8/22 Neurotransmission - Glendinning Flashcards Preview

M2 Neuron Brain Behavior > 8/22 Neurotransmission - Glendinning > Flashcards

Flashcards in 8/22 Neurotransmission - Glendinning Deck (26):
1

steps in neuron activation

1. receive stimuli

  • sensory input: pseudouni- and bipolar
  • synaptic input: bi- and multipolar

2. integrate the input

3. APs are activated at trigger zone (area with increased number of Na channels, can initate AP)

2

resting membrane potential

 

number

what generates it?

-65mV 

 

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

 

Na, Cl, Ca (out > in)

K (in > out)

3

electrical inputs in a nerve cell

 

neuronal inputs as graded potentials

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

4

 EPSP vs IPSP

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

5

"impact factor"

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

6

4 neuron-to-neuron synapses

AD - axodendritic

AA - axoaxonal

AS - axosomatic

DD - dendrodendritic

7

summating effection on action potentials

 

spatial vs. temporal

spatial : number of inputs received summed

temporal : timing of inputs builds up to AP

 

 

8

what's the point of inhibition/summation?

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

9

presynaptic inhibition

 

postsynaptic inhibition

presynaptic inhib:

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

 

postsynaptic inhib:

inhibiory inputs on POSTSYN NEURON → can inhibit entire neuron

10

saltatory conduction

 

axon diameter implications

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

11

factors affective conduction velocity

1. amt of myelin

2. conduction velocity

12

chemical synaptic transmission

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,

13

two families of postsynaptic receptors

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

14

major neurotransmitters

 

excitatory vs inhibitory

PNS

  • excitatory : Ach (nicotinic)

CNS

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

15

glutamate

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)

 

16

NMDA receptor

 

name

type of gated-ness : how do you open?

role

 

fun fact: inhibition

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

long term potentiation

 

example of NMDA

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

glutamate toxicity

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

tirpartite synapse

 

role of glia

close association of presynaptic cellpostsynaptic cellglial cells

 

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

20

GABA

 

type A and B : actions of each

drugs action on them

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

ascending neurotransmitter systems

mostly neuromodulators

mainly originate in brainstem and project widely

affect: cognition, wakefulness, attn

 

*target for many psych drugs!

22

norepinephrine (NE)

projections originate in : LOCUS CERULEUS and LATERAL TEGMENTAL AREA

 

fx:

  • sleep/wakefulness
  • attention
  • consciousness
  • pain modulation

 

drugs that stimulate NE release:

  • amphetamines
  • methylphenidate

23

dopamine

projections originate in : VENTRAL TEGMENTAL AGEA and SUBSTANTIA NIGRA

24

acetylcholine (ACh)

projections originate in : BASAL FOREBRAIN and PONS

 

fx:

  • arousal
  • memory
    • nucleus basalic degenerates in Alz disease

25

endogenous opioids

peptide neurotransmitters

 

location: spinal cord, brainstem, forebrain

fx: pain, reward

26

unconventional nts

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

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