Membranes and Receptors - Session 5

A type of transmembrane ion channel that allows calcium ions (Ca2+) to pass through the cell membrane.

The process by which action potentials trigger the opening of calcium channels in cell membranes.

Calcium channels come in different forms, with varying properties and functions.

The rapid transmission of signals between nerve cells (neurons) via specialized junctions called synapses.

A type of ion channel that opens when a specific molecule binds to it, like a key fitting into a lock.

A type of ion channel that opens in response to changes in the electrical potential across the cell membrane.

A type of ion channel that opens when a specific molecule binds to it.

The process of moving the membrane potential of a cell to a more positive value.

A positively charged ion that plays important roles in many cellular processes, such as muscle contraction and neurotransmitter release.

The process by which ions move into or out of a cell through a membrane channel.

The process by which neurotransmitters bind to receptors on ion channels, causing these channels to open and allowing calcium ions to flow into the cell.

Calcium ions are vital for neurotransmitter release. They trigger vesicles, which hold neurotransmitters, to fuse with the cell membrane and release their contents into the synapse.

Ligand-gated calcium channels are opened by the binding of a neurotransmitter to the receptor. This binding triggers a conformational change, opening the channel and allowing calcium ions to enter the cell.

The speed of synaptic transmission in neurons is directly influenced by the rate of calcium influx. The more quickly calcium enters the cell, the faster neurotransmitters are released.

Ligand-gated calcium channels allow the influx of calcium ions, triggering the release of neurotransmitters into the synapse. This process facilitates rapid communication between neurons.

The point on a muscle cell where a motor neuron connects, allowing the release of acetylcholine (ACh).

A type of receptor protein on the muscle cell that binds to ACh, triggering muscle contraction.

The initial change in membrane potential of a muscle cell caused by the binding of ACh to nAChR.

The process of reaching a certain level of depolarization, triggering the release of calcium ions and muscle contraction.

The electrical signal that travels down the muscle cell membrane, triggering the muscle to contract.

An autoimmune disease where antibodies attack the acetylcholine receptors (AChR) on skeletal muscle, leading to muscle weakness.

Patients with Myasthenia Gravis experience weakness in their muscles, which worsens with physical exertion.

Antibodies in Myasthenia Gravis damage acetylcholine receptors, leading to a reduction in the number of functional receptors.

The loss of functional acetylcholine receptors reduces the size of the endplate potentials, resulting in weaker muscle contractions.

Myasthenia Gravis can lead to fatigue and muscle weakness due to impaired signal transmission at the neuromuscular junction.

Drugs that bind to the same site as acetylcholine (Ach) on nicotinic receptors, preventing Ach from binding and blocking the receptor's activation.

These blockers work by blocking the binding of acetylcholine to its receptor site.

Tubocurarine is one example of a drug that acts as a competitive blocker of nicotinic receptors.

Agents block the receptor's activation by binding to a different site from acetylcholine.

These blockers target the receptor and modify its structure, preventing it from responding to acetylcholine.