cerebrocortical

cerebrocortical

pertaining to the cerebral cortex.

cerebrocortical malacia
cerebrocortical necrosis
References in periodicals archive ?
Myricetin inhibits the release of glutamate in rat cerebrocortical nerve terminals.
sup][37] Propofol induced GABA and glutamate release in cerebrocortical synaptosomes, and the glutamate release is through presynaptic voltage-dependent Na [sup]+ channels as a molecular target.
Retrospective analysis of cases with diagnosis of cerebrocortical necrosis and its relation with type 5 bovine herpesvirus.
Bauer, "Detecting the signature of reticulothalamocortical communication in cerebrocortical electrical activity," Clinical Neurophysiology, vol.
Valproate inhibits oxidative damage to lipid and protein in primary cultured rat cerebrocortical cells.
The Na + -Ca2 + exchanger activity in cerebrocortical nerve endings is reduced in old compared to young and mature rats when it operates as a Ca2 + influx or efflux pathway.
However, in-vitro studies demonstrated that lamotrigine reduce the release of GABA in the cerebrocortical slices of rats in doses higher than that required to reduce release of glutamate and aspartate.
Furthermore, enhancement of neurite outgrowth in cerebrocortical neurons by 1 was reported at a concentration of 30-100 nM after 24 h incubation.
The results demonstrated that terbutaline increased microglial activation in the subjects' cerebral cortex, cerebellar, and cerebrocortical white matter [23].
The company provides primary neuronal culture models of neuroinjury and neurotoxicity, including cerebrocortical cultures, cerebellum granule neurons, and hippocampal neurons; protease enzyme assays; cell-based protease assays; and others.
The cerebrocortical areas in normal brain aging and in Alzheimer's disease: noticeable differences in the lipid peroxidation level and in antioxidant defense.
Similarly, a study of cerebrocortical cell cultures found that 3 days of exposure to 1% oxygen increased activities of glycolytic and its related enzymes (hexokinase, lactate dehydrogenase, and pyruvate kinase), as well as decreased activities of the TCA cycle related enzymes (citrate synthase and glutamate dehydrogenase), suggesting that neurons are capable of adapting to prolonged hypoxia by upregulating glycolysis and downregulating oxidative energy metabolism [72].