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When EPSP and IPSP happened?
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Post synaptic ( anxon- dendtries (most common) / anxon -somatic) @ associate cell membrane Two side direction<--
How ligand-binding site works?
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Ach (NTm) binding on receptor , then Na+ channel open Local depolarization
What are agonist and antagonist ? what are the possibility of combinations?
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Agonist / antagonist ( increase NT effect / decrease NT effect)
Agonist + Ex= increase firing (EPSP) ; Agonist + In= Decrease firing ( IPSP) Antagonist + Ex = decrease firing(IPSP); Antagonist + In = increase firing(EPSP)
What is agonist ? receptor agonist? Competitive antagonist? Noncompetitive agnosit / antagonist? - - -
Agonist ( NTm) bind- channel opens- usually endogenous ligand = Ntm
Competitive antagonist : Ntm cann’t bind because of block (exogenous ligand= drugs) Noncompetitive antagonist/agogist : binding differently ( bind but not open/close channel)
What is the common EPSP? IPSP?
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EPSP (excitatory )- GLUTAMATE & MOST NTM- (+) DEPOLARIZATION IPSP ( inhibitory)- GABA- HYPERPOLARIZTION- (-)
In jerk-kick experiment, when excitatory ( EPSP) happen? What its effect?
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AP @ axon terminals cause release of glutamate increase likelihood of EPSP (firing) . then trigger AP in motor neuron
Then EPSP passively spread to anxon hillock -> AP …. Release of Ach as Ntm- neuromuscular junction potential
What inhibitory interneurons do?
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Enable excitatory neuron have indirectly inhibit effect on other neuron
What is multiple transmitter effect?
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Different transmitter have different (epsp/ipsp ) effect on cell body
What’s the pathway of Dopamine (DA)? What its effect ? cause? Treatment? - - - -
Substantial nigra (VTA) to Basil ganglia - loss of DA , Parkinson’s disease Effect volnetary motor actitivity Genetic + environment
Deep brain Stimuli , drug (DA)
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2023-02-20
