Lectures 3 and 4: Neurophysiology
Lectures 3 and 4: Neurophysiology NSC 3361
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This 7 page Class Notes was uploaded by Rachael Couch on Thursday February 4, 2016. The Class Notes belongs to NSC 3361 at University of Texas at Dallas taught by Van S Miller in Summer 2015. Since its upload, it has received 20 views. For similar materials see Behavioral Neuroscience in Neuroscience at University of Texas at Dallas.
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Date Created: 02/04/16
Lectures 3 and 4: Neurophysiology Neural Signals The Big Picture: How neurons communicate Under light microscope start with nerve cells, then can zoom in see neurons Under electron microscope, can see the synapse synaptic cleft neuronal membrane ion channel Ionic forces underlie electrical signaling Neurons have a semipermeable membrane (a screen door) Diffusion causes ions to flow from areas of high to low concentration, along their concentration gradient Electrostatic pressure causes ions to flow towards oppositely charged areas (electrical gradient) o Like charges repel/move away from each other Cell membrane The cell membrane is a lipid bilayer Ion channels are proteins that span the membrane and allow ions to pass in and out o Necessary because ions are surrounded by water and the membrane repels water Ion channels are mostly closed (gated) Gated channels open and close in response to… o voltage changes o chemicals (drugs, SSRIs, cocaine) o mechanical action (can be physically pulled open) Resting potential Neurons are just batteries – they store charge to use when needed Inside of the axon is negatively charged (60 millivolts) Outside of the axon is positively charged Dead neuron – if electrode put inside, it would read 0 volts Origin of the resting membrane (equilibrium) potential 2 forces act against each other – electrical and concentration gradient o When these 2 balance = reach equilibrium (force driving in = force driving out) o Charge at equilibrium = 60mV (+ or – 10) Neuronal membranes are not permeable to big negatively charged proteins (anions) o Anions are stuck inside the cell unless the cell dies; cannot pass through membrane negative charge on the inside of the neuron Neurons are selectively permeable to K+ it can enter or leave the cell freely o At rest, K+ ions move into the negative interior of the cell because of electrostatic pressure o As K+ ions build up inside the cell, they also diffuse out along the concentration gradient Prevents all the K+ coming in o K+ reaches equilibrium when ion movement out is balanced by ion movement in o Potassium channel is always open; more inside than outside because the proteins inside are negatively charged + The membrane is slightly permeable to sodium ions (Na ) so they slowly leak in o Sodiumpotassium pump pumps Na out and K in, to maintain the resting potential o 3 sodium out, 2 potassium in – net gain = 1 positive charge o Running the pump requires energy 40% of brain energy is used for pumps o Sodium – always trying to get into cell Na + K + Cl Ca2+ Proteins Outside Cell Many Few Many Many Few Inside Cell Few Many Few Few Many Only thing many of in the cell is K+ and proteins Ion channels are selective filters K+ ions pass through this filter more easily than Na+ o Recall: each ion has its own channel Channelopathy – genetic abnormality of ion channels o Ex: epilepsy, migraine, weakness How is the stored charge used? 2 sections of a neuron: graded potentials and action potential Graded potentials o Occur in dendrites o Neuron is always ready to fire waiting for instructions to do so o Info enters at the synaptic site on the dendrite o Inject positive charge (depolarization) response Could be sodium, calcium, or other positive charge More depolarization = more response “Grades” not all or none – proportionate to intensity of stimulation o As graded potentials spread across membrane, they diminish ”Ripples in a pond” get weaker as they get further away from the source o If membrane reaches threshold (great enough positive charge; 40mV) it triggers an action potential Action Potential o Occurs in axons Starts at axonhillock o Large spike in positive charge o “All or none” neuron fires at full amplitude or not at all “Firing a gun” – either fires or doesn’t o Action potentials increase in frequency with increased stimulus strength o Can fire multiple times as long as it has the charge o Conduction speed is faster on a myelinated axon Unmyelinated