Communication Between Neurons Flashcards
the synapse
synapse is the point of interaction between neurons. at the tip of the axon is the axon terminal (has alot of mitochondria). post synaptic has special proteins on the membrane called receptors to receive the released neurotransmitters. 3 types of synaptic connection: axodendritic, axosomatic, axoaxonic.
synaptic neurotransmitter release
when action potential reaches the terminal it changes the membrane potential there as well (depolarized). specific voltage gated calcium channels open (more depolarized). each action potential releases several vesicles. neurotransmitter passively diffuses to post synaptic membrane (concentration gradient). neurons are relatively neurotransmitter selective.
termination of synaptic transmission
3 ways = enzymatic metabolism, reuptake, uptake by glial cells
enzymatic metabolism
inside the synaptic cleft, there are enzymes that are always present. when neurotransmitters are released into the synaptic cleft, the enzymes immediately metabolize them. very efficient and quick progress. most get metabolized before getting to the other terminal.
reuptake
an efficient process. the membrane of the pre synaptic neuron has pumps/transporters. these pumps are specific to the neurotransmitter and they are taken up again and recycled. it gets metabolized inside the terminal.
uptake by glial cells
all synapses in the brain have glial cells - maintenance and support cells. they supply the neuron with energy and metabolites and remove garbage. remove neurotransmitters from the synapse and stored where it can be reused. if they dont remove the neurotransmitter, signal would stay on longer
synaptic potentials
post synaptic response can be excitatory (EPSP) or inhibitory (IPSP).
EPSP
post synaptic membrane has depolarized - membrane is not as negatively charged as before. might make it easier to cross the threshold for an action potential.
IPSP
post synaptic membrane becomes even more negative, reverses a depolarization that had already occurred. might make it harder to fire an action potential
2 types of EPSPs
- opening channels permeable to NA+ (enters cell)
- closing leaky K+ channels (K+ cannot leave cell)
2 types of IPSPs
- opening channels permeable to Cl- (enters cell = hyperpolarization)
- opening K+ channels (leaves the cell = hyperpolarization)
spatial summation
several inputs act on a relatively limited area at the same time. the membrane potential in that area is summed up to a much stronger change. strong intensity of potential more resistant to interference.
temporal summation
a single axon fires very rapidly multiple action potentials that are summed to produce a greater potential.
neurotransmitter synthesis
- necessary enzymes are transported to the terminal where synthesis is taking place (ACh, DA). DA is synthesized from tyrosine converted into L-Dopa by tyrosine hydroxylase. L-Dopa is converted to DA by Dopa decarboxylase.
- neuropeptides precursors are synthesized in the soma and carried to the terminal via vesicles (replenishment is slower)
pharmacology of the synapse
- agonist = imitates effects or increases effects of the neurotransmitter
- antagonist = reducing or inhibiting the effect of the neurotransmitter
- L-Dopa precursor to DA = agonist
- PCPA inhibits synthesis of serotonin = antagonist
- reserpine prevents storage of monoamines in vesicles = antagonist
- blackwidow spider venom stimulates release of ACh = agonist - (increased ACh not good)
- botulinum toxin inhibits release of ACh = antagonist
- nicotine, muscarine stimulates postsynaptic ACh receptors = agonist
- curare, atropine blocks postsynaptic ACh receptors = antagonist (complete paralysis)
- apomorphine stimulates DA autoreceptors = antagonist
- yohimbine blocks NE autoreceptors = agonist (increased NE causes anxiety)
- cocaine blocks DA, NE, serotonin reuptake = agonist
- physostigmine inactivates acetylcholinesterase (increases ACh) = agonist