NeuroScience Exam Notes (Some main topic)
Receptors and Synaptic Transmission
Receptor Types: Nicotinic Acetylcholine (ACh) receptors are ionotropic (ligand-gated ion channels); Muscarinic ACh receptors are metabotropic (G-protein coupled).
Synaptic Delay: Time between presynaptic action potential (AP) and postsynaptic potential.
Electrical synapses: no delay.
Directly-gated chemical synapses: <0.5 \text{ ms}.
Indirectly-gated chemical synapses: >0.5 \text{ ms}.
Inhibition:
Presynaptic: Reduces neurotransmitter release via calcium channel modulation at axoaxonic synapses.
Postsynaptic: Produces IPSPs by opening potassium or chloride channels at axosomatic/axodendritic synapses.
Action Potentials and Membrane Potentials
Action Potential (AP) Initiation: Most likely at the axon hillock due to high density of voltage-gated sodium channels; requires local potential to reach threshold ().
Resting Membrane Potential (RMP): Primarily driven by non-gated potassium channels; kept stable by the Na+/K+ pump maintaining ion gradients.
AP Height: Influenced by the external sodium concentration (gradient for sodium influx).
Nodes of Ranvier: Exposed gaps in myelinated axons, concentrated with voltage-gated ion channels for saltatory conduction.
After-Hyperpolarization (AHP): Membrane becomes more negative than RMP after an AP, due to prolonged opening of voltage-gated potassium channels.
Glial Cells and Nerve Conduction
Myelin-Producing Glia:
Oligodendrocytes: In the CNS, myelinate up to different axons.
Schwann Cells: In the PNS, myelinate a single axon.
Conduction Velocity:
Unmyelinated axon: .
Myelinated axon: .
MS Functional Recovery: Occurs via migration of voltage-gated sodium channels into previously myelinated areas, not remyelination.
Neurotransmitter Deactivation
Mechanisms:
Diffusion: Minor mechanism for all neurotransmitters.
Enzymatic Breakdown: Primary for Acetylcholine (ACh) via acetylcholinesterase.
Active Reuptake: Primary for most other neurotransmitters (e.g., GABA, glutamate, serotonin) back into the presynaptic terminal.
SSRIs (Selective Serotonin Reuptake Inhibitors): Block the active reuptake of serotonin, thereby increasing its concentration in the synaptic cleft to treat mood disorders.