Neurotransmitters: GABA and Glycine

The primary inhibitory neurotransmitter in the brain.

An enzyme responsible for converting glutamate (excitatory) into GABA (inhibitory).

Specialized neurons that release GABA.

A type of GABAergic neuron that acts as a local inhibitor. Examples include basket cells and stellate cells.

A type of GABAergic neuron that transmits signals to other areas of the brain. An example is the Purkinje cell.

A type of GABA receptor that acts as an ion channel, allowing chloride ions to pass through.

The influx of chloride ions through the GABA-A receptor causes the neuron to become less likely to fire.

Astrocytes help regulate the levels of GABA and glutamate by recycling them.

GABA-A receptors are ionotropic, allowing chloride ions to flow into the cell, causing hyperpolarization and inhibiting neuronal activity.

GABA-C receptors are also ionotropic, but they have a different subunit composition and pharmacological profile than GABA-A.

GABA-B receptors are metabotropic, meaning they indirectly influence neuronal activity through complex signaling pathways involving G-protein coupled receptors.

Bicuculline is a selective antagonist for GABA-A receptors, blocking their action.

GABA-A receptors are composed of five subunits, which can vary, creating functional diversity. These subunits bind different compounds at specific sites.

GABA-C receptors are homomeric, meaning they are formed by the same type of subunit, the rho subunit.

GABA-B receptors are heteromeric, made up of two different subunits, GABA-B1 and GABA-B2, which must work together to create a functional receptor.

GABA-B receptors are found in both the presynaptic and postsynaptic compartments of neurons, where they play a crucial role in regulating neurotransmitter release and neuronal activity.

Activation of GABA-B receptors leads to the closure of voltage-gated calcium channels, which prevents the fusion of synaptic vesicles with the membrane and subsequent neurotransmitter release.

GABA-B receptors reduce the release of various neurotransmitters, including GABA itself and glutamate, by decreasing calcium influx into the presynaptic terminal.

In the presynaptic terminal, GABA can activate GABA-B receptors, leading to a decrease in calcium influx, depolarization of the terminal, and ultimately a reduction in the release of neurotransmitters.

Activation of GABA-B receptors in the presynaptic terminal acts as a feedback mechanism that limits the further release of GABA or glutamate, leading to a balanced level of neurotransmitters in the synapse.

During high-frequency stimulation, activation of GABA-B receptors in the presynaptic terminal reduces further GABA release, effectively limiting inhibition and facilitating the induction of long-term potentiation (LTP).

GABA-A receptors are inhibited by convulsants like bicuculline, leading to increased neuronal activity and potentially convulsions.

Drugs can either activate or inhibit GABA receptors, impacting neuronal activity and potentially leading to various effects, such as convulsions or sedation.

Skeletal muscle relaxants, like Baclofen, act by activating GABA-B receptors, which reduces neuronal activity and leads to muscle relaxation.

In early embryonic development, GABA is an excitatory neurotransmitter. This is because chloride ions are more concentrated inside the cell, so when GABA channels open, chloride flows out, causing depolarization and increased neuronal activity.

Ethanol, as a dose-dependent drug, primarily interacts with GABA-A receptors, enhancing their activity, leading to a range of effects from excitement and relaxation to severe outcomes like coma and death.

Ethanol directly enhances GABA-A receptor activity, but the involvement of GABA-B receptors further amplifies these effects. This shows both GABA receptor types play a role in ethanol's effects.

When GABA-B receptors are silenced, ethanol has a more pronounced effect on GABA-A receptors, demonstrating the inhibitory role of GABA-B receptors on GABA release.

Glycine acts as a co-agonist of NMDA receptors, meaning it's required for these receptors to open.

Glycine is an inhibitory neurotransmitter that silences neuronal activity, contributing to its crucial role in various brain functions.

GABA transaminase (GABA-T) deficiency can lead to increased GABA levels, resulting in a build-up of GABA in the brain.

A type of transporter found in synaptic vesicles that transports both GABA and glycine. It helps regulate vesicular concentration of these inhibitory neurotransmitters.

Glycine can inhibit the uptake of GABA into vesicles, and vice versa. This means they compete for transport by VIAAT.

Glycine receptors are composed of α and β subunits. The α subunit binds glycine, and the receptor can be composed of only α subunits or a combination of α and β subunits.

Glycine's effect changes during development due to the expression of different chloride transporters. Initially, glycine acts excitatory, then becomes inhibitory after a few days postnatally.

Ethanol and other substances like anaesthetics can enhance the function of glycine receptors, amplifying their inhibitory effects. This is an example of allosteric modulation.

Glycine is the primary inhibitory neurotransmitter in the mature CNS, while in the developing nervous system it acts as an excitatory neurotransmitter.

Glycine is an amino acid that plays a critical role in inhibitory neurotransmission in the central nervous system. It acts as a neurotransmitter at glycine receptors, mediating inhibitory postsynaptic potentials (IPSPs).

Strychnine is a competitive antagonist of the glycine receptor, meaning it blocks the binding of glycine to the receptor and prevents its activation.