PYSC 106 Lecture 4
Synapse and Neurotransmitter Release
Components of a Synapse
Presynaptic terminal
Postsynaptic terminal
Postsynaptic structures can include:
Dendrites
Soma
Axon
Neurotransmitter Release Process
Change in voltage along the presynaptic membrane triggers opening of voltage-gated calcium channels.
Calcium rushes into the presynaptic terminal.
Causes vesicles containing neurotransmitters to fuse with the presynaptic membrane.
Vesicles release their contents into the synaptic cleft.
Neurotransmitter Diffusion and Receptor Interaction
Released neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic membrane.
Types of Receptors:
Ion Channels:
e.g. AMPA receptors (for glutamate).
G-Protein Coupled Receptors (GPCRs):
e.g. NMDA receptors (require binding of multiple ligands).
AMPA and NMDA Receptors
AMPA Receptors
Ion channel receptor that mediates fast synaptic transmission.
Upon binding of glutamate, it opens to allow positive ions to flow into the postsynaptic neuron.
NMDA Receptors
Complex receptor that requires both glutamate and glycine to bind for activation.
Uses a magnesium block that prevents ion flow until membrane depolarization occurs, allowing excitation of the neuron.
Requires two events for activation:
Binding of glutamate and glycine.
Depolarization to remove the magnesium block.
Comparison of Postsynaptic Neurons
Neuron A: 2 AMPA receptors and 1 NMDA receptor.
Neuron B: 3 AMPA receptors and 1 NMDA receptor.
More AMPA receptors lead to higher initial depolarization in Neuron B due to more binding sites for glutamate.
Action Potential and Synaptic Responses
Process of Depolarization
AMPA receptors open first, allowing positive ions into the cell, leading to depolarization.
Higher AMPA activation increases the likelihood of reaching the action potential threshold.
NMDA receptors can allow for an additional influx of positive ions providing a further depolarization boost after AMPA activation.
Synaptic Plasticity and Receptor Regulation
Concept of Plasticity
Neurons adjust receptor levels based on past neurotransmitter activity, facilitating learning and memory.
Activity-Dependent Receptor Insertion:
More active synapses can lead to increased AMPA and NMDA receptor insertion to adapt to increased glutamate presence.
GABA as an Inhibitory Neurotransmitter
GABA Receptors
Types of GABA Receptors:
GABA A: Ion channel allowing chloride ions to enter the neuron.
GABA B: G-Protein coupled receptor.
Clinical implications:
Many drugs (e.g., alcohol, benzodiazepines) act on GABA receptors, enhancing their inhibitory effects.
Neurotransmitter Clearance Mechanisms
Primary Mechanisms of Neurotransmitter Clearance:
Reuptake:
Specialized transporters remove neurotransmitters from the synapse back into the presynaptic neuron.
Example: Cocaine inhibits dopamine reuptake, increasing synaptic dopamine levels.
Enzymatic Breakdown:
Enzymes degrade leftover neurotransmitters in the synaptic cleft (e.g., degradation of acetylcholine).
Diffusion:
Neurotransmitters can diffuse away from the synaptic cleft.
Role of Glial Cells in the Central Nervous System
Types of Glial Cells:
Astrocytes: Provide structural support, transport nutrients and regulate neurotransmitter levels.
Oligodendrocytes: Form myelin sheaths around CNS axons for insulation and effective signal transmission.
Microglia: Act as immune cells in the CNS, removing debris and dead neurons.
Blood-Brain Barrier
Function of the Blood-Brain Barrier (BBB):
A selective barrier that restricts the passage of substances from the bloodstream into the brain, preserving neuronal health.
Facilitated by astrocytic end-feet that surround blood vessels.
Neurotransmitter Dynamics
Synthesis and Recycling:
Astrocytes help synthesize neurotransmitters (e.g., converting glutamate to glutamine, which can be reused by neurons).
Turnover of Receptors:
Receptors undergo recycling based on activity levels to maintain optimal synaptic signaling.
Final Notes
Understanding these processes is crucial for exploring neuronal communication, learning and memory mechanisms, and the effects of various pharmacological agents on brain function.