Kainic Acid Receptors (Kainate Receptor)

09/01/2008 - "This study shows that the stimulation of the GLU(K5) kainate receptor subtype rescues the kindling-induced impairment of LA-LTP at least within 48 h after the last seizure. "
09/01/1992 - "This study was conducted to assess the functional integrity of the kainate receptor-mediated seizure response in aged rats. "
04/23/2014 - "Olfactory bulb kindling developed similarly in wild-type, GluK1, and GluK2 knock-out mice, demonstrating that GluK1 kainate receptors are not required for epileptogenesis or seizure expression in this model. "
04/23/2014 - "We found that systemic ATPA, acting specifically via GluK1 kainate receptors, causes locomotor arrest and forelimb extension (a unique behavioral characteristic of GluK1 activation) and induces myoclonic behavioral seizures and electrographic seizure discharges in the BLA and hippocampus. "
01/01/2009 - "Recent analysis of genetically modified mice deficient in different kainate receptor (KAR) subunits have strongly pointed to a role of the GluK2 subunit, mediating the vulnerability of the brain towards seizures. "

09/01/2004 - "Kainate receptor antagonists could thus be useful for the treatment of certain forms of allodynia and hyperalgesia."
05/30/2003 - "The present study demonstrates that administration of a high-potency ligand that selectively desensitizes kainate receptors attenuates the development of mechanical and heat hyperalgesia and attenuates ongoing inflammatory hyperalgesia."
10/11/2002 - "These results suggest that a selective upregulation of kainate receptor subunit expression contributes to inflammatory hyperalgesia."
10/01/2006 - "The present studies provide further evidence that selective Glu(K5) kainate receptor subtype antagonists can reverse allodynia and hyperalgesia, particularly in persistent pain states."
10/11/2002 - "Activation of spinal kainate receptors after inflammation: behavioral hyperalgesia and subunit gene expression."

06/01/2007 - "The selective targeting of kainate receptors with an antagonist could therefore be a novel pharmacological mechanism to treat anxiety disorders."
04/01/2006 - "These data along with those in the literature suggest that AMPA and/or kainate receptor blockade may be an important component to producing anxiolytic-like effects and may therefore be a target for compounds with efficacy in the therapeutic treatment of anxiety disorders."
04/01/2006 - "In vitro and in vivo studies in rats with LY293558 suggest AMPA/kainate receptor blockade as a novel potential mechanism for the therapeutic treatment of anxiety disorders."
06/01/2008 - "Although emerging number of data supports the role of glutamate receptors and the potential of their antagonists in anxiety disorders, the involvement of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors in anxiety is less well characterized. "

01/01/1991 - "In contrast to ischemia and hypoglycemia, however, damage is mediated at a different excitatory CNS receptor, namely the kainate receptor. "
08/24/1998 - "The high vulnerability of oligodendrocytes and their precursors to AMPA/kainate receptor excitotoxicity may represent an important mechanism of white matter damage resulting from trauma or ischemia in the perinatal and adult central nervous system (CNS)."
07/01/1995 - "To test the hypothesis that the period of vulnerability of the developing human brainstem to hypoxia-ischemia correlates with a transient elevation in kainate receptor binding, we compared the quantitative distribution of [3H]kainate binding in brainstem nuclei between four fetuses (19-26 gestational weeks), four infants (one to nine months), and three "mature" individuals (one child and two adults) without neurological disease. "
08/01/2000 - "NBQX, an AMPA/kainate receptor antagonist, reduced ischemia-induced white matter injury and improved locomotor function."
11/10/2004 - "Similar morphological alterations (neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina."

11/01/2013 - "Kainate receptor RNA editing is markedly altered by acute spinal cord injury."
01/01/2001 - "Excitotoxic mechanisms involving alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA)/kainate receptors play an important role in mediating cellular damage in spinal cord injury. "
06/01/1997 - "Delayed antagonism of AMPA/kainate receptors reduces long-term functional deficits resulting from spinal cord trauma."
10/18/2011 - "To evaluate bladder function recovery after spinal cord injury (SCI) in response to a combination treatment of an acutely administered AMPA/kainate receptor antagonist and delayed transplantation of neuronal precursors. "
05/26/2010 - "Glutamate excitotoxicity mediated via kainate receptors has been implicated in the neuropathology of both EAE and spinal cord injury, and has been identified as a trigger that reduces PMCA2 levels in pure spinal cord neuronal cultures through degradation of the pump by calpain without affecting PMCA2 transcript levels. "