Clase 10 Fisiología - Neurofisiología Sensitivo 1 (IG:@doctor.paiva)

General Overview

In this segment, the instructor introduces the topic of neurophysiology, specifically focusing on sensory neurophysiology. Key concepts discussed include the generalities of the nervous system, types of synapses, neuronal anatomy, neurotransmitter release, receptor proteins, ion channels, and mechanisms of excitation and inhibition.

Generalities of the Nervous System

• The central nervous system comprises two main systems: sensory (afferent) and motor (efferent).

• Sensory neurons transmit information from the periphery to the central nervous system.

• Motor neurons convey information from the central nervous system to the periphery for muscle contraction.

Neuronal Structure and Synapses

• Neurons are the fundamental functional units of the central nervous system.

• A neuron consists of a cell body (soma), nucleus, axon, myelin sheath, dendrites, and synapses.

• Synapses serve as communication points between neurons; they involve pre-synaptic terminals releasing neurotransmitters to post-synaptic receptors.

Types of Synapses

• There are two primary types of synapses: chemical and electrical.

• Chemical synapses involve neurotransmitter release into synaptic clefts for signal transmission.

• Electrical synapses rely on open fluid channels for direct electrical conduction between cells.

Chemical Synapses Mechanisms

• In chemical synapses, neurons release neurotransmitters like acetylcholine or adrenaline into synaptic gaps.

• These neurotransmitters bind to receptors on post-synaptic neurons to trigger excitatory or inhibitory responses.

Electrical Synapse Characteristics

• Electrical synapses feature open fluid channels that facilitate rapid electrical conduction between cells.

Anatomy and Physiology of Synapses

In this section, the anatomy and physiology of synapses are discussed, focusing on the structure of dendrites and soma, as well as the types of synaptic buttons present.

Anatomy and Physiology of Synapses

• The soma contains dendrites with 10,000 to 20,000 synaptic buttons.

• These synaptic buttons can be excitatory or inhibitory based on the type of stimulus received.

• Examination of a presynaptic terminal reveals mitochondria, transmitter vesicles, receptor proteins, and calcium channels.

• Mitochondria provide ATP for neurotransmitter synthesis.

• Vesicles in the presynaptic terminal can be excitatory or inhibitory based on their content.

• Mitochondria contribute to neurotransmitter synthesis by providing energy like acetylcholine for choline production.

• The release of transmitter vesicles from the presynaptic neuron to the postsynaptic neuron is facilitated by calcium ions.

• Calcium influx triggers vesicle fusion with the membrane for neurotransmitter release.

Mechanism of Neurotransmitter Release

This section delves into how neurotransmitter release occurs through calcium ion involvement in membrane depolarization.

Mechanism of Neurotransmitter Release

• Voltage-dependent calcium channels open upon membrane depolarization in the presynaptic neuron.

• Calcium influx leads to neurotransmitter release into the synaptic cleft due to membrane permeability changes.

• Membrane depolarization alters channel sensitivity to trigger calcium influx into the presynaptic neuron.

• Calcium entry induces vesicle exocytosis towards the synaptic cleft for neurotransmission.

Neurotransmitter Receptor Activation

This part explores how neurotransmitters bind to receptors and initiate ion channel opening for signal transmission.

Neurotransmitter Receptor Activation

• Acetylcholine binds to its receptors leading to ion channel opening allowing ion passage such as chloride or sodium ions.

Estimulación Neuronal y Mecanismos de Excitación e Inhibición

This section delves into the stimulation of neurons, mechanisms of excitation and inhibition, and how changes in ion channels affect neuronal activity.

Stimulation and Excitation Mechanisms

• Neuronal excitation can occur through depolarization by closing potassium chloride channels or both.

• Closing potassium chloride channels leads to increased positive charges inside the cell, enhancing excitation.

• Changes in the internal metabolism of postsynaptic neurons can alter excitability by adjusting receptor numbers.

Inhibition Mechanisms

• Neuronal inhibition can result from opening chloride channels, allowing negative ions to leave the cell.

• Enzymes inhibiting metabolic functions can modulate receptor numbers, affecting synaptic transmission.

Action Potential and Ion Channels

• Action potential involves sodium influx at chemical-gated channels, leading to depolarization at the threshold.

• Repolarization involves potassium efflux and closure of sodium channels, causing hyperpolarization.

Hyperpolarization Effects on Neuronal Activity

Hyperpolarization impacts neuronal excitability thresholds and necessitates stronger stimuli for depolarization.

Impact of Hyperpolarization

• Hyperpolarized cells require higher stimuli for depolarization due to a more negative resting membrane potential (-100mV).

• Increased stimulus strength is needed for depolarization when cells are hyperpolarized.

Inhibition via Chloride Channel Opening

Opening chloride channels induces hyperpolarization, requiring stronger stimuli for subsequent depolarizations.

Chloride Channel Effects

New Section

In this section, the discussion revolves around the opening of sodium channels and the impact on membrane potential.

Opening of Sodium Channels

• The entry of sodium leads to a change in membrane potential.

• Example provided: From -75mV to -90mV, a stimulus of 25,000 volts is needed. With the sodium channel open, only 10,000 volts are required for excitation.

New Section

This part focuses on how small stimuli can trigger depolarization in cells near their excitability threshold.

Threshold of Excitation

• Individuals near the excitability threshold may experience depolarization with minor stimuli.

• Examples given include skeletal muscle and neurons where proximity to the excitability threshold can lead to conditions like epileptic seizures.

New Section

The discussion shifts towards the role of acetylcholine receptors in triggering sodium influx and inhibition via calcium channel blockade.

Acetylcholine Receptors and Calcium Channel Blockade

• Acetylcholine at neuromuscular junctions initiates sodium influx through specific channels.

• Blocking voltage-dependent calcium channels prevents calcium entry into presynaptic neurons, hindering vesicle release into synaptic clefts.

New Section

Here, the consequences of blocking voltage-dependent calcium channels on neurotransmission are explored.

Effects of Calcium Channel Blockade

• Blocking calcium channels inhibits vesicle release at synapses.

• Lack of vesicle release disrupts stimulation transmission; morphine is cited as an example that blocks calcium channels to impede information flow.

New Section

The final segment discusses how inhibiting vesicle release impacts neuronal transmission using morphine as an illustrative example.

Impact on Neuronal Transmission

• Morphine's action involves blocking calcium channels to halt information transfer.