Test 2 Flashcards
Ch. 6 slide 12 - Ch. 11 Slide 11
What are the events @ the synapse?
AP reaches end of presynaptic terminal
Calcium is released into presynaptic terminal
vesicles move towards release site
terminal releases neurotransmitter
neurotransmitters bind to post-syn membrane receptor
membrane channel changes shape, and ions enter
transporters and enzymes enter synapse to clear and re-set for next AP
What are the three types of synapses?
axoaxonic - axon - axon
axodendritic - axon-dendrite
axosomatic - axon-somite
Which type of synapse(s) can increase/decrease chances of AP? Change number of neurotransmitters sent?
Chances of AP - axodendritic, axosomatic # sent -axoaxonic
Describe an EPSP’s.
Excitatory post-synaptic potential
local
depolarize
Na+/Ca++ into cell
Describe IPSP’s.
Inhibitory post-synaptic potential
local
hyper polarize
Cl- in/ K+ out
Describe the two Presynaptic potentials
pre-syn facilitation
Increases influx of Ca++
pre-syn Inhibition
decreases influx of Ca++
Differences between Neurotransmitters and Neuromodulators.
Neurotransmitter - released into synaptic cleft, acts on receptors, excites or inhibits, quickness’s and short
Neuromodulator - act at distance, can affect many neurons, slow and long
What are the 3 kinds of synaptic receptors?
- ligand-gated
- G-Protein
- G- Protein 2nd messenger
What does an agonist do?
bind and mimic
enhance release
What does an antagonist do?
bind and block
diminishes releasing
ACl
facilitatory/excitatory, depolarize
fast: pns-neuromuscular jx -nicotinic
slow: ans and cns - muscarinic
Glutamate
Facilitatory/Excitatory/depolarize
brain works - too much =toxic
Fast: CNS (AMPA most prevalent excitatory in CNS)
slow: NMDA CNS
GABA
inhibitory - most prevalent in CNS
hyper polarize
fast: GABAa
slow: GABAb
Dopamine
slow acting nt
motor act, cognition, behavior
pleasure - associated with addiction
Norepinephrine
slow acting nt
increases attn. to sensory info in and
sympathetic fight/flight
serotonin
slow acting nt
blood and perception of P
adjusts arousal
Histamine
slow acting nt
inflammation of nt
endogenous opioids
peptide
inhibit perception of P
substance P
peptide
transmitter/modulator
send signal or enhances route
chronic pain - substance p is overactive
What kind of neurotransmitters are in the PNS?
only excitatory
In terms of receptor regulation, what does it mean to “down-regulate?” - re-map
decrease chance of AP
inactivate - protein in synapse but not used
internalize
In terms of receptor regulation, what does it mean to “up-regulate?”
increase chance of AP
activate - unlock gate and allow ions to flow in
externalize - bring receptor from outside cell into membrane
What does LTP do?
Turns up cell signaling passive --> active Ca released by NMDA AMPA active into post-sun membrane split into two dendritic spines less effort required
What does LTD do?
Turns down cell signaling
active to passive
remove ampa
less likely to depolarize when glutamate is released
penumbra
cells that fall asleep because of reduced O2
excitotoxicity glycolysis protease protein enzymes solute
too much glutamate - too much Ca++ lactic acid> decrease in pH degrade cell protein O2 free radicals cell swelling > pop
What happens to connection in an axonal injury?
distal axon and myelin degenerates, Mm atrophy
collateral axonal injury
the denervated is innervated by intact neighbors * ----- * ----- * \--- *----- regenerative sprouting * ----- * ----- * -----/
regenerative sprouting
axon and target cell damage, injured axon sprouts
- —– * —–
- —–/
Is there final regeneration in the CNS
no
recovery of synaptic effectiveness
decrease swelling and wake up sleeping cells
denervation hypersensitivity
new receptors at remaining terminals