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Neuroscience Ch5

gap junctions site of (rarer) electrical synapses. spanned by special proteins called 'connexins', six of which form a channel which allow ions to pass directly. bi. usually found in invertebrates btwn sense and motor neurons [thus "electrotonically coupled"] bc fast
gray's type 1 synapse synapse wherein the membrane on the post-synaptic side is thicker than presynaptic; excitatory
gray's type 2 synapse synapse wherein membrane is similar thickness at post and pre synapse; usually inhibitory b/c there are more gates down closer to the soma to open and let Cl in and inhibit.
secretory granules larger vesicles [than synaptic vesicles] located in the axon terminal, containing soluble protein (neurotransmitter: peptides). AKA large dense-core vesicles.
active zones proteins that jut into the terminal from the presynaptic side. site of neurotransmitter release. they differentiate pre and post (or not, in inhibitory)
postsynaptic density protein accumulated in and under the postsynaptic membrane. these are the receptors for neurotransmitters
amino acid transmitters examples: gamma-amino butyric acid (GABA), glutamate (Glu), Glycine (Gly) (small, organic, contain nitrogen)
amines (neurotransmitters) ex: acetylcholine (ACh), dopamine (DA), epinephrine, histamine, noorepinephrine (NE), serotonin (5-HT) (small, organic, contain nitrogen)
neuromuscular junction what it sounds like. also: reliable, w/big synapses. post-synaptic membrane is called the motor end-plate. neurotransmitter: acetylcholine
peptides stored in and released from the secretory granules. larger molecules. made in the rough ER, and sorted/cleaved by the golgi apparatus, where they are put in their secretory granules. takes more than one AP to release them.
glutamate one of the 20 amino acid "building blocks" (so abundant)
glycine one of the 20 amino acid "building blocks" (so abundant)
GABA only made by the neurons that release it
transporters special proteins embedded in the membrane of the synaptic vesicles, whose job it is to get the neurotransmitters into the vesicles
exocytosis as Ca2+ floods into the presynaptic terminal (since the depolarization opened up the calcium gates), this is the process by which the calcium causes the vesicles to fuse w/the membrane and release their contents. unfortunately, actual mechanism is unknown
endocytosis process by which vesicle is recovered after exocytosis
transmitter-gated ion channels unlike voltage gated ion channels, these channels, opening upon reception of a neurotransmitter, are less selective. neverthless the net effect will be depolarization, and therefore excitatory
g-protein-coupled receptors AKA metabotropic receptors. upon neurotransmitter arrival, these receptors activate G-proteins, which activate "effector" proteins
effector proteins can be a) G-protein gated ion channels, or b)enzymes that generate molecules called secondary messengers, which can activate additional enzymes in the cystol that can regulate ion channel fxn and alter cell metabolism
IPSP inhibitory post-synaptic potential. Cl- floods in, forcing the cystol to tend towards a negative voltage. glycine-gated and GABA-gated ion channels both do this
autoreceptors receptors at the presynapse which are sensitive to the transmitters that that presynapse releases. often are g-protein-coupled receptors which work on secondary messengers to inhibit. (overflow safety drain dealio?)
acetylcholinesterase an example of neurotrasmitter removal, AChE is used after a neuromuscular presynaptic firing releases ACh. If ACh stayed there, the post-synapse would become desensitized to its presence, and further APs would do nothing. AChE binds to ACh, removing it
miniature postsynaptic potential aka mini. low rate of continual nt release causes low base postsynaptic response. since its one vesicles, its the quanta
integration of EPSPs CNS neurons fire very weak synapses, and numerous EPSPs on the dendrites ("spatial summation") or multiple APs must combine succesively within 1-15msec ("temporal summation") to make the postsynapse depolarize
dendritic length constant the distance at which the depolarization of the dendrite is 37% of that of the base (rand number? no, based on e)
internal resistance inverse of conductance of a neuron's dendrite, depending on thickness and electrical properties of cytoplasm. stays fairly constant for any given neuron
membrane resistance resistance of a neuron's dendrite's membrane, depending on the number of open ion channels, which is very variable. (number of holes in leaky hose)
shunting inhibition inhibition where, b/c so much chloride is coming in, voltage stays around -65mv and APs don't happen
modulation synptc trans where EPSPs are not created but modified in effctvnss. effect (eg, chnging K+ conc and thus incr conduct) can last longer than cause (conversion of ATP into cAMP, stimulation by cAMP of protein kinases, phosphorylation by protein kinases)
Created by: jwdink