Topic: Synapses and Neurotransmitters
Focus: Understanding neuronal communication, synapse structure, neurotransmitter functions, and their physiological effects.
Key Structures in Neurons:
Presynaptic Axon: Sends impulses to the synapse.
Dendrites: Receive signals at the receiving end of the neuron.
Axon Hillock: Initiates action potentials based on synaptic input.
Axon Initial Segment: Site where action potentials are generated.
Node of Ranvier: Gaps between myelin sheath that facilitate rapid signal transmission.
Synaptic Potentials:
Excitatory Postsynaptic Potentials (EPSPs) increase likelihood of action potential.
Inhibitory Postsynaptic Potentials (IPSPs) decrease likelihood.
Neurotransmitter Release: Involves telodendria that transmit impulses across the synaptic cleft.
Definition:
Junction between two neurons or between neuron and effector (muscle/gland).
Components:
Presynaptic Neuron: Sends neurotransmitters into synaptic cleft.
Postsynaptic Neuron: Receives neurotransmitters.
Synaptic Cleft: Gap between presynaptic and postsynaptic neurons.
Chemical Synapses:
Mechanism: Release of neurotransmitters from presynaptic neuron, binding to receptors on postsynaptic neuron.
Electrical Synapses:
Mechanism: Direct ion flow between cells via gap junctions.
Key Features:
Axon Terminal: Contains synaptic vesicles storing neurotransmitters.
Voltage-Gated Ca2+ Channels: Open upon action potential arrival, allowing Ca2+ influx, triggering neurotransmitter release.
Synaptic Vesicles: Contain neurotransmitters for exocytosis.
Receptors: Located on postsynaptic neurons, bind neurotransmitters.
Reuptake Mechanisms: Remove neurotransmitters from the synaptic cleft after action.
Phases of Response:
Presynaptic Activation: Causes opening of voltage-gated Ca2+ channels.
Neurotransmitter Release Process:
Vesicles fuse with plasma membrane.
Released neurotransmitters bind to receptors on postsynaptic neuron.
Resulting Ionic Changes:
EPSP: Inward Na+ movement causes depolarization.
IPSP: Inward Cl- movement/hyperpolarizes.
Definition: Summation of multiple synaptic inputs influencing overall neuron output.
Types of Summation:
Temporal Summation: Same synapse activated multiple times in rapid succession.
Spatial Summation: Simultaneous inputs from multiple synapses.
Mechanisms:
Facilitation Increases: Enhances likelihood of neurotransmitter release.
Inhibition Decreases: Prevents neurotransmitter release.
Inhibitory/Excitatory Effects:
Binding of neurotransmitters can lead to different postsynaptic responses based on receptor types and ion channels.
Neurotransmitter Types:
Acetylcholine (ACh): Major in PNS, involved in muscle activation, breaking down by Acetylcholinesterase.
Biogenic Amines: Includes dopamine, norepinephrine, serotonin; regulate mood and response systems.
Amino Acids: e.g., Glutamate (excitatory) and GABA (inhibitory); important in overall neural function.
Neuropeptides: Include endogenous opioids, which manage pain and stress responses.
Clinical Importance:
Recognizing changes in neurotransmitter functions is key in diseases like Alzheimer’s, Parkinson's, and depression.
Investigating receptor sensitivity and modulation can aid in treatment strategies (e.g., MAO inhibitors for depression).
Describe the communication at synapses and compare EPSP vs. IPSP.
Explain synaptic integration and the significance of neuronal summation.
Identify neurotransmitter roles and implications for conditions such as Alzheimer’s and depression.