GAMALATE SOLUTION

Indications

• Epilepsy
• Seizure disorders
• Anxiety disorders
• Muscle spasms

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines.

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

GABA exerts its effects by binding to GABA receptors, which are ligand-gated ion channels. This binding results in the opening of ion channels that allow the influx of chloride ions into the neuron, leading to hyperpolarization and a decreased likelihood of action potential generation. Consequently, GABA reduces neuronal excitability and can help prevent seizures.

Pharmacodynamics

GABA's primary action as an inhibitory neurotransmitter is critical in maintaining the balance between excitation and inhibition in the brain. By enhancing GABAergic activity, antiepileptic medications that target GABA pathways can effectively reduce seizure frequency and severity. The modulation of GABA receptors can also influence various other neurological and psychiatric conditions, such as anxiety disorders and depression.

Pharmacokinetics

GABA is not extensively absorbed when administered orally, and its pharmacokinetics can vary based on formulation and route of administration. When utilized as a medication, its effects may be influenced by factors such as protein binding, metabolism, and excretion. The half-life and clearance rates can differ depending on the specific GABAergic drug used in therapy.

Pregnancy

Consult relevant guidelines, as safety during pregnancy is not established.

Breast-feeding

Consult relevant guidelines, as safety during breastfeeding is not established.

Storage

Store in a cool, dry place, away from light.

Formulations

• {'formulation': 'Capsules', 'strength': '100 mg'}
• {'formulation': 'Tablets', 'strength': '300 mg'}
• {'formulation': 'Oral solution', 'strength': '250 mg/5 mL'}

Indications

• Partial seizures in adults and children
• Neuropathic pain
• Restless legs syndrome

Dosage

Children: Refer to the BNF for Children for appropriate dosing information based on age and weight.

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated and patient factors.

Mechanism of action

Gabob primarily acts by inhibiting voltage-gated calcium channels on neurons, which reduces the release of excitatory neurotransmitters. This mechanism is believed to contribute to its anticonvulsant and analgesic effects. Additionally, gabapentin may enhance GABA-mediated inhibition in the central nervous system, although it does not bind to GABA receptors directly.

Pharmacodynamics

Gabob exhibits dose-dependent effects on seizure control and pain relief. It is thought to modulate the excitatory neurotransmitter release in the central nervous system, resulting in decreased neuronal excitability. The drug's ability to stabilize neuronal membranes contributes to its efficacy in treating seizures and neuropathic pain. The therapeutic effects are typically observed within a few days to weeks after initiation of treatment.

Pharmacokinetics

Gabob is well absorbed after oral administration, with peak plasma concentrations occurring approximately 2 to 3 hours post-dose. It has a bioavailability of about 60% to 80%, which decreases with increasing doses. The drug is not extensively metabolized by the liver and is primarily excreted unchanged in the urine. Gabapentin's half-life is approximately 5 to 7 hours, and its pharmacokinetics are not significantly affected by food. Special populations, such as those with renal impairment, may require dose adjustments due to altered clearance.

Pregnancy

There is insufficient data on the use of gabob in pregnant women. Consult healthcare professionals for individual assessment.

Breast-feeding

It is not known if gabob is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Cognitive enhancement
• Neuroprotective strategies in neurodegenerative diseases
• Potential roles in mood disorders

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Refer to BNF for specific dosing information.

Mechanism of action

Glutamate activates both ionotropic (AMPA, kainate, and NMDA receptors) and metabotropic glutamate receptors. It is primarily involved in neuronal signaling and synaptic transmission. Due to its inability to cross the blood-brain barrier, it is converted into L-glutamine for utilization in the brain.

Pharmacodynamics

As an excitatory neurotransmitter, glutamate is essential for normal brain function. It is a key player in neurotransmission and synaptic plasticity, influencing learning and memory. Moreover, it acts as a precursor for GABA synthesis in GABAergic neurons.

Pharmacokinetics

Glutamate is not freely available in significant quantities in the brain due to the blood-brain barrier. Instead, it is synthesized from glucose and other precursors. Its metabolism involves conversion into L-glutamine, which is then utilized in the brain. The transient nature of glutamate makes it challenging to study pharmacokinetically.

Pregnancy

Glutamate is generally regarded as safe during pregnancy when consumed in normal dietary amounts, but excessive intake, particularly in supplement form, should be approached with caution.

Breast-feeding

Glutamate is considered safe during breastfeeding as it is naturally present in various foods and is not expected to pose a risk to nursing infants.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Mechanism of action

Glutamate activates both ionotropic and metabotropic glutamate receptors. The ionotropic ones being non-NMDA (AMPA and kainate) and NMDA receptors. Free glutamic acid cannot cross the blood-brain barrier in appreciable quantities; instead it is converted into L-glutamine, which the brain uses for fuel and protein synthesis. It is conjectured that glutamate is involved in cognitive functions like learning and memory in the brain, though excessive amounts may cause neuronal damage associated in diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Also, the drug phencyclidine (more commonly known as PCP) antagonizes glutamate at the NMDA receptor, causing behavior reminiscent of schizophrenia. Glutamate in action is extremely difficult to study due to its transient nature.

Pharmacodynamics

In addition to being one of the building blocks in protein synthesis, it is the most widespread neurotransmitter in brain function, as an excitatory neurotransmitter and as a precursor for the synthesis of GABA in GABAergic neurons.