When EPSP and IPSP happened? - - Post synaptic ( anxon- dendtries (most common) / anxon -somatic) @ associate cell membrane Two side direction<-- How ligand-binding site works? - - Ach (NTm) binding on receptor , then Na+ channel open Local depolarization What are agonist and antagonist ? what are the possibility of combinations? - - - 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? - - EPSP (excitatory )- GLUTAMATE & MOST NTM- (+) DEPOLARIZATION IPSP ( inhibitory)- GABA- HYPERPOLARIZTION- (-) In jerk-kick experiment, when excitatory ( EPSP) happen? What its effect? - - 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? - Enable excitatory neuron have indirectly inhibit effect on other neuron What is multiple transmitter effect? - 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) 本文来源：https://www.wddqw.com/doc/1ec5af4a5727a5e9856a61fb.html