neurochem Flashcards
neuron structure
dendrites go out, cell body, nucleus, axon, myelin sheath, terminal fibers, synapse and synaptic cleft
- nucleus has mito
synapse
1 nerve ending and dendrite meet
- presynaptic and post synaptic with vescicles and receptors
resting membrane potential
70 mv with high - inside. k is inside, cl and na outside
action potential
- membrane is lowered to -50
- allows na in and k out
- potential is +30 now, gives impulse
- happens in 1 sec
- na k atapse pumps na out and k in
na k permeability
voltage gated channels, only open when nerve impulse hits axon and terminal fiber to allow/nnot allow nerve impulse
calciym
release of NT from cleft is ca dependent
- AP causes ca to enter cleft
blood brain barrier
- endothelial cell lined wiyh tight junctions
acetylcholine
- see structure
- associated with skeletal muscle, motor neurons and attention and self awareness in CNS
- EXCITATOTIR
acetylcholine made + how it works
made in presyn
- see reaction
- binds to receptor on post syn, na channel is opened to let na in
- neuron is depolarized (closer to threshold so more +)
- after it has boumd it gets attacked by acetylcholineesterase
acetylcholineesterase
- see reaction
- acetate and choline taken back up into presyn
nicotinic
- nicotine is mimicing action of acetylcholine (agonist)
- found in skeletal muscle
- cobra toxin binds to this type + blocks receptor
muscarinic
- binds atropine
- smooth muscle and brain
myasthenia gravis
- some disease to do with antibodies against nicotinic receptor
- muscle weakness
catecholamines
- dopa and norepi
- excit/inhibit depending on
- often inhibtory using cl- ions and increase camp by increasing adenyl cyclase
dopamine
- dopamine controls movement
- parkinsons is death of dopamine neurons so less dopamine is made
- shiophroena is excess dopamine transmission so also less dopamine
serotonin
- mediate sleep and sensory perception
- LSD binds to this to decfease it?
gaba
inhibitory
- increases cl transport into post synapse
- hyperpolarizes
- valium binds here
- some reaction written
glial cells
non neuronal.
- microglia clean debris
- macroglia make myelin (white matter) and guide axons in brain dev
- astrocytes are star shaped that buffer ions and metabolites
glutamate
- excitatory
- involved in plasticity and neurotoxicity
plasticity
involves long term potentiation or depression
- potentiation means long lasting enhancement in synpase efficacy
- depression is reduction
nerve impulse and glu
glu is released as impulse reaches pre synaptic end and ninds to receptor causing na release
- made inside astrocyte where g.u is converted to gln
glycine
- inhinitory of spinal chord and brain stm
cocaine
- plant alkaloid from coca shrub
- blocks re-uptake of norepi from synpatic cleft
brain opiates
- analgesic (releive pain)
- produce euphora (well being feeling)
- addictive with emotional/physical dependence
- tolerance (take more to get effect)
- withdrawl
opium from poppy
10 is morpheine
- see structure
- if you acetylate, you get heroin
antagonist
drug that produce none of the effects of the parent drug and blockj the effects
mixt agonist
antagonist. drug that makes some effects of parent drug but blocks others
enkephalin, met and leu
met enkephaline is a penta peptide (tyr, gly, gly, phe, met)
leu enkephain is tyr, gly,gly, phe, leu
- bind to train receptors
b endorphin
protein with pentapeptide sequence
acth
made in pituitary gland
- naturally make b endorphins
enkephalin effect
- decrease na flo
- inhibit neurons that normally are excitatory
- involved in modulation of neurons that reulate pain, keep pain threshold high so no pain
drug mechanism: tolerance
- increase degradative enzymes so more drug to make more effect
drug mech: enkephalin
- without drugs, we have a level of enkephalin
- with drugs, drug binds in place of enkephalins so down reg of it and fewer enkephalins
- tolerance
- withdrawl
drug mech: adennylate cyclase
- cell needs camp,
- enkephalins inhibit so less camp
- body increases receptors to restore levels of camp
- more drug = more inhibit
