BMS 300 Exam 2 Notes
BMS 300 Exam 2 Notes BMS 300
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Date Created: 10/09/16
EXAM 2 NOTES 9/21/16 OUTLINE The nervous system as a machine The 3box model o DATA – in – sensory From the periphery o Analysis – integration CNS (brain and spinal cord) o DATA out – motor Biological definitions: o Peripheral nervous system: Sensory in Afferents o “Toward” the CNS Motor out Efferents o “Away” from the CNS o Central nervous system Brain and spinal cord Sensory transduction: o Change in form of energy Conversion to ion movements across membranes o Types of energy: Electromagnetic Mechanical Chemical The neuron doctrine o The neuron as the fundamental structural and functional unit of the nervous system 3Box Model Data in Analysis Data out Take this simple 3 step paradigm and apply it to the nervous system o In this case, the data coming in is sensory information Take the sensory info and integrate it o Motor out As we sit here and currently don’t worry about things like lions, we still have sensory info coming in o We make decisions to sit still, stay put, or leave o The idea of integration is pretty much mysterious Sensory information in: o Sensory afferents means “to carry toward” Integration unit: o Central nervous system (CNS) Brain and spinal cord If we define integration units as CNS, then the sensory info carried toward the integrating unit is the PNS Once you have decided to move (integration), we now go back into the PNS o Motor out Motor efferents (Latin: “to carry away”) Sensory Transduction Changing the energy form o Changing – transducing one form of energy to the movement of ions across a membrane The way the nervous system signals requires the movement of ions across membranes o Generate a battery o Use that energy to signal one neuron to the next Electrical signal o If we’re going to signal from one neuron to the next, the first place we start is the idea of moving ions across a membrane Changing one energy into another Electromagnetic Mechanical Chemical We know what’s going on around us because of these 3 forms of energy o Electromagnetic: light o Mechanical: pressure on skin (for example) Hair cells of the inner ear sensing motion generated by sound waves o Chemical: taste and smell Electromagnetic spectrum: o Violet infrared o Gamma rays radio waves Other animals have different ways of transducing this same information and relating it to their own environment Infrared: heat o Night goggles show the heat signature of some warm object Giving off infrared light Mechanical: o Moving the tips of cells opens channels Ions move across the membrane 9/22/16 OUTLINE The Neuron Doctrine o The neuron is the fundamental functional and structural unit of the nervous system Source of the Doctrine o Santiago Ramon y Cajal o Camillo Golgi Golgi stain o Cellularists Said nervous system is structured with individual neurons o Reticularists Said every neuron is connected to another neuron by cytoplasmic bridges One long mesh o Law of dynamic polarization Says there’s unidirectional flow of info in neurons Structural description of neuron organization o Dendrite, cell body, axon Functional description o Input, conductile, output o Determined by type and distribution of ion channels Cell Biology of Neurons o Logistics of asymmetric cells Axoplasmic transport Fast transport: 200400 mm/day Slow transport: 0.52 mm/day Experiments on transport to determine protein type Neuron Doctrine Argument that the neuron is the fundamental structural and functional unit of the nervous system Cellularists: o Said we have individual cells in the nervous system Began to think about synapse but hadn’t fully formed the idea Reticularists: o Said the nervous system is a connected system There is cytoplasmic continuity among neurons Every neuron is connected to other neurons This conflict was resolved by Camillo Golgi o He was interested in using microscopes to study tissues One of the problems in studying the nervous system is that when you use the standard dyes used for other organs, there were so many nervous cells that you couldn’t differentiate Started using stains Came up with silver nitrate and chromium nitrate salts By using precipitates of silver and chromium, he could begin to see neurons in their entirety o The problem with the stain: only labeled about 2% of cells Santiago Romano y Cahal: o Developed Golgi stain o Could recognize