neurophysiology Flashcards

1
Q

2 types of electrical signals b/t neurons

A

action potentials - travel long distances

graded potentials local membrane changes

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2
Q

Segments of a neuron

A
  • Cell body = receptive segment–> binds neurotransmitters to create graded potentials
  • Axon Hillock = initial segment - summation of graded potentials and initiation of action potential
  • axon = conductive segment - propagation of action potential
  • axon terminal = transmissive segment - AP causes release of neurotransmitters
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3
Q

Types of Ion Channels

A
  • Leakage = always open -> more K+ ones than Na+ ones
  • Ligand gated = open and close in response to stimulus (results in neuron excitability)
  • voltage gated = respond to change in membrane potential
  • mechanically gated = respond to mechanical vibration or pressure
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4
Q

RMP

  • what is the #
  • where’s + vs -
A
  • the rmp is -70mV
  • exists bc extracellular fluid is rich with Na+ and Cl- and inside is rich with K+, organic phosphate and AAs
  • inward flow of Na+ can’t keep up with outward flow of K+
  • Na+/K+ pump removes Na+ as fast in leaks in
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5
Q

Graded potentials

A
  • small deviations from -70mV
  • vary in amplitude depending on strength of stimulus
  • lovalized
  • occur most often in dendrites and cell body
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6
Q

2 types of graded potentials

A
  1. EPSP
    - opens Na+ and K+ chem-gated channels
    - Na+ influx > K+ efflux
    - depolarization
  2. IPSP
    - Neurotransmitter binding causes hyperpolarization
    - opens K and/or Cl chem-gated channels
    - K efflux and/or Cl influx
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7
Q

Generation of APs

A

voltage gated na and k channels open in sequence

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8
Q

all or none principle

A

if stimulus reaches threshold the ap is always the same –> a stronger stimulus won’t cause a larger impulse

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9
Q

Depolarizing phase

A
  • chem or mech stimulus causes graded potential to reach at least -55mV
  • voltage gated na channels open and na enters cell
  • Resting membrane: inactivation gate of na channel is open and activation gate is closed
  • when -55mV is reached, both open
  • inactivation gate closes again really fast–> 20,000 Na get in

-positive feedback process

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10
Q

Repolarizing Phase

A
  • When -55mV is reached, K channels open, but do it really slow
  • K finally open once Na have already closed
  • K outflow causes repolarization and often hyperpolarization to -90mV
  • k channels close and rmp goes to -70mV
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11
Q

Refractory period

A
  • period when neuron can’t generate another AP
  • absolute refractory = even strong stimulus won’t do anything –> inactivated Na channels have to go back to resting state first
  • relative refractory period = a suprathrshold stimulus will start and AP –> k channels are still open, but Na channels have closed
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12
Q

continuous vs saltatory conductions

A

continuous = step-by-step depolarization of each portion of the length of the axolemms

Saltatory = depolarization at nodes of ranvier where there’s high density of voltage gated channels –> current carried by ions flows through extracellular fluid from node to node

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13
Q

Factors that affect speed of propagation

A
  1. amount of myelination : more myelin = faster
  2. axon diameter: bigger diameter = faster
  3. temp: warmer = faster

NOT related to strength of stimulus

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14
Q

fiber types, biggest to smallest

A

A fibers = 5-20 microns and 130 m/s –> myelinated somatic sensory and motor

B fibers = 2-3 microns and 15 m/s –> myelinated visceral sensory and autonomic preganglionic

C fibers = 0.5 - 1.5 microns and 2 m/s –> unmyelinated sensory and autonomic motor

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15
Q

2 types of synapse

A
  1. electrical = fast, 2-way, ionic current goes to next cell through gap junction
  2. chemical= 1 way info transfer from presynaptic to postsynaptic neuron (axodendritic, axosomatic, and axoaxonic)
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16
Q

chemical synapse

A
  • AP reaches end bulb and voltage gated ca channels open
  • ca influx triggers release of neurotransmiters
  • neurotransmiters cross synaptic cleft and bind to ligand gated receptors (more neurotransmitters= bigger change in postsynaptic cell)
  • synaptic delay = 0.5 msec
17
Q

neurotransmitters

A
  • can be excitatory and inhibitory –> same one can be both depending on location
  • acetylcholine, glutamate, aspartate, gamma aminobutyric acid (GABA), glycie, norepinephrine, epinephrine, dopamine
18
Q

Small molecule neurotransmiters

A

Ach = released by many PNS neurons and some CNS –> exitatory on NMJ, but inhibitory on others –> inactivated by AchE

AAs = glutamate= released by almost all excitatory neurons in brain --> inactivated by glutamate specific transporters
-GABA = inhibiting neurotransmitter for 1/3 of all brain synapses (valium enhances GABA activity)
19
Q

Ionotropic and Metabotropic receptors

A
  • Ionotropic = ligand gated (channel-linked)

- Metabotropic = 2nd messenger protein (G prot linked)

20
Q

G-prot linked receptor

A

-neurotrans binds to it, activating G protein–> G prot controls production of 2nd messenger (cAMP/cGMP)–> 2nd messenger open/close channels, activate kinases, phosphorylate channel prots, or activate genes to induce prot. synth

  • responses= indirect, complex, slow and prolonged
  • involves transmembrane prot. complexes
  • cause widespread metabolic change
21
Q

channel linked receptor

A
  • ligand gated channel
  • action is immediate and brief
  • Excitatory receptors = channels for small cations (influx contributes to depolarization)
  • Inhibitory receptors allow influx that causes hyperpolarization
  • e.g. ach and aa
22
Q

Removal of neurotransmitter

A
  1. diffusion = move down conc. gradient
  2. enzyatic degradation = AchE
  3. Uptake by neurons or glia cells = neurotransmitter transporters (prozac= seratonin reuptake inhibitor)
23
Q

Summation

A
  • if several presynaptic end bulbs release neurotransmitters at same time, combined effect may generate a nerve impulse due to summation
  • may be spatial or temporal
24
Q

spatial summation

A

multiple axon terminals release neurotransmitters to one neuron
-effects are added

25
Q

temporal summation

A

presynaptic neuron releases neurotransmitters in rapid succession, so the effects pile up on top of themselves

26
Q

results of summation

A

Excitatory > inhibitory but < threshhold = facilitation

excitatory > inhibitory and threshhold = AP

inhibitory > excitatory = Inhhibition

27
Q

Modifications of neurotransmitters

A
  • Agonists = enhance the effects

- Antagonist = blocks its action

28
Q

types of neural circuits

A
  • diverging
  • convergins
  • reverberating
  • parallel after-discharge
29
Q

regeneration/ repair

A
  • limited ability for repair –> PNS can repair damaged dendrites or axons, but CNS can’t repair stuff
  • Plasticity is maintained, though –> new dentrites/ proteins and changes in synaptic contacts
30
Q

Repair in PNS

A
  • Damage causes chromatolysis = swelling of cell body (peaks 10-20 days aft injury)
  • Wallerian degeneration of distal portion of neuron days 3-5
  • retrograde degeneration of proximal portion to first neurofibril node
  • Regeneration after chromatolysis = synthesis of RNA and proteins favoring rebuiding of axon (several months) –> schwann cell/neurolemma on each side of injury repairs tube and axonal buds grow down the tube
31
Q

requirements for PNS repair

A
  • no damage to cell body
  • schwann cells remain active and form tube
  • scar tissue doesn’t form too fast
32
Q

Neurogenesis in CNS

A
  • formation of new neurons from stem cells doesn’t happen
  • no neurogenesis in CNS
  • This is bc neuroglial cells inhibit it, no growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue