, obviously different receptors for different tastes -Receptor activates phospholipase C, which activates calcium stores in the cell, increasing cytosolic calcium concentration -This causes depolarization of the cell membrane, opening the voltage gated ion channels, causing neurotransmitter release -T1R receptor family or T2R receptor family -Bitter: T2R family receptors -Sweetness: T1R2 + T1R3 -Umami: T1R1 + T1R3 -Capsaicin -Chemical in chili pepper called capsaicin activates thermal nociceptor, and so does heat -Neural coding of taste: there is much overlap in terms of response to different stimuli when it comes to taste -Type III receptors only innervated by nerve bundles (salty, sour) -Type II receptor cells (sweet, bitter, umami) can release ATP to send signal to Type III receptor cells •Central Taste Pathways -Goes to hindbrain, and then projected to the diencephalon (thalamus) and then the cortex -Ipsilateral projection: the opposite of contralateral, taste are projected to the same side -Aguesia: a disease in which taste is impaired •Olfaction -Pheromones -Smell: a mode of communication -Important signals: reproductive behavior, territorial boundaries, identification, aggression -Olfactory epithelium -You can find the olfactory epithelium in the upper wall of the nose chamber -Dogs have an olfactory epithelium 17 times larger than humans: density of receptor cells is also higher in dogs than in humans -Olfactory receptor cells are actually neurons, as opposed to taste receptor cells -Olfactory bulb is a unique receptor cell directly connected to the brain -You can find three types of cells here: lifespan is a little longer than taste cells, about 8 weeks rather than 2 -Supporting cells produce layer of mucus that is required for smell -Olfactory transduction: cAMP gates channels -Odorant molecule receptor protein activates adenylyl cyclase, which creates cAMP using ATP -Increase in cellular cAMP opens cAMP gated cation channels -Calcium and sodium come in, and the increase in calcium open chlorine channels, and chlorine rushes out -This depolarizes the membrane, thus generating an action potential -Central olfactory pathways -Glomerulus is the synapse between the second-order olfactory neuron dendrite and the olfactory receptor cell axon terminal. This is in the olfactory bulb -These are selective: so the senses are already organized when they get to the glomerulus -Neural coding of smell: population coding Somatic Sensation •Mechanical receptors -Bending of the hairs will innervate hair follicle receptors •Four types of receptors -Mechanoreceptors: sensitive to mechanical stimulation -Nociceptors: pain receptors -Thermoreceptors: sensitive to temperature -Proprioceptors: allow you to detect the position of body parts when you can't see them •Receptive field -Can define receptive field for a sensory neuron by taking a probe and seeing what generates an action potential -Pacinian has larger receptive field -Overlapping and not static (dependent upon stimulation) •Mechanoreceptors 1) Pacinian corpuscle: Large RF, fast adaptation, HF stimuli 2) Meissner's corpuscle: Small RF, slow adaptation, LF stimuli -Different discrimination abilities: minimal distance at which you cannot tell that two stimuli are actually one •Nociceptors -Free, unmyelinated nerve endings -Four subtypes: mechanical, thermal, chemical, and polymodal -Skin, bone, muscle, and internal organs -But NOT in the brain tissues -We have headaches because there are nociceptors in blood vessels in the brain and meninges •Thermoreceptors -Cold receptor -Warm receptors •Proprioceptors -Sensing positions of limbs and guiding movements -Muscle spindles and Golgi tendon organs -Primary afferent nerves: dorsal root, size, segmental organization -Spinal cord: cervical, thoracic, lumbar, and sacral -Dermatomes •Primary afferent axons -Fibers innervating temperature and pain are small fibers (no myelin sheath) •Dermatomes Cervical: 8 Thoracic: 12 Lumbar: 5 Sacral: 5 •Somatosensory pathways -Three somatosensory pathways -Dorsal column-medial lemniscal pathway: touch and proprioception -Dorsal column nuclei -Ipsilateral ascension to the brain -When it gets into the brain, crosses over to contralateral side and projected to the thalamus and cortex -Spinothalamic pathway: pain and temperature -Contralateral ascension to the brain -Projected to contralateral side of the brain (thalamus and cortex) -Trigeminal touch pathway: crosses to contralateral side and is projected to the contralateral side of the brain -Parietal lobe: S1, S2, and posterior parietal cortex -Primary sensory cortex: 3b -Secondary somatosensory cortex: 1,2,3a -Posterior parietal cortex: 5, 7 -Rat "Barrel cortex" whiskers of rat Synaptic Transmission •Two types -Electrical synapses and chemical synapses -Most synapses in the brain are chemical synapses -Sir Charles Sherrington first used the word synapse, Otto Loewi discovered the first neurotransmitter (ACH), Furshpan & Potter discovered electrical synapses •Electrical synapses: gap junctions -Connexon: proteins connecting the