individual neurons Functional Neuron Axon o Can cover long distances o Conductile region o Voltagegated channels Charge sensitive channels Output region: o Vgated calcium channel Govern release of neurotransmitter by exocytosis Dendrite Input region: receives signals from neighboring neurons o Type of transmembrane protein channels o Ligandgated channels Fancy way of saying neurotransmitter operated channels Confined to dendrite and cell body Trigger zone: o Area between axon and cell body where there is a cluster of charged channels o Enough charge here propagates the A.P. down the neuron Asymmetric Organization of the Cell There are microtubules along the axon o Vesicles move along the microtubules Experiments for Axoplasmic Transport There are ganglia cells in the retina o Only cells in the retina that send axons into the optic nerve Optic nerve into brain (thalamus) o Have neuronal cell bodies in retina Proteins made and delivered along axons o Generated two curves on a graph One slow and one fast Slow: Axoplasmic transport (cytoplasmic proteins) Actin Troponin Glycolytic enzymes Made on free ribosomes Fast: Axoplasmic transport (microtubule/vesicle transport) Transmembrane proteins o Made on Rough ER Proteins are synthesized in the slow component o Special enzymes cut out a chunk of the cytoplasm This piece of cytoplasm moves quickly with traffic when it’s riding on microtubules/vesicles (hitch hiker analogy) Movement is intermittent 9/23/16 OUTLINE Glia in the central and peripheral nervous systems o Glia maintain the environment for the neuronal function o Glial cells in the CNS Astrocytes Regulate extracellular environment, regulate K levels and neurotransmitter concentrations Oligodentrocytes Ensheathe axons in concentric layers of myelin (their plasma membranes) Glia in the PNS Schwann cell Microglia Early on, scientists thought these were smaller glia and called them glia o Not actually glia at all Macrophages in CNS o Part of macrophages defense system is to release free electrons Generate hydrogen peroxide May well be damaging viruses and bacteria in the CNS but also killing our own neurons High price to pay o Immune function Neurons electrically excitable cells o Starting energy across a membrane + The K battery o The Nearst Potential E K= RT/ZF ln [K ]0i o Role of Na channels in shifting the gradient Astrocytes in the Glial Cells of the CNS Astrocytes are responsible for regulating the extracellular environment in the CNS In the CNS, we have 100,000,000 of these individual neurons o We have to squeeze all these cells into our brain and spinal cord Very little extracellular space left over So the CNS has minimal extracellular space Space between output region and the neighboring input region of the next cell (12:17) o The output region of this neuron has synaptic vesicles that release neurotransmitters Neurotransmitter is released from neurons, binds to receptors in the input region of the next cell Receptors for neurotransmitters Neurotransmitter binding site: on the input region of the neurons o Channels open and there’s an influx of ions o The gap is tiny between neurons The volume of ions is tiny as well, so it doesn’t take a huge concentration of them to have an effect To keep receptors functioning with such a large concentration of ions in the channels, we need to get the neurotransmitter out of there after it’s bound to the cell to keep the process moving swiftly That’s the job of astrocytes – maintain the extracellular space o Their other role is to use Na/K pumps to control extracellular potassium [K] Plasma membrane of astrocytes: o Receptors are in the membrane that pick up neurotransmitters from the space o Astrocyte clears neurotransmitter in the synaptic cleft Neurons are packed in close together o Little extracellular space CNS Glial Cell – Oligodentrocyte (12:30) Plays the role to form myelin wraps around axons o These wraps are plasma membranes of oligodentrocytes o Turn the neuron with its axon 90 degrees to look at oligodentrocytes (12:32) Axoplasm (cytoplasm) of the axon o The cell body of the oligodentrocyte wraps around and makes contact with the axon’s plasma membrane The end (leading tip) of the oligodentrocyte wraps and “snuggles” under the plasma membrane The leading edge circumnavigates the edge and lays down the 2 plasma membrane layers – squeezes out the cytoplasm so there are concentric rings of oligodentrocytes