GYKI 52466: Difference between revisions

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'''GYKI 52466''' is a non-competitive [[AMPA receptor]] antagonist that has been widely used in scientific research. By blocking the AMPA receptor, GYKI 52466 is able to inhibit fast synaptic transmission in the [[central nervous system]]. This property makes it a useful tool in the study of the brain and the systems that govern its function.
== GYKI 52466 ==


==Pharmacology==
[[File:GYKI_52466.svg|thumb|right|Chemical structure of GYKI 52466]]
GYKI 52466 is a selective antagonist for the AMPA receptor. Unlike most other AMPA receptor antagonists, it does not compete with the [[glutamate]] binding site, instead it binds to a modulatory site on the AMPA receptor and inhibits its function. This makes GYKI 52466 a non-competitive antagonist.


==Uses in Research==
'''GYKI 52466''' is a chemical compound known for its role as a non-competitive [[AMPA receptor]] antagonist. It is primarily used in [[neuroscience]] research to study the effects of AMPA receptor inhibition on [[synaptic transmission]] and [[neuroprotection]].
Due to its ability to inhibit the AMPA receptor, GYKI 52466 has been used in a variety of research contexts. It has been used to study the role of the AMPA receptor in [[neurotransmission]], [[neuroplasticity]], and [[neurodegeneration]]. It has also been used to investigate the potential therapeutic effects of AMPA receptor antagonists in conditions such as [[epilepsy]], [[stroke]], and [[chronic pain]].


==Potential Therapeutic Applications==
== Mechanism of Action ==
While GYKI 52466 is primarily used in research, it has potential therapeutic applications. Its ability to inhibit the AMPA receptor could make it useful in the treatment of conditions characterized by excessive glutamate activity, such as epilepsy and neurodegenerative diseases. However, more research is needed to fully understand the potential therapeutic benefits and risks of GYKI 52466.


==See Also==
GYKI 52466 functions by binding to the AMPA receptor, a type of [[ionotropic glutamate receptor]] in the [[central nervous system]]. Unlike competitive antagonists, GYKI 52466 does not compete with [[glutamate]] for binding at the receptor's active site. Instead, it binds to an allosteric site, causing a conformational change that reduces the receptor's activity. This non-competitive inhibition results in decreased [[excitatory synaptic transmission]], which can be beneficial in conditions characterized by excessive neuronal excitation.
* [[AMPA receptor]]
 
* [[Glutamate]]
== Applications in Research ==
* [[Neurotransmission]]
 
* [[Neuroplasticity]]
In [[neuroscience research]], GYKI 52466 is utilized to explore the role of AMPA receptors in various physiological and pathological processes. It has been instrumental in studies investigating [[epilepsy]], [[ischemic stroke]], and [[neurodegenerative diseases]] such as [[Alzheimer's disease]]. By inhibiting AMPA receptor activity, researchers can assess the contribution of these receptors to [[neuronal excitotoxicity]] and [[cell death]].
* [[Neurodegeneration]]
 
== Potential Therapeutic Uses ==
 
The neuroprotective properties of GYKI 52466 have sparked interest in its potential therapeutic applications. In preclinical models, it has shown promise in reducing [[neuronal damage]] following [[ischemic events]] and in mitigating [[seizure]] activity. However, further research is needed to evaluate its safety and efficacy in humans.
 
== Chemical Properties ==


==References==
GYKI 52466 is a member of the [[2,3-benzodiazepine]] family, characterized by its unique chemical structure that allows for selective inhibition of AMPA receptors. The compound's structure is depicted in the accompanying image, highlighting its distinct molecular configuration.
<references />


{{medicine-stub}}
== Related Pages ==


* [[AMPA receptor]]
* [[Ionotropic glutamate receptor]]
* [[Neuroprotection]]
* [[Excitotoxicity]]
* [[Epilepsy]]
[[Category:Neuroscience]]
[[Category:Pharmacology]]
[[Category:Pharmacology]]
[[Category:Neuroscience]]
[[Category:Chemical compounds]]
[[Category:AMPA receptor antagonists]]

Latest revision as of 03:31, 13 February 2025

GYKI 52466[edit]

Chemical structure of GYKI 52466

GYKI 52466 is a chemical compound known for its role as a non-competitive AMPA receptor antagonist. It is primarily used in neuroscience research to study the effects of AMPA receptor inhibition on synaptic transmission and neuroprotection.

Mechanism of Action[edit]

GYKI 52466 functions by binding to the AMPA receptor, a type of ionotropic glutamate receptor in the central nervous system. Unlike competitive antagonists, GYKI 52466 does not compete with glutamate for binding at the receptor's active site. Instead, it binds to an allosteric site, causing a conformational change that reduces the receptor's activity. This non-competitive inhibition results in decreased excitatory synaptic transmission, which can be beneficial in conditions characterized by excessive neuronal excitation.

Applications in Research[edit]

In neuroscience research, GYKI 52466 is utilized to explore the role of AMPA receptors in various physiological and pathological processes. It has been instrumental in studies investigating epilepsy, ischemic stroke, and neurodegenerative diseases such as Alzheimer's disease. By inhibiting AMPA receptor activity, researchers can assess the contribution of these receptors to neuronal excitotoxicity and cell death.

Potential Therapeutic Uses[edit]

The neuroprotective properties of GYKI 52466 have sparked interest in its potential therapeutic applications. In preclinical models, it has shown promise in reducing neuronal damage following ischemic events and in mitigating seizure activity. However, further research is needed to evaluate its safety and efficacy in humans.

Chemical Properties[edit]

GYKI 52466 is a member of the 2,3-benzodiazepine family, characterized by its unique chemical structure that allows for selective inhibition of AMPA receptors. The compound's structure is depicted in the accompanying image, highlighting its distinct molecular configuration.

Related Pages[edit]