Exocytosis beta

Neuron States and Potentials• Resting State: Affects the entire neuron where the inside of the neuron is more negative compared to the outside, leading to a stable environment for potential action. The resting potential is typically around -70mV.• EPSP (Excitatory Postsynaptic Potential): Occurs in dendrites and cell bodies, characterized by depolarization, decremental flow, and graded responses. When an excitatory neurotransmitter binds to its receptor, sodium (Na+) channels open, allowing Na+ to flow into the neuron, causing depolarization. This change can lead to an action potential if the threshold is reached.• Impulse: Occurs in axons and is characterized by a rapid change in membrane potential. In myelinated axons, saltatory conduction allows impulses to jump between nodes of Ranvier, which increases the speed of conduction.• Release of neurotransmitters: From axon terminals into the synapse involves action potentials triggering calcium (Ca++) influx, leading to fusion of synaptic vesicles with the membrane and exocytosis of neurotransmitters.

Synaptic Function• Synapses: Form junctions between neurons where communication occurs. Key components include:

• Sending neuron (presynaptic): Contains synaptic knob or terminal that releases neurotransmitters into the synaptic cleft.

• Calcium ions (Ca++): Play a critical role in neurotransmitter release.

• Receptor sites: On the receiving neuron (postsynaptic) that bind neurotransmitters and initiate a response.

• Exocytosis: The process by which neurotransmitters are released from synaptic vesicles into the synapse.

Neurotransmitter RegulationBrief Impact Mechanisms:• Reuptake: The process by which neurotransmitters are reabsorbed by the presynaptic neuron.• Enzymatic inactivation: Neurotransmitters are broken down by enzymes (e.g., AChE for acetylcholine).• Absorption by glial cells: Support cells can take up neurotransmitters, influencing their availability.• Diffusion: Neurotransmitters can simply drift away from the synaptic cleft.

Specific Example:

• ACh inactivation: Achieved by the enzyme acetylcholinesterase (AChE), which hydrolyzes the neurotransmitter into acetate and choline, terminating its action.

Autoreceptors: Located on the presynaptic neuron, these receptors monitor and regulate neurotransmitter levels by providing feedback to inhibit further release when levels are sufficient.

Inhibitory Processes• Approximately 25% of neurons in the brain are inhibitory. They are more highly concentrated in specific brain regions, with up to 90% present in the cerebellar cortex.• Critical Functions:

• Selective attention: Allowing focus on specific stimuli while ignoring others.

• Response inhibition: Preventing inappropriate responses.

• Motor control: Coordinating smooth movements.

• Reflex override: Suppressing reflex actions when necessary.

• Sensory processing: Filtering and modulation of sensory input.

• Sleep regulation: Promoting sleep states through inhibitory signaling.

• Mental flexibility: Facilitating the switching of attention and tasks.

IPSPs (Inhibitory Postsynaptic Potentials)• Primary neurotransmitter: GABA (Gamma-Aminobutyric Acid)• Characteristics:

• Hyperpolarization: Leads to a shift in membrane potential towards -80mV, making it less likely to fire an action potential.

• Decremental and graded responses: The effect diminishes with distance from the synapse.

• Involves chloride (Cl-) influx and potassium (K+) efflux: This process stabilizes the neuronal membrane potential.

Drug and Poison Effects on NeurotransmittersClassification:• Agonists: Substances that increase neurotransmitter activity (e.g., enhancing release, mimicking neurotransmitter action).• Antagonists: Substances that decrease neurotransmitter activity (e.g., blocking receptor action or release).

Specific Examples

• Acetylcholine (ACh):

  • Botox (antagonist): Blocks ACh release, leading to paralysis of muscles.

  • Black widow venom (agonist): Causes excessive ACh release, resulting in muscle spasms.

• Dopamine:

  • L-Dopa (agonist): Used in treating Parkinson's disease by increasing dopamine levels in the brain.

  • Antipsychotic drugs (antagonists): Used to treat schizophrenia by blocking dopamine receptors.

• Serotonin:

  • SSRIs (agonists): Selective Serotonin Reuptake Inhibitors increase synaptic serotonin by blocking its reuptake.

Combined Effects:

• Stimulant drugs: Often boost dopamine levels but may reduce serotonin, affecting mood, sleep, and impulse control.

• Glutamate and GABA:

  • Anticonvulsants: Work by blocking glutamate receptors and enhancing GABA sensitivity to prevent seizures.

  • Drug X: Significantly decreases brain activity through chloride ion regulation, leading to sedation.

  • Drug Y: Increases brain activity through potassium ion regulation, which can heighten alertness.