o Thought to provide insulation around axon membrane Multiple Sclerosis is a demyelinating disease o You can go long periods of time where you’re not bothered by this disease o Myelin sheaths can re ensheathe if they’re damaged but there’s a limited amount of times this can happen People with MS should hold off as long as possible between re sheathing myelin The longer between the attacks of the disease, the better the prognosis We tend to remyelinate in the PNS faster than in the CNS (12:47) Looking at a longitudinal view of an axon of a neuron, there are sections along the axon that are covered in concentric rings of myelin o There are naked regions every so often Nodes of Ranvier The parts of the inner axon that are opposite the Nodes of Ranvier are called intermodal regions 9/26/16 OUTLINE Comparison of oligodentrocytes (CNS) and Schwann cells (PNS) Physiology of excitable cells o Generating a membrane potential and initiating an action potential The Potassium battery o How to stor+ energy cross a+phospholipid bilayer K ions, A ions, K leak channels The Nernst potential E KRT/2F ln (K )0(K) i Role of Na channels + o The Na channel Gated – can open and close o Role of permeability The membrane potential seeks the equilibrium potential for the ion whose permeability is dominant The action potential o Sequential opening and closing of channels o Concepts of voltage gating Change sensitivity o Concept of threshold Point where channels open almost simultaneously Remain open no more than a millisecond or two o Concept of channel inactivation Oligodentrocytes to Schwann Cells Schwann cells: peripheral nervous system (PNS) Oligodentrocytes: central nervous system (CNS) These cells largely do the same thing – play the role of myelination o But there’s a distinction between CNS and PNS: PNS: Schwann cells Neurons can regenerate from their cell bodies and regrow to their targets o Nerves in your bodies (legs, arms, hands, etc) can reinnervate over time CNS: Oligodentrocytes Nerves in your spinal cord and brain do not regenerate o Transmembrane proteins inhibit axon regrowth (12:18) Neurons as Electrically Excitable Cells Potassium (K ) battery o Separation of charge across the membrane (12:21) In a phospholipid bilayer, there are potassium leak channels o Always open Potassium on the inside of the cell is confined in a small concentration Potassium ions bounce across the membrane, find the leak channels, and move down their concentration gradient (in to out) Large impermeant anions are inside the cell (A) Potassium moves from inside the cell outside the cell, and A cells hold the charge steady o Equilibrium: between the tendency of K to leave down its concentration gradient and the tendency to be held in check by the charge on the large negative anion (A ) Nearst Potential: the equilibrium potential for an ion (in this case potassium) is equal to the gas constant + x temperature over 2F times the natural log of the concentration of K over the initial concentration of + K o E K RT/2F ln [K ]/ i o E K 0.58 log [K ]/0K] i o E K 58 log /100 o E = 58 mu K + + (12:33) If we put 100 mm Na ions outside the cell and 10 mm Na ions inside the cell: o Sodium bounces around the membrane, trying to get in or out If we “open the doors” sodium runs down its electrical gradient (out to in) We have to have way more sodium channels than potassium channels + Creates a positive charge as Na E Na RT/2F ln [Na ]/0Na] i E Na +58 m. o (12:38) Polarity switches when the charges across the membrane change + Close Na channels to make potassium the dominant permeability again Voltage gated K channels only allow potassium to pass through (selective) o The difference between these and the potassium leak channels: gate is open Na channels close o Inactivate If potassium channels are all open, the dominant permeability is potassium (12:43) Look at graph Dr. Walrond draws So, o Open Na channels o Depolarizes o Accumulation of positive charge increases the probability of a Na channel opening o Threshold: sodium channels are opening so fast that potassium leak channels are unable to return the membrane potential to E K o All sodium channels open nearly simultaneously 9/28/16 OUTLINE Action Potential Generation o K leak channels E Kse+s membrane potential o Vgated Na channels Charge sensitive Depolarize membrane potential + Ina+tivate to close Na channels o Vgated K channels Repolarize membrane