@entity159 results in an @entity1024 receptor-dependent inhibition of Ca2+/calmodulin-dependent kinase II activity in the XXXX .

@entity410 @entity3175 @entity1024 @entity2134 @entity460 @entity35 @entity159
@entity159 is a major medical emergency that results in significant alteration of neuronal function. @entity159 involves @entity410 activity recurring frequently enough to induce a sustained alteration in brain function. This study was initiated to investigate how @entity159 affects the activity of @entity460 and calmodulin-dependent kinase II in the brain. @entity460 and calmodulin-dependent kinase II is a neuronally enriched signal transducing system involved in the regulation of neurotransmitter synthesis and release, cytoskeletal function, gene transcription, neurotransmitter receptor function and neuronal excitability. Therefore, alteration of this signal transduction system would have significant physiological effects. @entity159 was induced in @entity35 by @entity2134 injection, allowed to progress for 60 min and terminated by repeated @entity3175 injections. Animals were killed at specific time-points and examined for @entity460 and calmodulin-dependent kinase II activity. @entity460 and calmodulin-dependent kinase II activity was significantly reduced in cerebral cortex and hippocampal homogenates obtained from @entity159 @entity35 when compared with control animals. Once established, the @entity159 -induced inhibition of @entity460 and calmodulin-dependent kinase II activity was observed at all time-points tested following the termination of @entity410 activity. However, @entity460 and calmodulin-dependent kinase II activity was not significantly decreased in thalamus and cerebellar homogenates. In addition, @entity159 -induced inhibition of @entity460 and calmodulin-dependent kinase II activity was dependent upon activation of @entity1024 subtype of glutamatergic receptors. Thus, @entity159 induced a significant inhibition of @entity460 and calmodulin-dependent kinase II activity that involves @entity1024 receptor activation. The data support the hypothesis that inhibition of @entity460 and calmodulin-dependent kinase II activity may be involved in the alteration of neuronal function following @entity159 .
