Glutamate is an amino acid that also serves as the brains' primary excitatory neurotransmitter
The glutamate hyperfunction hypothesis of schizophrenia has been proposed largely on the basis of studies in post-mortem brain and the lack of efficacy of glutamate agonists as antipsychotic drugs
Lamotrigine, a drug which inhibits glutamate release, has been investigated as an adjunctive treatment in schizophrenia
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In early studies, patients with epilepsy who were taking lamotrigine reported increases in a subjective sense of well-being, and this led to its exploration as a psychotropic drug (3)
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Often, patients with treatment-resistant depression (TRD) who respond to ketamine require serial infusions and Lamotrigine oral tablet is a prescription medication used to treat seizures in people with epilepsy and bipolar disorder
Lamotrigine acts on the central nervous system to control the number and severity of seizures
This was a double-blind, placebo-controlled, parallel group study of lamotrigine, an agent that modulates glutamate release
Lamotrigine (LTG) stabilizes presynaptic neuronal membranes by blocking voltage-dependent sodium channels and thereby preventing the release of excitatory amino acids, especially glutamate and aspartate
Further study is needed
Lamotrigine is an anticonvulsant thought to inhibit voltage-dependent sodium channels causing decreased glutamate release
Similar suppressive effects of the drugs were observed on formalin-induced increases in spinal aspartate, except that gabapentin and lamotrigine produced effects only during the second phase
Although many studies have been published, there is still not enough data on the effect of ketamine in combination with other medications
Lamotrigine is a voltage-dependent blocker of voltage-sensitive sodium channels
Glutamate is the principal excitatory neurotransmitter in the adult brain
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Ketamine induces glutamate level and so increases GBCr in prefrontal cortex
Recent studies have highlighted the involvement of LTG in modulating the activity of voltage-gated ion channels, particularly those related to The aim of the current study was to review the clinical evidence for therapeutic utility of glutamate-modulating drugs as an augmentation or monotherapy in OCD patients
Neuroprotective effects of the mood stabilizer lamotrigine against glutamate excitotoxicity: roles of chromatin remodelling and Bcl-2 induction Whether lamotrigine is a more selective glutamate release inhibitor than other antiseizure agents is uncertain
Purpose: The dentate gyrus (DG) is a gateway that regulates seizure activity in the hippocampus
3 , 4 Recent evidence suggests that the ubiquitous excitatory neurotransmitter glutamate is dysregulated in OCD, and that this dysregulation may contribute to the pathophysiology of the disorder
Lamotrigine is the first medication since lithium granted Food and Drug Administration (FDA) approval for the maintenance treatment of bipolar type I
Lamotrigine: a reduces glutamate release in the cortex
Lamotrigine, an antiepileptic that reduces presynaptic glutamate release, has also been proposed as a potential adjunctive medication in schizophrenia
The anticonvulsant, lamotrigine decreases spontaneous glutamate release but increases spontaneous GABA release in the rat entorhinal cortex in vitro 2000 Aug
Researchers Dursun and Deakin (2001) describe lamotrigine as being a “glutamate excess release inhibitor” and suggest that it may be useful for the
We investigated the site of action of lamotrigine (LTG), an effective anticonvulsant, in the regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and N
In summary, our novel results revealed the strong neuroprotective effects of LTG against glutamate excitotoxicity in CGC cultures
Excitatory glutamatergic neurons participate in virtually every circuit and system in the central
The proposed mechanisms of action explaining the beneficial effect of lamotrigine in bipolar disorder include inhibiting voltage-sensitive sodium channels, glutamate release and the calcium channel blockade
Recent reports have also suggested that the addition of lamotrigine, a glutamate excess release inhibi
It also increases the effects of a neurotransmitter called GABA, which is a calming neurotransmitter
64 Its anticonvulsant and mood-stabilizing properties make it a treatment of Another reason Lamictal may be effective against OCD is because of its ability to modulate glutamate
27 It is unclear whether effects on other neurotransmitter systems are direct
The efficacy of lamotrigine in the treatment of focal epilepsies have already been reported in several case reports and open studies, which is thought to act by inhibiting glutamate release through voltage-sensitive sodium channels blockade and neuronal membrane stabilization
It’s available in generic forms and as the brand-name drugs Lamictal LAMOTRIGINE, a novel antiepileptic drug, is known to block sodium channels in a use-dependent manner and to inhibit glutamate release in the striatum, cortex and hippocampus
The aim of this study was to evaluate the efficacy of lamotrigine, a glutamate antagonist blocking voltage-sensitive sodium channels, in the prophylaxis of migraine aura symptoms
It is thought to suppress the activity of certain parts of the brain Weeks 1 and 2: 25 mg every other day
Lamotrigine is an antiepileptic agent, which has also been used as a mood stabilizer
Glutamate is the ligand that activates it, leading to excititory effects, but it's not directly what causes glutamate release
From: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose (Fourth Edition), 2007