potential o Voltage changes result from charge movement These movements have VERY little effect on ion concentrations o Only gradient available to repolarize membrane is K + Propagating the action potential o Propagation along membrane that only has leak channels Decay/decrement of A.P. amplitude o Propagation along membranes with vgated Na and K channels evenly distributed – unmyelinated 1 2 meters/second o Propagation along myelinated axons Potential is regenerated at each Node of Ranvier Resting Membrane Potential If we put an electrode across a membrane, the Resting membrane potential is about 70 mV + Add voltagegated Na channels to a membrane o Concentration normally of Na outside the membrane = 130 mm + o Concentration normally of Na inside the membrane = 10 mm Since there is a much higher concentration outside the membrane, it’s a chemical gradient This increase in + charge on the cytoplasmic side opens the gate + Na ions can move in through the membrane o Depolarizes the membrane o Goes from 70 mV 40 mV Potassium ions (12+15): o 110 mm K ions inside the cell o 4 mm K ions outside the cell This repolarization due to potassium efflux + o Na channels inactivate closing Charge opens the channel and time with the ball and chain closes it We can use potassium leak channels to bring the membrane potential back + o We use the + charge, which has accumulated inside the cell, to open the vgated K channels We gain speed of repolarization with K gated channels o Delayed rectifier What’s the distinction between the gates and the ballandchain? o They are different parts of a molecule o Ball and chain: down in the cytoplasm o Gates: alphahelical regions that go across the membrane 4 repeats of helical regions (12:28) Sodium channels open really fast but potassium channels take longer o This is why they’re called delayed rectifiers Action Potential Propagation in Membranes that Have Predominantly K Leak Channels All along a membrane, we add potassium leak channels o All must have them if they’re going to generate a membrane potential Begin to incorporate voltage gated sodium channels o Only in one section of the membrane This region has a + charge inside the membrane Gates open and sodium ions flow through the channels into the membrane Positive charge gathers inside This + charge leaks out the potassium channels as K If we take recordings along the cylinder membrane, the potential goes from a large difference in charge to a smaller difference 70 mV 40 mV, then further down is 70 mV 10 mV, then further down is 70 mV 20 mV, etc. What this means is that the charge put into the cell in sodium gated channels rapidly dissipates across leak channels (12:42) If you touch a hot stove, that action potential doesn’t generate past your first knuckle Now look at distributed sodium channels along the membrane: Propagation of Action Potentials in Membranes where VGated Sodium Channels are Evenly Distributed Potassium leak channels all along the membrane But also voltagegated sodium channels evenly distributed along the membrane Sodium comes into the vgated sodium channel o Sodium flows in and tells the next vgated sodium channel to open One opens the next, opens the next, opens the next, etc o If we take recordings in intervals along the axon, we’ll see that we go from 70 mV 40 mV all along the axon o We have regenerated this potential at each of these points by sequentially opening the vgated sodium channels o If we myelinate the axon and have inter nodal regions, only at certain regions these vgated sodium channels can cluster In between the Nodes of Ranvier 9/29/16 OUTLINE Action potential conduction – why is it such a good insulator? o Lipid bilayer as a capacitor Offsetting capacitance before permitting ion movement through ion channels (the negative charge inside have to be offset) Role of myelin in reducing capacitance o Move the inter nodal regions further and further apart Rapid conduction of EMF through salt solution of axoplasm Generator potential to action potential in a sensory afferent o Role of stretch activated channels The number that open is proportional to the strength of the stimulus Charge from generator potential begets action potential Summation of charge at trigger zone Clustering of Vgated channels at trigger zone Producing all or nothing action potential (AP) at trigger zone o AP as an invariant signal Frequency coding with action potentials o Duration