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Brain and Behavior Exam 1 > Lec 4 Electrophysiological Basis of Neurotransmission > Flashcards

Lec 4 Electrophysiological Basis of Neurotransmission Flashcards

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1
Q

What is Ohm’s Law?

A 
V = I x R
I = V/R
R = 1/g
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2
Q

What is g? units?

A 
conductance = the ease by which charge moves = 1/R
units = Siemens, pS
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3
Q

What is R? units?

A 
resistance = impeding the movement of charge = 1/g
units = Ohms, MW
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4
Q

What is I? units?

A 
current = movement of charge
units = Amps, nA or pA
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5
Q

What is V? units?

A 
voltage = separation of charges across some resistance
units = Volts, mV
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6
Q

What is the inside charge of cell relative to outside?

A
  • inside is negative relative to outside

the potential/voltage = -70 mV = resting membrane potential Vm

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7
Q

What happens to Vm of neuron in response to stimulus?

A
  • goes from -70 mV toward 0 [depolarize]

- reaches a threshold Vm at which all-or-none action potential is triggered

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8
Q

What is capacitance?

A
  • ability to store charge

- capacitance slows voltage response to a change in current

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9
Q

What is Ek? Ena? Ecl?

A 
Ek = -75 mV
Ena = +40 mV
Ecl = -80 mV
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10
Q

What is electrical effect of K flow?

A
  • [K] is high in cell, flows outward

- opening of K channels is hyperpolarizing

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11
Q

What is electrical effect of Na flow?

A
  • [Na] is high outside cell, flows in

- opening of Na channels is depolarizing

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12
Q

What is electrical effect of Cl flow?

A
  • [Cl] is high outise cell, flows in

- opening of Cl channels is hyperpolarizing

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13
Q

What is electrical effect of Ca flow?

A
  • [Ca] is high outside cell, flows in

- opening of Ca channels is depolarizing

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14
Q

At rest whcih of K, Na, and Cl channels are open?

A

At rest K channels are slightly open, Na and Cl are mostly closed

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15
Q

What ion flow triggers action potential?

A

usually voltage gated Na channels opening and Na flowing into cell

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16
Q

What is difference between action potential mediated by Ca vs Na?

A

Ca mediated = broader action potential = lasts longer than Na mediated

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17
Q

What are the ion steps in action potential?

A
  1. at resting -70 mV potential
  2. Na channels opens and depolarize toward +40 mV
  3. Na channels close/inactivate
  4. voltage gated K channels open and repolarize
  5. get “after hyperpolarization” due to open K channels
  6. get back to normal resting -70 mV
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18
Q

What is an example of drug that blocks voltage-gated Na channels/

A
  • all local anaesthetics –> cocaine, lidocaine, procain, etc
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19
Q

What is the axon hillock?

A
  • the starting point of the neuron’s main axon

- synaptic potential summate in cell body, if reach threshold, AP is triggered from axon hillock

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20
Q

What is path of AP leading to neurotransmitter release?

A
  1. AP triggered in cell body and travels down axon
  2. AP reaches nerve terminals
  3. nerve terminals rich in voltage-gated Ca channels that open when nerve terminal is depolarized
  4. entry of Ca into nerve terminals triggers rapid release of neurotransmitter via exocytosis
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21
Q

What is the NMJ?

A
  • specialized synapse between axon from cholinergic motor neuron in anterior horn of spinal cord and the muscle endplate
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22
Q

What two things about the NMJ make it such that muscle cells reliably contract in response to almost ever presynaptic AP?

A
  • there is high probability of ACh release in response to each AP
  • the muscle endplate provides large surface area of nicotinic ACh receptors
23
Q

What is myasthenia gravis?

A
  • disease caused by autoimmune antibodies directed against postsynaptic nicotinic ACh receptor at NMJ
  • most common NMJ disorder
24
Q

What are symptoms of myasthenia gravis?

A
  • muscle weakness
  • ptosis [drooping eyelid], diplopia [double vision], blurred vision
  • worsens with muscle use
25
Q

What is diagnostic test for myasthenia gravis?

A
  • give cholinesterase inhibitor

- if weakness instantaneously relieved = positive sign of myasthenia

26
Q

What is lambert-eaton syndrome?

A
  • autoantibodies to presynaptic Ca channels at NMJ, causes decrease in amount of ACh released
27
Q

What are symptoms of Lambert-Eaton syndrome?

A
  • muscle weakness of upper and lower limbs
  • dry mouth, impotence
  • improves with muscle use
28
Q

What happens if you give cholinesterase (AChE) inhibitor to pt with lambert-eaton?

A

minimal effect

29
Q

What is the Na/K pump?

A
  • NA/K ATPase
  • pumps 3 NA out of cell in exchange for 2K in
  • restores ionic gradient and membrane potential
30
Q

What is mech of cardiac glycosides? example of drug? Function?

