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- author "JLeezy"
- tags "PSL"
- description "Lectures 9-11"
- fileName "Neurons"
- freezingBlueDBID -1.0
- Four regions/parts of neurons
- Dendrites, cell body, axon, axon terminal.
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Neurons' resting potential (and why is it this number?)
- -70 mV
- K+'s is -90 mV, and Na+'s is +60 mV, so a neuron's falls between the two.
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About graded potentials
Conducted, not propogated. Not all-or-nothing like AP. Potential's strength varies with size of stimulus.
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What causes AP?
The rapid opening of Na+ channels, signalled by crossing the threshold at around -50 mV.
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Electrical synapses vs. chemical synapses
- Electrical synapses are the conduction of a graded potential via gap junctions
- Chemical synapses involve neurotransmitters crossing the synaptic gap.
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How does a chemical signal transmit the AP?
The AP triggers the opening of Ca++ channels, allowing Ca++ to enter the axon. This influx of Ca++ stimulates SNARE activity, causing vesicles to dump their contents (neurotransmitters) into the synaptic gap, where they bind to receptor cites on the next neuron's dendrite.
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Ionotropic vs. metabotropic
- In ionotropic neurotransmitter receptors, the neurotransmitters bind directly to the channel protein (ex: nAchR, glutamate)
- In metabotropic neurotransmitter receptors, neurotransmitters bind to a GPCR, which then activates the channel protein (ex: dopamine, norepinephrine)
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Glomeruli
The locations in the olfactory bulb where olfactory sensor neurons synapse with mitral cells.
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Mitral cells
- The carry on the neuronal olfactory messages that they receive from olfactory sensory neurons.
- *Mitral cells also synapse with each other, so there is "cross-talk."
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What does cocaine do?
- GETS YOU CRUNK AS FUCK
- No but in all seriousness, it blocks the reuptake of dopamine. Thus, the dopamine stays in the synaptic gap and more of it bins to the receptor sites.
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What does nicotine do?
Increases neurotransmitter release, increasing the opportunity for binding to receptor sites.
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What is Long-term Potentiation (LTP) and how does it work?
- Basically, "practice makes perfect."
- Glutamate (ligand) binds to AMPA (opens immediately, allowing Na+ to enter post-synaptic terminal) and NMDA (doesnt open yet) receptors --> stimulus causes depolarization at post-synaptic terminal --> depolarization unblocks NMDA receptor, allowing Ca++ to enter post-synaptic terminal --> Ca++ activated Calmodulin --> Calmodulin activates Calmodulin-dependent kinase --> CaMKinase phosphorylates AMPA receptor (allows it to stay open longer --> more Na+ in cell), SNARES (vesicles with new AMPA receptors are delivered), and itself (meaning it is now self-sufficient! LTP has happened!)
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AMPA receptors
Once they bind glutamate, they allow Na+ into the post-synaptic terminal.
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NMDA receptors
Bind glutamate, but still require a strong depolarization (stimulus) before opening and allowing Ca++ to enter the post-synaptic terminal.
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