of bout of action potentials o Frequency of action potentials in the bout Synapse structure and function o Concept of chemical communication between neurons o Neurotransmitters and their receptors Plasma Membrane Charge and Its Effect on Opening Channels We have negative charges in the axoplasm and positive charges outside the cell membrane The electromagnetic field is like a magnet This separation of charge across the lipid bilayer is said to create a capacitor o The charges are separated from each other by the membrane but they interact with each other Voltage gated sodium channels o Sodium from outside comes in o The charge on sodium is positive o We must discharge the capacitor before opening the vgated sodium channels Looking at a lipid bilayer of an axon membrane: o Nodes of Ranvier along the membrane The unmyelinated sections are similar to the plasma membrane discussed above With the electromagnetic field o Vgated sodium channels open and let sodium in Positive charge The sodium coming in has an electromagnetic field o The myelin sheath that is wrapped around the membrane is made of concentric circles It protrudes out a bit, creating a space between the inside of the membrane and the outside world This region of the membrane is a poor/weak capacitor There are much fewer charges sitting in the intermodal regions than a regular plasma membrane o The electromagnetic field propagates easily from node to node If you block the nodes, there’s an adequate positive charge moving 2 or 3 nodes down the line to open channels Regular plasma membrane: o Channel opens driving force, sodium comes in sodium in has capacity to offset membrane charge more sodium has to come in to offset negative charge because there’s so much Input Regions and Stretch Activated Channels On a hand, imagine the input region is at a finger tip o Input region of a sensory afferent stretch activated channels The number of stretch activated channels that open is proportional to the strength of the stimulus o The more we pull on the membrane, the more channels open o Measure the depolarization produced by stretching the membrane Amplitude of the depolarization is proportional to the strength of the stimulus We need to be able to regenerate this potential o The role of generating the potential falls to the vgated sodium channels o At the trigger zone, vgated sodium channels are clustered o Where does the charge come from? Opening the stretch activated channels Threshold: the membrane potential where sodium influx is precisely balanced by potassium efflux through potassium leak channels o Opening of all vgated sodium channels in the neighborhood 9/30/16 OUTLINE Structure and Function of the Chemical Synapse o The term – synapse To clasp or hold o Concept of receptive substance – (receptors) o Concept of chemicals released from neurons to affect target o Synapse structure Presynaptic element Vesicles, C2 channels, exocytosis, USNARES, TSNARES o Fate of the neurotransmitter Bind to receptor Uptake by glia Breakdown by enzyme Neurotransmitter Effects o Ligandgated ionotropic channels Opened by neurotransmitters They bind to channel swings open ions flow through o Excitatory postsynaptic potential + Na influx Graded depolarization EPSP – decay Gets smaller with distance The Synapse Primary Sensory Neuron: Neuron in a hand: o Input region on finger tip o Cell body located down the arm o On the spinal cord – output region Synapses onto another neuron Vgated channels show beginning of conductile region Neuronal cell body – part of conductile region The synapse: o Site of chemical communication between neurons Sherrington: o Professor at Cambridge o Knew there must be a cite where neurons communicate Synapse Some form of chemical communication Frog Heart Connected to a frog heart is the vagus nerve o The heart beats on its own If we chop the heart of a frog out and put it in a dish, it’ll continue to beat Stimulate the vagus nerve: o Slowed the heartbeat Take a frog heart attached to the vagus nerve and put it next to a frog heart without the nerve o If the solution surrounding the frog heart + nerve is put next to the heart without the nerve, it is still slowed down Tells us that is something released by vagus nerve affecting the heart Acetylcholine Acetylcholine and Action Potentials In order for neurotransmitter to be released from presynaptic cell, Vgated calcium channels are necessary o If