Term
What are the difference between classic neurotransmitters (like
acetylcholine) and peptide neurotransmitters (like GABA, glycine,
glutamate)?
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-Classic have small, clear storage vesicles, peptide have larger, denser
vesicles.
, -Classic are synthesized in nerve terminus, most peptide synthesized in
cell body as prohormones
Sodium Influx: EPSP (makes potential more positive)
Potassium Efflux: IPSP (makes the potential more negative)
Chloride Flux: IPSP
Extracted from millet grain, prevents polymerization.
Also induces cells to extrude their nuclei and prevents cytokenisis.
As more sodium channels open, the membrane potential is further depolarized,
which causes more voltage gated sodium channels to open and the cycle
continues.
Sodium stimulates this positive feedback
Potassium is negative feedback
(Also consider the important role of spontaneous inactivation of Voltage gated
sodium channels)
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How are skeletal and cardiac muscle APs different?
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, Cardiac has a significant plateau phase
-NT will activate signal until it is removed! We want removal to be fast
and short acting so elimination is super important.
Random, small, quantal release is what stimulates miniature EPPs.
When nerve impulse reaches terminus, quantal release increases and
large EPP is formed, which then spreads across membrane and brings
downstream membrane into full AP.
-Acetylcholine is synthesized in the nerve terminus. Parasympathetics,
CNS, nueron/neuron junctions all utilize this! Very diverse!
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Consider the following scenario: You have an EPSP and an IPSP with
equal voltages. The IPSP is closer to the axon hillock. What will the
overall voltage change be?
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Hyperpolarization because the IPSP is closer to the axon hillock.
, -NT will activate signal until it is removed! We want removal to be fast
and short acting so elimination is super important.
-AMPLIFICATION is key
-Can be inhibitory or excitatory
Made up of 5 subunits.
Alpha 1 and 2, gamma, and delta affect current amplitude and channel
kinetics
Beta subunit acts as a regulatory phosphorylation site
Inactivation depends on type of alpha 1 protein
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What are the structural units of Actin Filaments? What happens when
they are bound to ATP vs ADP? How does this differ in
microtubules?
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