Myasthenia Gravis and Cholinergic Pathways

A chronic autoimmune disease that causes weakness in muscles by interfering with the communication between nerves and muscles at the neuromuscular junction.

Myasthenia Gravis arises when antibodies attack acetylcholine receptors at the neuromuscular junction. This prevents acetylcholine from binding, disrupting the signal for muscle contraction.

Acetylcholine is a neurotransmitter crucial for muscle contraction and plays a role in brain functions like memory and attention.

Nicotinic receptors are ion channels that are activated by acetylcholine. They are found in muscles and the brain and are crucial for muscle contraction and neuronal signaling.

Muscarinic receptors are activated by acetylcholine and are found in organs like the heart, lungs, and glands. They play a role in regulating smooth muscle activity and glandular secretions.

ACh is synthesized in the presynaptic terminal of a neuron, where the enzyme choline acetyltransferase combines choline and acetyl coenzyme A.

Curare is a substance that blocks the activity of nicotinic receptors. It can cause muscle paralysis by preventing acetylcholine from binding.

Atropine is a substance that blocks the activity of muscarinic receptors. It can affect heart rate, breathing, and digestive processes.

These receptors are found in skeletal muscles and are responsible for muscle contraction. They have a unique structure containing either a δ or ε subunit.

These receptors are located in neurons and are involved in neurotransmission. They have a diverse subunit composition, with 10 α-subunits and 4 β-subunits.

This receptor contains the α7 subunit and is highly permeable to calcium ions (Ca²⁺). It requires all five acetylcholine (ACh) binding sites to be activated.

This receptor is the main pathway for sodium ions (Na⁺) flow. It has two binding sites for acetylcholine (ACh).

These receptors belong to the G-protein-coupled receptor family and are responsible for slower responses in the body.

This condition is caused by an autoimmune attack on acetylcholine receptors, leading to muscle weakness and fatigue.

These medications are used to treat Myasthenia Gravis by preventing the breakdown of acetylcholine (ACh), allowing it to last longer at the synapse.

These drugs are used to treat Myasthenia Gravis by temporarily improving muscle strength, confirming the diagnosis.

A neurotransmitter that activates NMDA receptors, but requires the presence of another molecule called a co-agonist for full activation.

A molecule that binds to a site on an NMDA receptor, distinct from the glutamate binding site, and is essential for receptor activation.

Glycine and D-serine are important co-agonists for NMDA receptors. They increase the sensitivity and activity of the receptors.

A drug that blocks the activity of NMDA receptors. Ketamine selectively inhibits NMDA receptor-mediated signaling, reducing neuronal firing.

The most common type of NMDA receptor, made up of two GluN1 and two GluN2 subunits. They are well-studied and involved in many brain functions.

NMDA receptors that contain GluN3 subunits in addition to GluN1 and/or GluN2 subunits. Their functions and roles are less well understood.

A type of NMDA receptor with two different subunit types (e.g., GluN1 and GluN2).

A type of NMDA receptor composed of three different subunit types (e.g., GluN1, GluN2, and GluN3).

A type of neurotransmitter receptor responsible for ion conduction. It participates in fast synaptic transmission and is activated by glutamate.

A type of neurotransmitter receptor that activates G-proteins, leading to slower and more complex signaling pathways. It's involved in various brain functions, including learning and memory.

The enzyme that converts glutamine into glutamate. It's a crucial step in the synthesis of this important neurotransmitter.

A type of glial cell responsible for removing glutamate from the synaptic cleft. It plays a vital role in regulating glutamate levels and preventing excitotoxicity.

A subtype of iGluRs that is activated by N-Methyl-D-Aspartate (NMDA). It requires glycine as a co-agonist and is crucial for learning, memory, and plasticity.

A subtype of iGluRs that is activated by AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid). It is responsible for fast excitatory synaptic transmission.

A subtype of iGluRs that is activated by kainic acid. It is involved in neuronal signaling and is sometimes implicated in neurological disorders.

A co-agonist required for activation of the NMDA receptor. It binds to a separate site on the receptor and is essential for calcium influx and neuronal signaling.

NMDA receptors are blocked by Mg²⁺ at negative membrane potentials, reducing ion flow. As the membrane potential becomes more positive, the Mg²⁺ block is relieved, allowing ion flow through the receptor.

Different GluN2 subunits (e.g., GluN2A, GluN2B) exhibit varying sensitivities to Mg²⁺. GluN2A and GluN2B are more sensitive to Mg²⁺ block than GluN2C and GluN2D.

GluN2A expression increases with brain development, while GluN2B expression remains consistently high.

The assembly of NMDA receptors involves the combination of GluN1 and GluN2 subunits. This process involves individual subunits dimerizing and then forming a tetramer.

Different GluN2 subunits influence the receptor's sensitivity to glutamate and glycine, impacting the strength of the resulting ion currents.

NMDA receptors exhibit voltage-dependent block by Mg²⁺, where the block is strongest at negative potentials and weakens as the membrane potential becomes more positive.

NMDA receptors play a crucial role in synaptic plasticity, learning, and memory formation. Their activity is altered by factors such as Mg²⁺ block and subunit composition.

GluN2 subunits are differentially expressed across various brain regions, suggesting specialized functions.

A type of glutamate receptor that is activated by glycine. They are found in the brain and are involved in learning and memory.

A molecule that blocks the action of glycine at the GluN1/N3 receptor.

A test that measures the electrical activity of cells in response to a stimulus.

Involves the removal of a specific gene from an organism. This allows scientists to study the function of that gene.

A condition characterized by excessive brain activity, often causing seizures. NMDARs are implicated in this disease.

Damage to brain tissue caused by excessive stimulation of neurons. NMDARs are involved in this process.

A drug that blocks the action of NMDARs. It has anesthetic and antidepressant effects.

A drug that blocks the action of NMDARs. It is used to treat Alzheimer's disease.