8/22 Neurotransmission - Glendinning Flashcards

1
Q

steps in neuron activation

A
  1. receive stimuli
  • sensory input: pseudouni- and bipolar
  • synaptic input: bi- and multipolar
  1. integrate the input
  2. APs are activated at trigger zone (area with increased number of Na channels, can initate AP)
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2
Q

resting membrane potential

number

what generates it?

A

-65mV

  • osmotic and electrical forces
  • selective permeability
  • energy dependent Na/K pump

Na, Cl, Ca (out > in)

K (in > out)

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3
Q

electrical inputs in a nerve cell

neuronal inputs as graded potentials

A

inputs stimulate or inhibit an action potential

  • stimulate: depolarizing (positive, excitatory)
  • inhibit: hyperpolarizing (negative, inhibitory)

neuronal inputs are graded potentials → show small changes in RMP in response to inputs

  • size of change varies based on strength of input → leads to varied AP firing rate/nt release
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4
Q

EPSP vs IPSP

A

EPSP: excitatory postsynaptic potential

  • depolarizing
  • excitatory, graded : usually from opening of Na or Ca channeles
  • < 1mV

IPSP: inhibitory postsynaptic potential

  • hyperpolarizing
  • inhibitory, graded : usually from opening of K or Cl channels
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5
Q

“impact factor”

A

graded membrane potentials attenuate (weaken) rapidly with distance from start point

“IMPACT FACTOR” depends on:

  • location (impact could be greater if stim closer to trigger zone!)
  • strength of synapse
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6
Q

4 neuron-to-neuron synapses

A

AD - axodendritic

AA - axoaxonal

AS - axosomatic

DD - dendrodendritic

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7
Q

summating effection on action potentials

spatial vs. temporal

A

spatial : number of inputs received summed

temporal : timing of inputs builds up to AP

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8
Q

what’s the point of inhibition/summation?

A

don’t always want the SAME level of response to an AP! sometimes, want a bigger response than other times

consider:

  • postural demands
  • environmental changes (ex. terrain)
  • goal of movement

combo of excitatory and inhibitory inputs leads to summed state → differential firing rate and force of contraction for diff levels of response

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9
Q

presynaptic inhibition

postsynaptic inhibition

A

presynaptic inhib:

inhibitory inputs at AXON TERMINALS → selective blocking of synaptic output!

postsynaptic inhib:

inhibiory inputs on POSTSYN NEURON → can inhibit entire neuron

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10
Q

saltatory conduction

axon diameter implications

A

myelination produces segments of axon that are insulated - CANT trigger AP there

AP instead jumps to successive nodes of Ranvier

greater axon diameter leads to…

  • increased conduction velocity!
    • higher space constants : signal can move further before decaying
    • larger internodal spaces
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11
Q

factors affective conduction velocity

A
  1. amt of myelin
  2. conduction velocity
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12
Q

chemical synaptic transmission

A

when AP makes it to the axon terminal…

  1. Ca channels open (Ca influx into terminal) → synaptic vesicles fuse with presynaptic terminal
  2. nt is released → binds to receptors on postsynaptic membrane
    * leads to opening of ion channel!
    * *fate of nt released via exocytosis?*

degradation by enzymes, removal by glial cells, reuptake by presyn cell, diffuse away,

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13
Q

two families of postsynaptic receptors

A

1. ligand gated ion channels

  • ionotropic : receptor linked directly to ion channels
  • FAST (<1 ms)

2. G protein coupled receptors

  • metabotropic : receptor does not have channel, affects G-protein activation instead
    • G-protein dissociates and interacts directly or indirectly with ion channel
    • bc of the Gprotein middleman → slower!
  • responsible for neuromodulation
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14
Q

major neurotransmitters

excitatory vs inhibitory

A

PNS

  • excitatory : Ach (nicotinic)

CNS

  • excitatory : glutamate
  • inhibitory : GABA or glycine (spinal cord)
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15
Q

glutamate

A

major excitatory nt in CNA

  • contained in approx 50% of all neurons (virtually all excitatory neurons)

receptors:

ionotropic (excitatory)

ex. AMPA receptor (Na in, K out)
ex. NMDA receptor (Na/Ca in, K out)
ex. kainate

metabotropic (excitatory or inhibitory depending on state of neuron)

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16
Q

NMDA receptor

name

type of gated-ness : how do you open?

role

fun fact: inhibition

A

N-methyl-D-aspartate receptor

voltage gated AND ligand gated

  • NEEDS glutamate AND voltage change
    • at RMP/hyperpol, receptor is blocked by Mg
    • when depolarized, no Mg block → Na/Ca in, K out → EXCITATORY
  • opening of Na/Ca ion channel portion of NMDA potential (when postsyn depol occurs) can lead to long term potentiation (LTP)

role in learning/plasticity AND cytotoxicity

NMDA receptor inhibited by hallucinogenic drugs (PCP and ketamine) → hallucinations that resemble schizophrenia

17
Q

long term potentiation

example of NMDA

A

incrased responsiveness of postsyn neurons after repeated stim of neurons (ex. in hippocampus)

ex. NMDA lets in Ca → Ca-dependent signaling cascades →→→ long term potentiation

  • insertion of additional AMPA receptors (increased responsiveness)
  • changes in dendritic spines

other long term synaptic changes affect:

  • devpt of synapses
  • regulation of neural circuits
  • learning/memory (LTP)
18
Q

glutamate toxicity

A

trauma/disease that impairs ATP generation can cause increased Glu release OR decreased Glu reuptake

  • Glu NMDA channels allow Ca leak into cells
  • increased Ca → inc water update, stim of intracellular enzymes → degradation of proteins/lipids/n.a.s

conditions believed to be assoc: ALS, Alzheimers, tumors, O2 def, ischemia, trauma, repeated seizure

19
Q

tirpartite synapse

role of glia

A

close association of presynaptic cell, postsynaptic cell, glial cells

astrocytes (glia) take up nt and excess K at synapses

20
Q

GABA

type A and B : actions of each

drugs action on them

A

major inhibitory nt of CNS

GABAA : ionotropic receptors → open Cl channels

GABAB : metabotropic receptors → open K, close Ca channels

drugs that act on GABA : anti-anxiety, hypnotics, anti-epileptics, anesthetics

21
Q

ascending neurotransmitter systems

A

mostly neuromodulators

mainly originate in brainstem and project widely

affect: cognition, wakefulness, attn

*target for many psych drugs!

22
Q

norepinephrine (NE)

A

projections originate in : LOCUS CERULEUS and LATERAL TEGMENTAL AREA

fx:

  • sleep/wakefulness
  • attention
  • consciousness
  • pain modulation

drugs that stimulate NE release:

  • amphetamines
  • methylphenidate
23
Q

dopamine

A

projections originate in : VENTRAL TEGMENTAL AGEA and SUBSTANTIA NIGRA

24
Q

acetylcholine (ACh)

A

projections originate in : BASAL FOREBRAIN and PONS

fx:

  • arousal
  • memory
    • nucleus basalic degenerates in Alz disease
25
Q

endogenous opioids

A

peptide neurotransmitters

location: spinal cord, brainstem, forebrain
fx: pain, reward

26
Q

unconventional nts

A

not stored in synaptic vesicles, not released by exocytosis

  • ENDOCANNABINOIDS: excite receptors activated by THC
    • lipid metabolites that cross presyn membranes → act as neuromodulators (affect neuronal excitability)
    • can decrease transmission of pain, decrease nausea/vomiting
  • NO, CO
    • gases that permeate plasma membrane
    • act through 2nd messenger systems
    • might be involved in neurodegen processes