axon – slow (10 m/s) Stops at every sodium channel Myelinated axon – rapid; fewer stops; only stops at nodes of Ranvier; myelin covers up any other sodium channels so that conduction doesn’t stop there If node of Ranvier is covered up (which happens in MS where you have to remyelinate), the potential may not be able to reach all the way to the end and so will not fire Also requires less energy to conduct the signal Ionic basis of action potential 1) Voltagegated Na channels (in the axonhillock) open in response to initial depolarization (graded potential) o Increase in amount of Na+ outside of the channel increase in pressure on the gated channel which eventually cause the channel to open o Initial depolarization comes from the opening of sodium channels in the dendrites and soma + o Once it reaches 40mV the Na channels open up o Na+ flow down the concentration gradient to the inside of the cell and along the electrical gradient into the negatively charged cell + 2) More voltagegated channels open and more Na ions enter until membrane potential reaches +40 mV o Na goes past 0 because of the concentration gradient; still less sodium ions inside the cell than outside the cell + 3) Voltagegated Na channels close o At peak, concentration gradient pushing Na ions in equals positive charge (electrical gradient) driving them out + 4) As inside of cell becomes more positive, voltagegated K channels open 5) K moves out and the resting potential is restored Refractory Periods – after firing Limits to how fast the neuron can fire Absolute refractory phase (AR) no more action potentials can be produced o Right after reaching + 40mV; very short o Inactivation gate on sodium channel closes Relative refractory phase (RR) only strong stimulation can produce an action potential o Charge becoming more negative, still not restored o Action potentials are regenerated along the axon o Action potentials travel in one direction (axon hillock to axon terminal) because of the refractory state of the membrane after depolarization Inactivation gate = lock on an axon/ion channel Not the same as closing the channel; block at the cytoplasmic side of the channel Happens during refractory periods and prevents the action potential from firing backwards Multiple ion channels along the axon; can’t go backwards because the door to the left is “locked” Sequence of transmission at chemical synapses 1) Action potential travels down the axon to the axon terminal o The point of an action potential is to get the charge to the terminal 2) At the axon terminal, voltagegated calcium channels open and Ca enters the cell o Wants to get in because no/few calcium ions in the cell (concentration gradient) 3) Synaptic vesicles form in the terminal which transmitter molecules in them and then fuse with membrane and release transmitter into the synaptic cleft 4) Transmitter molecules bind to the postsynaptic receptor causing EPSP or IPSP 5) Transmitter may bind to presynaptic autoreceptors, decreasing release o Feedback regulation 6) After binding, the neurotransmitter is inactivated by: degradation or reuptake o Reuptake Molecules pull the transmitters back into the presynaptic neuron Requires energy o Degradation Breakdown/inactivation of transmitter by an enzyme Example: acetylcholinesterase (AChE) breaks down acetylcholine (Ach) Cuts the molecule in half – gets rid of half and recycles choline Raid blocks AChE – causes excess of Ach excessive twitching Postsynaptic potentials Excitatory postsynaptic potential (EPSP) – small local depolarization, pushing cell closer to threshold o Depolarization = moving the charge closer to 0, making the neuron more likely to fire (60 to 50, etc.+ o EPSPs result from Na ions entering the cell, making inside more positive Inhibitory postsynaptic potential (IPSP) – small local hyperpolarization, pushing cell away from threshold o IPSPs result from Cl ions entering cell, making inside more negative o Hyperpolarization = moving the charge further away from 0, making the neuron less likely to fire (60 to 70, etc.) EPSPs and IPSPs are integrated by the axon hillock – more positive than negative charges fire Electrical Synapses Ions flow directly through large channels into adjacent neurons, with no time delay Benefit: faster, allows neurons to synchronize, saves energy Not common because no control/regulation o If one cell fires, they all fire Ex of electrical synapses: heart – want everybody on the same page at the same time Review: + Transmitter release from presynaptic neuron opens ion channels (e.g., Na ) in postsynaptic membrane. This creates a depolarizing current (EPSP) that passively flows down to axon hillock to trigger action potential that is conducted down the axon to presynaptic terminal and the cycle continues, from toe to brain (or brain to toe) Ligands Ligands fit receptors to activate or block them: lockandkey Any substance that binds a receptor is a ligand Endogenous ligands – neurotransmitters and hormones Exogenous ligands – drugs and toxins from outside the body Ex: Acetylcholine Receptor Number of receptors in a neuron varies over time Drug binds receptor causing it to open up allowing ions to follow through Receptor number changes rapidly – esp. during development, with drug use, learning Upregulation is an increase in number of receptors o Ex.: nicotine receptors when you start smoking o = sensitization (not addiction) Downregulation is a decrease in the number of receptors o Ex.: benzodiazepines (Valium, sleeping pills, etc.) downregulate their receptors o = tolerance (also not addiction) Electroencephalogram (EEG) is a recording of brain potentials: A functional test Records brain potentials/brain waves Normal – waves, mini ups/downs in EEG, neurons talk to each other Abnormal spike in EEG Seizure Disorders Reasons for seizures o Bunches of neurons get together and all fire at the same time; cells are linked, they’re not supposed to be; they’re supposed to be independent operators o They become linked together by an electrical synapse o Drugs – decrease sodium conductance; hyperpolarize Could treat a long seizure with valium (hyperpolarizing) About 2% of people have epilepsy Clinical application – 3 triplets; all with seizures; Na+ channel stays open too long, depolarizes cell neuron more likely to fire o Kids can outgrow seizure because of neuroplasticity o INFC Older onset – less likely to go away because of decrease in neuroplasticity with increased age Generalized (wholebody and wholebrain) convulsions – abnormal activity throughout the brain o Characteristic movements are tonic and clonic contractions Tonic = stiffening, rigid Neurons all firing at once, inhibition lost Clonic = jerking Neurons getting tired, rest then all fire at once, repeated o Unconscious during seizure, entire body involved (entire brain involved) o Seizure is followed by confusion and sleep Neurons not firing after normally, tired – act as if in coma Absence seizure – brain waves show generalized rhythmic activity for a few seconds (much slower than tonicclonic), but hundreds of times a day o No unusual muscle activity, except for stopping and staring o Conscious part of the brain turned off but entire brain not turned off because still able to stand, breathe, etc. Entire brain without motor activity o Events during seizure are not remembered o Childhood onset, kids outgrow it, the brain makes the right types of receptors o Neurons fire 3 times/sec instead of 810/seconds like normal Partial seizures o Do not involve entire brain o Start in one area o May have jerking of one side o Can start in one hemisphere and during the seizure transfer to other hemisphere (travel across corpus callosum) o Right face twitching – defect in left hemisphere motor cortex o Reason it’s different from a tick is that it’s rhythmic o Simple partial seizure – normal awareness; can last for days/weeks o Complex partial seizure – impaired awareness; unaware Myoclonic seizures o Rapid, brief contractions of bodily muscles, which usually occur at the same time on both sides of the body o Myo – muscle; clonic – jerk o Chance of severe mental retardation – 98% Types of seizures o Partial onset Simple partial – only seizure with normal awareness Complex partial o Generalized onset Absence seizures (petitmal) Myoclonic seizures Generalized tonicclonic seizures (grandmal) Case: Fugu (pufferfish) A 32yearold man ate three bites of fugu, and then noticed tingling in his tongue and right side of his mouth followed by a "light feeling," anxiety, and "thoughts of dying." He felt weak and then collapsed. Collapse because he can’t breathe – respiratory paralysis; tetrodotoxin (made by pufferfish) – made in the internal organs, have to be cleaned out and thrown away Tetrodotoxin blocks sodium channels, have to have sodium in cell to fire the breathing muscles/diaphragm Tetrodotoxin blocks nerve action by binding to / blocking pores of voltagegated, sodium channels in neuron membranes
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