8/22 Neurotransmission - Glendinning Flashcards Preview

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

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)


resting membrane potential



what generates it?



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


Na, Cl, Ca (out > in)

K (in > out)


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



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


"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


4 neuron-to-neuron synapses

AD - axodendritic

AA - axoaxonal

AS - axosomatic

DD - dendrodendritic


summating effection on action potentials


spatial vs. temporal

spatial : number of inputs received summed

temporal : timing of inputs builds up to AP




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


  • 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


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


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


factors affective conduction velocity

1. amt of myelin

2. conduction velocity


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,


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


major neurotransmitters


excitatory vs inhibitory


  • excitatory : Ach (nicotinic)


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



major excitatory nt in CNA

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



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)



NMDA receptor



type of gated-ness : how do you open?



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


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)


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


tirpartite synapse


role of glia

close association of presynaptic cellpostsynaptic cellglial cells


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




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


ascending neurotransmitter systems

mostly neuromodulators

mainly originate in brainstem and project widely

affect: cognition, wakefulness, attn


*target for many psych drugs!


norepinephrine (NE)

projections originate in : LOCUS CERULEUS and LATERAL TEGMENTAL AREA



  • sleep/wakefulness
  • attention
  • consciousness
  • pain modulation


drugs that stimulate NE release:

  • amphetamines
  • methylphenidate



projections originate in : VENTRAL TEGMENTAL AGEA and SUBSTANTIA NIGRA


acetylcholine (ACh)

projections originate in : BASAL FOREBRAIN and PONS



  • arousal
  • memory
    • nucleus basalic degenerates in Alz disease


endogenous opioids

peptide neurotransmitters


location: spinal cord, brainstem, forebrain

fx: pain, reward


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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