Transmission across synapses a. Depolarization of presynaptic cell b. Increase in inward gCa ++ via voltage gated Ca ++ channels c. Vesicle migration and exocytosis of neurotransmitters d. NT diffusion across cleft

4-2 e. NT binding and activation of receptors

4-3 Receptors NT active without entrance Transmembrane proteins Specifically bind NT outside cell Initiate response in postsynaptic cell

4-4 receptor is channel, e.g., nicotinic ACh receptor is enzyme

4-5 Each NT has at least one receptor, usually more ACh = “cholinergic”, nicotinic and muscarinic Ep/Norep = “adrenergic”,  and 

4-6 f. Reception of NT results in change in ion permeability of subsynaptic membrane Leads to a change in the E M of the postsynaptic cell

4-7 f. Reception of NT results in change in ion permeability of subsynaptic membrane Leads to a change in the E M of the postsynaptic cell

4-8 f. Reception of NT results in change in ion permeability of subsynaptic membrane Leads to a change in the E M of the postsynaptic cell

4-9 Postsynaptic potential f. Reception of NT results in change in ion permeability of subsynaptic membrane Leads to a change in the E M of the postsynaptic cell

4-10 PSP is type of “passive potential” low and variable magnitude local: decreasing magnitude with distance from synapse

4-11 g. 2 possible responses of the postsynaptic cell Record from postsynaptic cell as you stimulate a.p.s in presynaptic cell

4-12 (1) “excitatory” synapses Reception of NT leads to passive depolarization of postsynaptic membrane NT reception makes the postsynaptic cell more likely to reach threshold “Excitatory PostSynaptic Potential” Receptor linked to depolarizing ion channels

4-13 (2) “inhibitory” synapses: Reception of NT leads to passive hyperpolarization NT reception makes the postsynaptic cell less likely to reach threshold “Inhibitory PostSynaptic Potential” Receptor linked to hyperpolarizing ion channels

4-14 Every synapse programmed chemically as inhibitory or excitatory by channels involved Most neurons receive both types of input

4-15 h. Degradation of NT, recovery of presynaptic cell PSPs are brief Therefore NT action must be terminated quickly

4-16 (1) NT can be enzymatically degraded in cleft e.g., acetylcholinesterase on subsynaptic membrane cleaves ACh A and Ch recycled presynaptically

4-17 (2) NT can be reabsorbed by presynaptic cell or glial cell e.g., norepinephrine is reabsorbed, metabolized, recycled

4-18 (3) Ca ++ is pumped out of presynaptic terminal Synapse restored to resting condition Synapse is one-way structure

Action potential generation in postsynaptic cell How are passive potentials converted to action potentials? a. Postsynaptic integration: incoming electrical activity is “summated” to depolarize postsynaptic membrane to threshold

4-20 b. Area of cell called “spike initiation zone” or “axon hillock” has lower threshold than other areas due to high density of sensitive sodium channels c. Summation Additive effects of multiple passive potentials on total membrane voltage

4-21 Multiple epsps summate to depolarize SIZ to threshold Ipsps cancel out epsps and prevent SIZ from reaching threshold Threshold for new postsynaptic cell action potential can only be reached in response to multiple epsps