A
  • digitalis, ouabain
  • inhibit Na/K pump
  • by depolarizing cardiac muscle cells –> increase strength of cardiac muscle contraction
  • used to treat CHF
31
Q

What is difference in AP non-myelinated vs myelinate axons?

A

in non-myelinated: slower conductance

in myelinated: greater speed of AP

32
Q

What type of channels are present in Nodes of ranvier?

A
  • lots of voltage gated Na channels

- bordered by regions rich in K channgesl

33
Q

What is multiple sclerosis?

A
  • autoimmune disorder that attacks myelin sheaths
  • over time can lead to degeneration of underlying axons
  • can affect any region of the CNS –> highly variable symptoms
34
Q

What are signs of multiple sclerosis?

A
  • optic neurits (sudden los of vission), hemiparesis, hemisensory smptoms, bladder/bowel incotinenct
35
Q

What is treatment for MS?

A

focused on immunosuppression

36
Q

What are the two paths of pain perception?

A
  • phenomenon of first and second pain –> perception of pain in two wzves
  • first wave mediated by large, myelinated axons (Aδ fibers)
  • second by smaller non-myelinated axons (C fibers)
37
Q

What are two types of synaptic summation? What does this mean?

A
  • synaptic summation = unlike NMJ, need dozens or hundreds of synaptic potentials added together to induce AP in target neuron of CNS
  • temporal or spacial summation
38
Q

What mediates EPSPs [excitatory postsynaptic potentials]?

A
  • glutamate acting on ionotropic [ligand] glutamate receptors, mostly AMPA
39
Q

What mediates IPSPs [inhibitory postsynaptic potentials]?

A
  • GABA acting on ionotropic [ligand] GABA receptors, mostly GABA-A
  • or in spinal cord also glycine acting on ionotropic glycine receptors
40
Q

What determines whether you will get AP at a neuron?

A
  • dozens or hundreds of EPSPs and IPSPs summating together determine what happens
41
Q

How do GPCR EPSPs/IPSPs differ from ionotropic EPSPs/IPSPs?

A
  • GPCRs produce smaller and slower signals
  • neurotransmitters that mediate these responses called “neuromodulators” because they modulate ability of ionotropic receptors to trigger AP

ex. fast EPSP to glutamate still might not get AP. But, if add fast EPSP to glutamate + EPSP to NE can reach depolarization threshold

42
Q

What is tonic firing vs burst firing

A

tonic = pacemaker activity, often mediated by HCN channel, have AP firing at intervals

burst: have lots of APs firing on top of each other, more likely to get neurotransmitter release

43
Q

What does EEG (electroencephalogram) measure?

A
  • surface electrodes, detect potential from surface areas of brain
44
Q

What is normal in EEG vs seizure vs sleep?

A
  • normal: can only detect small electrical potentials because most neural activity is unsynchronized
  • seizure: large number of neurons fire together, see very large potentials, large-amplitude oscillations
  • sleep: larger potentials than during wake, not as large as seizure
45
Q

What 2 mechs usually mediates short-term forms of neural plasticity?

A
  • Ca accumulation in presynaptic nerve terminal

- vesicle depletion in presynaptic nerve terminal

46
Q

What is post-tetanic potentiation (PTP)?

A
  • postsynaptic response to single stimulus is greater after a tetanus (period of high-frequency stimulation)
  • due to Ca accumulation
47
Q

What is paired-pulse facilitation (PPF)?

A
  • postsynaptic response is greater to single stimulus that occurs rapidly after prior stimulus
  • due to Ca accumulation
48
Q

What mediates LTP and LTD in the hippocampus?

A
  • NMDA glutamate receptors
49
Q

What is effect of teatnus on long term neurotransmission?

A
  • can cause long-lasting increase in postsynaptic responses (LTP)
  • can last days or weeks, mediated by altered gene expression
50
Q

What is mech of NMDAR-dependent LTP?

A
  • high frequency stimulation causes high levels of Ca to enter postsynaptic neuron through NMDA receptors
  • CA activates CAMKII (Ca/calmodulin dependent protein kinase II)
  • CAMKII phosphorylates AMPA glutamate receptors and causes them to insert into the synapse membrane
  • further made long term by changes in gene expression
51
Q

What is mech of NMDAR dependent LTD?

A
  • very low frequency stimulation causes smaller amounts of Ca to enter postsynaptic neuron through NMDA receptors
  • CA level not sufficient to activate CAMKII (Ca/calmodulin dependent protein kinase II) and instead activates Calcineurin
  • Calcineurin dephosphorylates AMPA receptors so they are removed from synapse
52
Q

What is mech of mGluR dependent LTD? What disease associated with?

A
  • metabotropic glutamate receptors trigger internalization of AMPA receptors
  • implicated in autism and mental retardatio
53
Q

What is mech of endocannabinoid-mediated LTD?

A
  • endocannabioids released from postsynaptic cell, act on nearby nerve terminals, suppress neurotransmitter rlease

Brain and Behavior Exam 1 (15 decks)

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