calcium is removed from external environment, no NT is released o If channels are blocked, no NT is released When positive charge being delivered by sodium through vgated sodium channels, channels swing open and calcium channels lead to release of NT o Positive charge opens gate, calcium comes in, triggered the fusion of the vesicle of the plasma membrane Exocytosis Had to be influx of calcium into cell to get exocytosis as an end result o But how does the positive charge caused from influx of Ca ions into the cell get close enough to the positively charged vesicle to merge membranes for exocytosis? Snare Hypothesis Snare Hypothesis: Proteins on vesicles and plasma membranes o Some interaction between these proteins led to exocytosis Vesicular membranes: Vesicleassociated membrane protein (VAMP): o Vsnare Postsynaptic: transmembrane protein called syntaxin o Tsnare (target snare) Membrane associated: SNAP 25 o Tsnare (target snare) Needs calcium o Vgated calcium channel When A.P. arrives, calcium comes in o Transmembrane protein called synaptotagmin is a calcium binding protein o Calcium pours through vgated calcium channels and binds to synaptotagmin o Mechanically pulls the membranes together – overcomes the energy repulsion from the positively charged membranes Neurotransmitter is then released in exocytosis 10/3/16 OUTLINE The fate of neuron transmitter and its effect on the post synaptic cell o Released into the cleft o Bind to ligandgated ionotropic channel o Uptake by glia in CNS o Enzymatic degradation in PNS Opening the ligandgated ionotropic channels o Glutamate most common in CNS o Acetylcholine most common in PNS Effect of opening the channel o Net influx (increase of sodium) o Excitatory post synaptic potential (E.P.S.P) o Small depolarization < 0.5 mV Summation at the trigger zone o Individual EPSPs add together o Role of R M embrane resistance) V = IR MOhm’s Law From one vesicle’s neurotransmitter o Role of R Min summation Inhibition o Role of Cl permeability GABA and glycine – operated channels Presynaptic and Postsynaptic Elements Presynaptic element: o Vgated calcium channels allow calcium to come in (enters the presynaptic element) It doesn’t take many molecules to change the concentration Postsynaptic element: o There are ligandgated ionotropic channels on it Can be glutamate receptors Tying to the molecule to allow ions to move CNS: the Neurotransmitter is glutamate o The binding of the neurotransmitter affects the structure of the channel Opens the gate So that sodium runs down its concentration and enters the cell Generates excitatory postsynaptic potential (E.P.S.P) If we imagine that we stick an electrode in this section, there is a depolarization so that 70mV 0.5 mV polarization If we’re going to dump neurotransmitter into the synaptic cleft, the concentration in the synapse rises o We can’t leave the concentration high for long – it must be regulated o In the synaptic cleft, astrocytes from the CNS take up glutamate o The neurotransmitter needs to be vacuumed out of the synaptic cleft to prevent influx of concentration again and again Motor Neurons (12:18) On the output of the lower motor neuron, there are nicotinic acetylcholine receptors (nAchlR) Postsynaptic: o nAchlR is found on the postsynaptic section of motor neurons Presynaptic: 2+ o Vgated Ca channels Extracellular proteins: acetylcholine esterase o Converts acetylcholine + acetate + choline So in the above section (CNS), neurotransmitters are vacuumed out of the cleft In this section (PNS), we use an enzyme to release the neurotransmitters from the cleft space On a Neuron (12:34) Output regions of neurons o Releasing the neurotransmitter glutamate Vgated Na channels clustered at the trigger zone + o Next to vgated K channels The trigger zone: o Decision point Recognizes how much positive charge has arrived Summation of E.P.S.P – drives the membrane potential toward threshold Ohm’s Law: o The change in voltage is equal to the current times the resistance V MIR M Current of number of sodium ions that enter the cell at a synapse A high resistance membrane takes a smaller potential to reach threshold A low resistance membrane takes a higher potential to reach threshold Inhibitory synapses: o GABA and glycineoperated chloride channels 10/5/16 OUTLINE Role of Inhibition in synapse integration o Concept of summation o Role of inhibition Effect on RM o Release of inhibitory