Recording-2025-02-26T14:37:26.014Z

Synapses Overview

• Synapses are connections where neurons communicate, primarily involving the transfer of ions between cells.

  • Fast ion transmission is rare and occurs in specific brain regions, eyes, and some pain glands.

  • The common type of synapse is a chemical synapse.

Chemical Synapses

• Chemical Synapse: This type involves the release of neurotransmitters across a gap between two neurons.

  • Synaptic cleft: The space between the presynaptic (sending) and postsynaptic (receiving) neurons.

  • Neurons do not physically touch; rather, they communicate via chemical signals.

Types of Synapses

• Neuromuscular Junction: Connection between a neuron and a muscle fiber.

• Neuroglandular Junction: Connection between a neuron and a gland.

Components of a Synapse

• Axon Terminal (synaptic terminal/synaptic knob): Contains synaptic vesicles housing neurotransmitters.

• Presynaptic membrane: The membrane of the neuron sending the signal.

• Postsynaptic membrane: The membrane of the neuron receiving the signal.

Neurotransmitter Function

• Neurotransmitters: Chemical messengers released into the synaptic cleft that influence the postsynaptic membrane.

  • They bind to receptors, leading to changes in the postsynaptic neuron.

  • Enzymes break down neurotransmitters after their action, preventing continuous activation.

Functional Role of Chemical Synapses

• Axon terminals release neurotransmitters, causing localized changes in the postsynaptic cell's permeability (graded potential).

• If the graded potential is sufficient, it can trigger an action potential in the postsynaptic neuron.

Action Potentials

• Graded potentials must reach a threshold (around -55 to -60 millivolts) to generate an action potential.

  • If sodium channels open, the neuron depolarizes (becomes more positive).

  • If potassium channels open, the neuron hyperpolarizes (becomes more negative).

Key Neurotransmitter: Acetylcholine

• Acetylcholine (ACh) is the most common neurotransmitter in the body, involved in cholinergic synapses.

  • Functions in neuromuscular junctions and various synapses in the central nervous system.

Synaptic Process and Events

1. Action Potential reaches the axon terminal.

2. Voltage-gated calcium channels open; calcium ions enter the cell.

3. Calcium triggers synaptic vesicles to release acetylcholine via exocytosis.

4. Acetylcholine diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane.

5. Binding opens ligand-gated cation channels, allowing sodium to enter and potassium to exit the muscle fiber.

6. A greater influx of sodium leads to depolarization of the postsynaptic membrane.

7. If the threshold is reached, an action potential propagates along the muscle fiber.

Clearing Neurotransmitters

• After neurotransmitter action, enzymes like acetylcholinesterase break down ACh into acetate and choline.

  • Acetate is metabolized by the body; choline is recycled to regenerate acetylcholine.

Synaptic Dynamics

• Synaptic Delay: A brief delay (0.2-0.5 milliseconds) occurs between action potential arrival and neurotransmitter release.

• Synaptic Fatigue: When prolonged activity depletes neurotransmitter levels, halting communication and muscle contractions.

Types of Neurotransmitters

• Excitatory Neurotransmitters: Cause depolarization (open sodium channels).

• Inhibitory Neurotransmitters: Cause hyperpolarization (open potassium channels).

• Some neurotransmitters can function as either, depending on the type of receptor they bind to.

Classes of Neurotransmitters and Their Effects

1. Acetylcholine: Main neurotransmitter; can be excitatory or inhibitory.

2. Norepinephrine: Primarily excitatory, important in the CNS.

3. Dopamine: Exhibits both excitatory and inhibitory effects; linked to Parkinson's disease and cocaine use.

4. Serotonin: Linked to mood regulation; too high or too low can lead to psychological issues.

5. GABA: Predominantly inhibitory, important for reducing neuronal excitability.

6. Nitric Oxide and Carbon Monoxide: Gases that can act as neurotransmitters.

Indirect Effects of Neurotransmitters

• Some neurotransmitters act via G-proteins leading to second messenger activation, affecting cellular responses indirectly.

• Direct Effects: Depend on neurotransmitters binding to receptors that open ion channels directly.

• Indirect Effects: Include activation of intracellular pathways that influence ion channels through second messengers.

Neuronal Interactions

• Neurons can receive thousands of connections leading to complex decision-making based on excitatory vs inhibitory signals.

