GABA and Glutamate Levels in the Substantia Nigra Reticulata Following Repetitive Cerebral Ischemia in Gerbils

Pre-ischemic treadmill training affects glutamate and gamma aminobutyric acid levels in the striatal dialysate of a rat model of cerebral ischemia

“…They consider that this is an important factor in brain injury. Shuaib et al (1997), using a repeated cerebral ischemia model in gerbils, tracked the release of GABA and glutamate in the reticular structure of the substantia nigra. They concluded that reduction in GABA level was one of the causes of neuronal injury after cerebral ischemia.…”

Overview of the Neuroprotective Effects of the MAO-Inhibiting Antidepressant Phenelzine

“…Studies on the possible role of acrolein in multiple sclerosis have received considerable interest in more recent years (Leung et al 2011;Tully et al 2018). Acrolein induces damage to myelin in the spinal cord of mammals (Shi et al 2011(Shi et al , 2015, and there have been reports of elevated levels of acrolein in the EAE mouse model of multiple sclerosis (Leung et al 2011;Tully et al 2018). Hydralazine, which like PLZ is a carbonyl scavenger, has been reported to improve symptoms (Leung et al 2011) and reduce spinal cord levels of acrolein in the EAE model (Tully et al 2018).…”

“…Our interest in possible neuroprotective/neurorescue actions of PLZ and PEH was stimulated by reports that various GABAergic drugs decreased neuronal cell loss in animal models of stroke (global and focal ischemia) (Chen Xu et al 2000 ; Leker and Neufeld 2003 ; Shuaib et al 1992 , 1997 ; Shuaib and Kanthan 1997 ; Sydserff et al 2000 ) and by suggestions that such agents were effective by counteracting the deleterious excitotoxic effects of the increased glutamate release that occurs in stroke (Green et al 2000 ; Schwartz-Bloom and Sah 2001 ; Shuaib and Kanthan 1997 ; Stumm et al 2001 ). Indeed, there is now a large body of literature indicating the importance of maintaining the exquisite balance between GABA and glutamate in the brain and suggesting that a disruption of that balance is a feature of several psychiatric and neurological disorders, including depression, mania, epilepsy, amyotrophic lateral sclerosis, schizophrenia, multiple sclerosis, and stroke (Cohen et al 2015 ; Foerster et al 2013 ; Green et al 2000 ; Ketter and Wang 2003 ; Kim and Yoon 2017 ; Luscher et al 2011 ; Naylor 2010 ; Potter et al 2016 ; Wassef et al 2003 ).…”

Neurovascular Unit as a Source of Ischemic Stroke Biomarkers—Limitations of Experimental Studies and Perspectives for Clinical Application

“…The reduction of tonic GABA-ergic inhibition, especially in the early postischemic period, apart from glutamatergic excitotoxicity, may enhance disturbances of synaptic plasticity. However, subsequently occurring increase in GABA content, through limiting damage, can be encountered among the neuroprotective processes [150]. Furthermore, increased tonic GABArelated inhibition, mediated presumably by GABA A receptors, might lead to improved motor function after ischemic stroke [151].…”

“…Moreover, a Glu/GABA ratio higher than 106 is regarded as a predictor of early neurological deterioration in 85% of patients with lacunar infarction. Subsequent increase in GABA secretion leading to reduction of this ratio signals lowering of the intensity of damage and promotion of reparative processes [150]. The Glu/GABA ratio can differ between the infarct core and peripherally localized penumbra [159].…”