presynaptic membrane to postsynaptic membrane, allowing chemicals to travel from one cell to another quickly -Small distances -Fast transmission •Chemical synapses -Presynaptic membrane thickens at the terminal -Active zone= the area where neurotransmitters fuse with the presynaptic membrane and are released into the synaptic cleft -Secretory granules: peptide neurotransmitters -Arrival of action potential triggers depolarization of the membrane and triggers response, opening calcium ion channels, influx of calcium ions -Postsynaptic membrane -Neurotransmitter receptors: differ from ion channels in that they trigger a response by being activated or inhibited by a neurotransmitter -Neurotransmitters do not enter the postsynaptic membrane -Types of CNS synapses -Axodendritic: axon-dendrite synapse -Axosomatic: axon-soma synapse -Axoaxonic: axon-axon synapse -Regulate neuronal activity -Presynaptic membrane surrounds the postsynaptic membrane so that depolarization causes membrane potential to reach the threshold and then generate an action potential •Types of Synapses -Gray's Type I: Asymmetrical, excitatory, depolarization -Gray's Type II: Asymmetrical, inhibitory, hyperpolarization -Neuromuscular junction: presynaptic= motor neuron, and postsynaptic is a muscle -Motor end plate innervated by motor neuron terminals -Folding in motor end plate to increase surface area •Neurotransmitters -3 types: Amino acids, amines, and peptides BE ABLE TO NAME SEVERAL EXAMPLES IN EACH GROUP, know EVERYTHING about ACH and its receptors (skeletal muscle, cardiac muscle) -Glutamate: excitatory -GABA: inhibitory -ACh -Epinephrine -Substance P: wrapped around by secretory granules -Amino acid and amine NTs: synthesized in axonal terminal -Peptide neurotransmitters: synthesized in the soma in the rough ER or in the spines in a dendrite -Neurotransmitter release -Depolarization: Ca2+ influx: vesicle docking: NT release by exocytosis -Vesicles move toward presynaptic membrane with influx of Ca -Vesicle SNARE attaches to the vesicle, and target SNARE attaches to presynaptic membrane -Neurotransmitter receptors -Transmitter-gated ion channels that are the receptor for neurotransmitters: fast transmission (membrane protein) -Several subunits -EPSP: excitatory post synaptic potential (depolarization) -IPSP: inhibitory postsynaptic potential (hyper polarization) -EPSP -Binding of neurotransmitter to a receptor causes influx of sodium ions and efflux of potassium ions -Membrane potential is smaller than 0, so influx is dominate -However, if membrane potential is greater than zero, the efflux of potassium becomes dominant, causing hyper polarization and IPSP -When the EPSP reaches the threshold, an action potential is generated -Graded potential: amplitude of graded potential (potential that has not reached the threshold) will decrease as distance traveled increased -Spatial (multiple synapses at different regions of the dendrite) and temporal summation (same synapse generates EPSPs close in time to one another) -IPSP -Binding of neurotransmitter causes influx of chlorine ions causing hyperpolarization -Neurotransmitter receptors -G protein coupled receptors: slow, long, lasting transmission -Autoreceptors: presynaptic membrane to control neurotransmitter release (feedback control) •Neurotransmitter recovery and regeneration -Some diffuse away in the synaptic cleft -Reuptake: neurotransmitter re-enters the presynaptic axon terminal -Enzymatic destruction inside terminal cytosol or synaptic cleft, AChE calves ACh to inactive state -If there is too much neurotransmitter, the receptors will become desensitized •Neuropharmacology -Receptor antagonist: Curare binds to receptors and takes the spot of neurotransmitters, shutting down response of ACh -Receptor agonist (mimic response of neurotransmitters): Nicotine mimics ACh -Defective neurotransmission: root cause of neurological and psychiatric disorders •Synaptic Integration -Dendritic properties -Cable-like dendrite (length constant is the distance at which the percent of depolarization drops to 37%) -By looking at a length constant, we can tell the excitability of the neuron -Quantal Analysis of EPSPs -Quantum: an indivisible unit -Mini EPSP: one synaptic vesicle release -Quantal analysis is used to determine the number of synaptic vesicles that release during neurotransmission -Neuromuscular junction: 200 vesicles, EPSP of 40 mV or more -CNS synapse much smaller -Shunting inhibition -Inhibitory synapse right near the cell body, causes influx of Cl- ions, cancels out EPSP -Rm reduction: resistance of the membrane so signal leaks out -Length constant reduction -Modulation -Synaptic transmission that modifies effectiveness of EPSPs generated by other synapses with transmitter-gated ion channels Spinal Control of Movement •Somatic motor system: skeletal muscles and motor neurons -Types of muscles -Smooth: digestive tract, arteries, related structures -Striated: cardiac and skeletal -Electric junctions in cardiac muscle and smooth m


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