Synaptic Transmission

Neural Conduction and Synaptic Transmission

  • Neural Conduction: The process of a single neuron firing is driven by action potentials that travel down the axon.

Key Definitions

  • Synaptic Transmission: The process by which a signal is passed from one neuron to another through neurotransmitters.

    • Presynaptic Cell: The neuron sending the signal (located at the axon terminals).

    • Postsynaptic Cell: The neuron receiving the signal (located at the dendrites).

  • Synapse: The junction where the presynaptic and postsynaptic neurons communicate.

    • Synaptic Cleft: The tiny gap between the presynaptic and postsynaptic neurons where neurotransmitters are released.

Structure and Function

  • Electron Micrograph: Images show terminal buttons of presynaptic cells and their close proximity to postsynaptic cells.

  • Neurotransmitters: Chemicals (e.g., dopamine, serotonin) stored in vesicles in the presynaptic cell. Released when action potential triggers vesicle fusion with the membrane.

  • Receptor Sites: Proteins on the postsynaptic membrane that bind to neurotransmitters, resulting in ion channel opening.

Mechanism of Transmission

  • Signal Transfer: Neurotransmitters cross the synaptic cleft and bind to receptor sites on the postsynaptic neuron.

  • Graded Potential: Binding leads to either excitatory or inhibitory post-synaptic potentials, affecting membrane potential and potential to trigger action potentials:

    • Excitatory Postsynaptic Potential (EPSP): Increases membrane potential toward threshold, known as depolarization.

    • Inhibitory Postsynaptic Potential (IPSP): Decreases membrane potential, moving it away from the threshold.

Action Potentials and Thresholds

  • Summation of Potentials: EPSPs and IPSPs are summed at the axon hillock. If the total reaches a critical threshold (around -55 mV), an action potential is initiated.

  • Basic Cycle of Action Potential:

    1. Resting State: Neuron is at -70 mV.

    2. Graded Potentials: Neurons receive multiple inputs; excitatory inputs increase potential; inhibitory inputs decrease it.

    3. Triggering Action Potential: When the threshold is reached, sodium channels open, causing depolarization.

    4. Repolarization: After reaching a peak, potassium channels open to restore negative charge.

    5. Refractory Period: The membrane potential temporarily overshoots resting state, then stabilizes at -70 mV again.

Neurotransmitter Fate

  • Post-synaptic Action: After binding to receptors, neurotransmitters are released and can:

    • Drift away (diffusion).

    • Be reabsorbed by presynaptic neuron (reuptake) for recycling.

    • Be broken down by enzymes in the synaptic cleft (enzyme degradation).

Role of Psychoactive Drugs ##### Graded Potential - **Graded Potential**: Binding of neurotransmitters to receptors on the postsynaptic membrane initiates changes in the membrane potential, producing either excitatory or inhibitory postsynaptic potentials. These changes significantly influence the neuron's likelihood of firing an action potential by modifying the overall membrane potential. - **Excitatory Postsynaptic Potential (EPSP)**: When neurotransmitters bind to specific receptors, they cause channels that allow positively charged ions (primarily sodium ions, Na+) to open, leading to an influx of these ions into the neuron. This process results in depolarization, where the membrane potential increases and moves closer to the critical threshold of approximately -55 mV. If sufficient EPSPs occur in quick succession (temporal summation) or at different locations on the neuron (spatial summation), they can collectively raise the membrane potential enough to trigger an action potential. - **Physiological Relevance**: EPSPs are crucial for neuronal communication and can amplify signals throughout neural circuits, contributing to the processes of learning and memory by enhancing the effectiveness of synaptic transmission over time. - **Inhibitory Postsynaptic Potential (IPSP)**: Conversely, when inhibitory neurotransmitters (such as GABA or glycine) bind to their receptors, they typically allow negatively charged ions (like chloride ions, Cl−) to enter the cell or lead to the opening of potassium channels, causing the efflux of K+. This hyperpolarizes the neuron, decreasing the membrane potential and making it less likely for the neuron to reach the action potential threshold. IPSPs counterbalance the effects of EPSPs, thus fine-tuning neuronal excitability and preventing excessive firing. - **Physiological Relevance**: IPSPs play a key role in maintaining neural network stability, processing inhibitory inputs, preventing overstimulation, and providing a mechanism for synchronization of neuronal activity. <!-- --> ##### Action Potentials and Thresholds - **Summation of Potentials**: At the axon hillock, the summed effects of EPSPs and IPSPs determine whether the membrane potential will reach the critical threshold necessary for generating an action potential. If the total surpasses approximately -55 mV, an action potential is initiated, representing a rapid, all-or-nothing response of the neuron. - **Basic Cycle of Action Potential**: 1. **Resting State**: The neuron has a resting membrane potential of approximately -70 mV, maintained by the sodium-potassium pump actively transporting Na+ out and K+ into the cell, along with the cell membrane's permeability properties. 2. **Graded Potentials**: As the neuron receives synaptic inputs, excitatory signals increase potential through Na+ influx, while inhibitory signals decrease it through Cl− entry or K+ efflux, leading to changes in the overall membrane potential based on the net influence of these signals. 3. **Triggering Action Potential**: Once the threshold is reached, voltage-gated sodium channels open, causing a rapid influx of Na+ and resulting in depolarization, where the membrane potential may rise toward +30 mV during the peak of the action potential. 4. **Repolarization**: Following the peak, sodium channels close, and voltage-gated potassium channels open, allowing K+ to flow out of the neuron. This restores the negative charge inside the cell and is responsible for returning the membrane potential back toward its resting state. 5. **Refractory Period**: The neuron briefly experiences a period of hyperpolarization, where the membrane potential drops below -70 mV (undershoot) before stabilizing back at resting levels. This refractory period prevents immediate re-excitation, ensuring that action potentials only travel in one direction along the axon, thereby facilitating proper signal transmission. <!-- --> ##### Neurotransmitter Fate - **Post-synaptic Action**: After neurotransmitters bind to their receptors, they must be cleared from the synaptic cleft to prevent continuous stimulation of the postsynaptic neuron. - **Diffusion**: Neurotransmitters may drift away from the synaptic cleft, reducing their concentration and, therefore, their action on the postsynaptic receptors. - **Reuptake**: Many neurotransmitters are reabsorbed by the presynaptic neuron through specialized transporters. This process allows for recycling of neurotransmitters, preparing the neuron for future signaling events. - **Enzyme Degradation**: Enzymes present in the synaptic cleft may break down neurotransmitters into inactive components, effectively terminating their action. For instance, acetylcholine is broken down by acetylcholinesterase into acetate and choline, which prevents overstimulation of postsynaptic receptors. - **Physiological Importance**: Efficient removal of neurotransmitters is crucial for maintaining synaptic integrity and ensuring that neurotransmission occurs in a time-sensitive manner for accurate and functional communication within the nervous system.

  • Mechanism: These drugs can mimic neurotransmitters and influence their receptor interactions, enhancing or inhibiting their effects by blocking reuptake processes.