neurotransmitters GABA, glycine o Ligandgated ionotropic channel for Cl o Effect of increased Cl on R M Spinal cord organization o Spinal cord structure o We’ll look at a cross section of the spinal cord and divide it into 2 big sets: Gray matter Dendrites White matter Myelinated axons Long distance communication Sensory afferents o Dorsal root ganglia o 1 Pa/segment o 31 segments Motor efferents o Lower motor neuron to muscle o Ventral horn (gray matter) o Ventral root (leading in from periphery to central) Carry sensory and motor information The patellar tendon tap reflex o Stretch receptors in muscle o Synapse of sensory afferent onto LMN o Sensory afferent synapse onto inhibitory interneuron Synapse in the Central Nervous System Ligandgated channels open when two molecules of transmitter bind Potassium leak channels affect the membrane resistance o More leak channels = lower membrane resistance o Fewer leak channels = higher membrane resistance Inhibitory synapses o Presynaptic element o We have lots of these vesicles o In the output region, there are voltagegated calcium channels o 12:20 Release neurotransmitters GABA (gamma amino butyric acid) Glycine Bind to ligandgated ionotropic channels o These ligandgated ionotropic channels are chloride channels when open Anion channel When GABA binds to receptor, it opens a passage for chloride to come in o Hyperpolarizes Due to chloride influx Membrane potential = more negative I.P.S.P. (inhibitory post synaptic potential) With chloride coming in, there is an influx of anions Potassium leak channels allow potassium to go out By changing number of potassium leak channels (increasing it), then you decrease the membrane resistance o It doesn’t matter to the cell if potassium leaves or chloride comes in because it does the same thing to the membrane resistance You can’t change the potassium leak channels, they’re fixed But you can change the chloride channels Effect of Open Chloride Channels on R M Open chloride channels, decrease RM If you have the same number of open cation channels, the current would be the same Time constant o T = duration of the EPSP o Tau = R CM M By changing R Mwe can change amplitude 12:38 When looking at a neuron, we look to see o How much energy is generated in the cell body, how much it excites the trigger zone, which is the analytical part of the neuron, and sending an action potential down the axon in an allor nothing response o Tetanus toxin – all motor neurons fire at once Spinal Cord Organization White matter: conductile regions o Region of action potential propagation Gray matter: input regions o Region of synaptic integration 10/6/16 OUTLINE The patellar tendon tap reflex and ascending pathways o The patellar tendonstretch receptor reflex Input regions of 1° sensory afferent in muscle Synapses directly on lower motor neuron Synapses on to muscle Inhibition of antagonistic muscle Electrical events Generation potential action potential to neurotransmitter release synaptic potential to action potential synaptic potential t action potential in muscle Ascending pathways o DCML (PCML) Tells us where we are in space, where we are in respect to our arms and legs, in respect to what’s around us, etc. 1° afferent nd 2 order neurons – crossed over 34d order to cortex o Spinothalamic tract – carries info about pain, pressure, and temp 1° sensory afferent nd 2 order crosses mid line in spinal cord Whenever you see 2 order, think it’s going to cross over the mid line 3 order to somatosensory cortex o Somatotopy Map of sensory input on post central gyrus – somatosensory cortex o Brown Sequard Syndrome On The Spinal Cord – Patellar Reflex (12:17) Quadriceps muscle has a tendon that attaches to a structure on the knee o Called the patella (kneecap) o The patellar tendon is tied into the bones in the lower leg o There is an input region on the quad 1° sensory afferent Stretchactivated channels Whack the tendon o Pulls on the quad muscle o Sets up a generator potential in the sensory afferent o If its large enough, generates A.P Propagate in the CNS Neuronal cell body travels to ventral horn Remember, everything above midline tends to be sensory And everything below midline tends to be motor Neuron travels through ventral root Out to the spinal nerve There is no inhibition in periphery Primary sensory afferent has a branch o Leads into the white matter of the dorsal posterior columns Neurons have