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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.
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.
About graded potentials
Conducted, not propogated. Not all-or-nothing like AP. Potential's strength varies with size of stimulus.
What causes AP?
The rapid opening of Na+ channels, signalled by crossing the threshold at around -50 mV.
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.
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.
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)
The locations in the olfactory bulb where olfactory sensor neurons synapse with 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."
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.
What does nicotine do?
Increases neurotransmitter release, increasing the opportunity for binding to receptor sites.
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!)
Once they bind glutamate, they allow Na+ into the post-synaptic terminal.
Bind glutamate, but still require a strong depolarization (stimulus) before opening and allowing Ca++ to enter the post-synaptic terminal.