B2W2 Flashcards
Information flow from dendrite to pre synaptic terminal
dendrite, soma, axon, nerve terminal, presynaptic terminal
Action potentials are found ….?
in the axon, within a neuron
Graded potentials are found …?
between neurons, synaptic potentials are graded (IPSPs and EPSPs)
Vrev for EPSP
0 mV
Vrev for IPSP
-71 mV
End plate potential location, transmitter, receptor, ions, effect and quantal content
NMJ, ACh, nicotinic AChR, (Na, K), depolarization, 100
EPSP location, transmitter, receptor, ions, effect, and quantal content
CNS, Glutamate, ionotropic voltage gated channels, (Na, K), depolarization, 1
IPSP location, transmitter, ions, effect, channel, quantal content
CNS, GABA (Brain), glycine (spinal chord), ionotropic voltage gated channels, (Cl-), hyperpolarization, 1
Glutamate ionotropic receptors have what kind of configuration
tetramers, different from ACh, seratonin, and GABA which are pentamers
AMPA receptors
point to point transmission, permeant to Na (in) , K (out), more likely to be active at -40 mV on the post synaptic membrane
NMDA receptors
has slower kinetics due to influx of Na,K AND Ca, needing both glutamate and depolarization of the cell to activate
Activation of NMDA receptors
Mg 2+ is released through depolarization of a cell, making it need both glutamate and depolarization to activate
Which receptors receive EPSP’s
AMPA, NMDA, and kainate
Quantal content v quantal size
Quantal content is the number of vesicles fusing to the presynaptic membrane, while quantal size is the amount of neurotransmitters in a vesicle
Facilitation v depression of EPSP
increases in quantal content v reduction in quantal content, requires a high frequency v low frequency, strongest when there is low ability for vesicle fusion v strongest when there is a high quantal content
Myasthenia Gravis v Lambert Eaton’s Disease in regards to membrane they affect
MG- autoimmune attack and affects AChR on the post synaptic membrane
LE- autoimmune attack and affects the Ca channels on the presynaptic membrane
LTP mechanism of memory formation
LTP has high frequency stimulation leading to higher Ca+ levels, due to the activation of AMPA and NMDA receptors, leading to calmodulin kinase and PKC activation and increase in AMPA receptors on the post synaptic membrane and increase in quantal content
LTD mechanism of memory loss
LTD has low frequency stimulation leading to moderate levels of Ca and increase in protein phosphatase activity
Main inhibitory neurotransmitter in the brain v spinal chord
brain - GABA
spinal chord - glycine
How do IPSP’s cause hyperpolarization
shunting with depolarizations - EPSP brings in Na into the cell while IPSP bring in Cl to equilibrate
Benzodiazepines affect on GABA channels
increases the frequency of GABA channels opening
Barbiturates affect on GABA channels
increases the duration of GABA channels opening
Top 5 most prescribed Benzodiazepines:
- Xanax (alprazolam)
- Ativan (lorazepam)
- Klonopin (clonazepam)
- Valium (Diazepam)
- Restoril (Temazepam)
Dense core vesicle release v small molecule vesicle release
Dense: takes longer, needs more Ca, need high frequency stimulation
Small: rapid release due to location to the terminal, less Ca needed
Ionotropic v Metabotropic receptors
ion: voltage gated ion channels leading to muscle contraction, uses glutamate, ACh, serotonin, ATP, uses (Na,K) for excitatory and (cl) for inhibitory
Meta: GPCRs, slow using cascades, lead to hyperpolarization when in cardiac myocytes, can be excitatory, inhibitory or modularly with use of peptides, opioids, NE, epi, serotonin, dopamine, glutamate, Ach, GABA
Neuromodulation of long depolarizations
Using NE you can reduce adaptation periods, and then restore adaptive depolarizations with washout of NE
Neuromodulations of short depolarizations
decrease after hyperpolarization’s by inhibiting slow Ca+ dependent K channels and then restore using washout
Phasic
frequent spiking of depolarizations followed by period of adaptation
Tonic
frequent spiking of depolarizations due to neuromodulation, leading to an increase of frequency
Divergent neurotransmitter
There is one neurotransmitter which is able to affect many receptors and elicit multiple different responses (ex. NE)
Convergent neurotransmitter
There are multiple neurotransmitters which are acting on the same channel/receptor leading to multiple signals converging !
Basic relay steps for synapse (general)
action potential travels down axon, Na channels open at the presynaptic terminal, voltage gated Ca channels open at presynaptic terminal, rise in Ca triggers vesicle fusion, followed by neurotransmitter release across the presynaptic cleft and into the postsynaptic cell, followed by neurotransmitter breakdown (diffusion, breakdown, reuptake)