an output region in the brain stem o Known as the dorsal column nucleus Said to be a cluster of neuronal cell bodies In the CNS Ganglia: cluster of neuronal cell bodies in PNS Nuclei: cluster of neuronal cell bodies in CNS Thalamic Relay Nucleus rd o Input regions on 3 order neurons Send processes that form synapses in a region of the brain known as the cerebral cortex Always composed of 6 neuronal cell body layers Input regions of the cerebral cortex Post central gyrus o Somatic sensory cortex Region across the midline: medial lemniscus o PCML (posterior column medial lemniscus) o DCML (dorsal column medial lemniscus) Both proprioception fine touch (12:31)!!!!! Spinothalamic Tract: o Bundle of conductile processes in the CNS o Spino: Cell body for input region o Thalamic: location of the neurons’ output region o Pain sensitive neuron sends a process all the way back in its cell body in the dorsal root ganglia Also sends a process in the CNS Almost immediately after entering the spinal cord and dorsal horn, the primary sensory afferent forms andynapse Synapses on a 2 order neuron This 2 order neuron crosses over the midline and enters the spinothalamic tract Forms a synapse in the thalamus o Sends a process to the cerebral cortex and forms synapse in somatosensory cortex Primary sensory afferent 2 order neuron 3 order neuron What happens if we cut the spinal cord only to the mid line? o What info is spared and what is intercepted? Above the cut still gets through, but what about below? 10/7/16 OUTLINE Brown Sequard Syndrome Somatotopy in the somatosensory and motor cortices o Sensory post central o Motor pre central gyrus Upper motor neuron cell body Internal capsule Skirt around the hypothalamus Cross over to the midline right above the first vertebrae Decussation of pyramids Lateral corticospinal tract Innervation of lower motor neuron Motor unit definition o Innervation of skeletal muscle by lower motor neuron Each individual LMN innervates several muscle fibers but only a small fraction of muscle fibers in a big muscle are activated by A.P. o The NMJ o EPSP A.P. Muscle cell structure Brown Sequard Syndrome If we precisely cut the spinal cord to the midline, what info gets in and what is blocked? o Primary sensory afferent never crosses over the midline nd o 2 order neurons always cross over the midline Importance of ascending and descending pathways in the spinal cord Postcentral Gyrus contains the Somatosensory Cortex Precentral gyrus: dedicated to motor Postcentral gyrus: somatosensory cortex Lower motor neurons dedicated to activated motor in the upper limbs is mostly found in the upper spinal cord Upper motor neuron stays in a bundle in the until the lumbar region where it synapses on the lower motor neuron in a site Motor Cortex of the Precentral Gyrus 6 neuronal cell body layers Layer 5 has a special neuron o Cell body of the upper motor neuron Aka the Betz cell Really big cell Processes out Bundle of conductile regions of upper motor neurons – the internal capsule The upper motor neuron skirts about the thalamus, hypothalamus (known as the diencephalon) o To the brain stem o And to the spinal cord (a continuation of the brain stem) o Area where it crosses over: Decussation of the pyramids Upper motor neuron finds its way to cervical spinal cord o Destined to innervate lower motor neurons that operate the hands o Finds it way into the ventral horn Synapses directly onto a lower motor neuron Leaves the CNS and goes to PNS to synapse on a muscle Root: White mater – carrying conductile processes Horn: Gray matter – neural cell bodies and synapses Lower Motor Neuron Communication with Muscles Innervation of a voluntary/skeletal muscle by lower motor neurons (LMN): o Motor unit: LMN + the group of muscle fibers/cells that it innervates Starts in periphery ventral root finds its muscle When we activate peripheral, certain muscles innervated by the same cell contract Large motor unit may contain one motor neuron and several hundred muscle fibers o Back, legs Small motor unit may contain one lower motor neuron innervating maybe 20 muscle fibers o Hands We determine the force of our muscle contractions by how many muscles we activate o Difference between whacking the C key on a piano versus gently tapping the note o Picking up something heavy, we activate many more muscle units than picking up a penny
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