  • This results in postsynaptic potentials where the neuron sums excitatory and inhibitory inputs to decide on action potential generation.

Facilitation and Summation

• Facilitation: When a neuron is close to generating an action potential due to excitatory input.

  • Temporal Summation: Multiple signals from the same neuron over time.

  • Spatial Summation: Signals from multiple neurons received simultaneously.

Presynaptic Modulation

• Presynaptic Inhibition: When an incoming signal is diminished by another neuron (reduces neurotransmitter release).

• Presynaptic Facilitation: Enhancement of neurotransmitter release due to an incoming signal, increasing the neuron's output.

Key Takeaways

• Action potentials are generated in response to neurotransmitter action at synapses.

• Chemical synapses allow for complex signaling pathways involving excitatory and inhibitory influences.

• Efficient neuronal communication requires study and understanding of neurotransmitter dynamics and synaptic function.

Action Potentials Definition

The process begins with a graded potential that brings the membrane to a threshold potential (typically around -55 mV).

Step 2: Sodium channel activation occurs; sodium ions (Na+) flood into the cell resulting in depolarization where the membrane potential becomes more positive (e.g., from -70 mV to +30 mV).

Step 3: Sodium channels become inactivated shortly after, halting further sodium influx.

Step 4: Voltage-gated potassium channels open, allowing potassium ions (K+) to exit the cell, thus initiating repolarization and restoring the membrane potential towards resting levels.

Step 5: After repolarization, sodium channels regain normal properties, which can briefly lead to hyperpolarization, making the inside of the neuron even more negative than the resting potential (e.g., -80 mV).

Summary: The overall process transitions from graded potential to repolarization, with a specific sequence of sodium and potassium ion movements that are crucial for action potential propagation.

Synaptic Vesicles

Location: Found at axon terminals. They are not found in dendrites or sublux (a spinal term referencing misalignment without physical injury).

Triggering Exocytosis of Synaptic Vesicles

Key Trigger: The arrival of an action potential at the axon terminal.

This causes voltage-gated calcium channels to open, which leads to the influx of calcium ions (Ca2+). This calcium spike is critical for triggering the exocytosis of neurotransmitters stored within synaptic vesicles.

Saltatory Propagation

Correct Statements: Both A & B are true; this reflects how myelin sheaths enhance action potential conduction speed across long axons.

The myelinated areas assist in more rapid conduction, while only the nodes of Ranvier (gaps in myelin) can respond to depolarizing stimuli effectively, allowing for faster information transmission compared to unmyelinated fibers.

Summation Types

Temporal Summation: Occurs when multiple impulses arrive at a synapse in quick succession, potentially creating a strong enough graded potential to reach threshold.

Spatial Summation: Involves simultaneous inputs from various presynaptic neurons that collectively contribute to reaching the action potential threshold. Both serve to enhance the likelihood of generating an action potential from individual Excitatory postsynaptic potentials (EPSPs).

Neurotransmitters Effects

Excitatory neurotransmitters: Lead to depolarization of the postsynaptic membrane (e.g., glutamate stimulates postsynaptic receptors).

Inhibitory neurotransmitters: Cause hyperpolarization (e.g., gamma-aminobutyric acid or GABA increases membrane permeability to Cl- ions, making inside more negative).

Cholinergic Synapses Process Sequence of Events

Action potential arrives at synaptic knob.

Calcium ions enter the cytoplasm from the extracellular space.

Acetylcholine is released from the synaptic vesicles via exocytosis into the synaptic cleft.

Acetylcholine binds to its receptors on the postsynaptic membrane, resulting in postsynaptic depolarization.

Acetylcholine is subsequently removed from receptors either by degradation via acetylcholinesterase or reuptake to prevent prolonged signaling.

Correct Order of Events: 1 (action potential) > 2 (calcium entry) > 3 (release) > 4 (binding) > 5 (removal).

Refractory Periods

Absolute Refractory Period: The time frame during which an excitable membrane cannot respond to further stimulation, ensuring one-way propagation of the action potential.

Puffer Fish Poison Impact

Effect on Neurons: Pufferfish poison contains tetrodotoxin which blocks voltage-gated sodium channels, thus preventing the generation of action potentials and potentially leading to paralysis due to disrupted neural communication.