Effect of Cortico‐Striate Pathway Lesion on the Activities of Enzymes Involved in Synthesis and Metabolism of Amino Acid Neurotransmitters in the Striatum

Sandberg, Mats; Ward, H. K.; Bradford, H. F.

doi:10.1111/j.1471-4159.1985.tb07110.x

Cited by 64 publications

(31 citation statements)

References 35 publications

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“…Lesioning the ipsilateral substantia nigra by 6-hydroxydopamine results in increased striatal levels of mRNAs encoding glumatic acid decarboxylase and proenkephalin; the changes in mRNA levels peaked on day 25 and lasted for a few months (Vernier et al, 1988). The time-courses of these two studies may be different from the present work because microsurgical dissection (Sandberg et al, 1985) or chemical lesion (Vernier et al, 1988) was used rather than focal ischemia, and because the brain region and the neurotransmitter systems studied are different. Our results do not differentiate whether the increase in neuropeptide levels in the amygdala is due to increased synthesis, increased axonal transport, or reduced release.…”

Section: Changes Of Npy 1-enk Dyn and Ntmentioning

confidence: 48%

“…Previous stildies have demonstrated compensatory changes in the levels of the enzymes or mRNA that are involved in the synthesis and metabolism of neurotransmitters within deafferented areas (Sandberg et al, 1985;Vernier et al, 1988). Sandberg and colleagues (1985) reported changes in levels of striatal enzymes for the synthesis and degradation of glutamate and glutamine following fronto-parietal decortication.…”

Section: Changes Of Npy 1-enk Dyn and Ntmentioning

confidence: 97%

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Time‐course of neuropeptide changes in peri‐ischemic zone and amygdala following focal ischemia in rats

Cheung

Diab

Cechetto

1995

J of Comparative Neurology

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Previously, using a middle cerebral artery occlusion model in Wistar rat, we showed autonomic disturbances similar to those seen clinically and observed striking neurochemical changes in cortical and subcortical sites at 5 days following stroke. The neurochemical changes may account for functional recovery and/or autonomic disturbances after focal ischemia. To understand the possible mechanisms and to facilitate future studies, it is necessary to define the time-courses of these changes. Using immunohistochemical staining with the peroxidase-antiperoxidase reaction, the changes in several neuropeptides over the peri-ischemic region and the ipsilateral central and basolateral nucleus of the amygdala were investigated at different times after middle cerebral artery occlusion. In the experimental group, neuropeptide Y immunoreactivity appeared to increase by 6 hours in the peri-ischemic region. Using image analysis to quantify the staining intensity, the change became statistically significant at 1 day, peaked around 3 days, and subsided at 10 days. There was a delayed increase in neuropeptide Y in the ipsilateral basolateral nucleus of the amygdala with a peak around 3 days. Immunoreactive staining for leucine-enkephalin, dynorphin, and neurotensin demonstrated an increase that was localized to the ipsilateral central nucleus of the amygdala with a peak around 3 days and a return to baseline levels by 10 days. The results support a specific time-course for each of the neuropeptides studied and indicate that a survival time of 3 days after focal ischemia is the critical period for examining the relationship between neuropeptide responses and neuronal or functional recovery.

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Section: Changes Of Npy 1-enk Dyn and Ntmentioning

confidence: 48%

Section: Changes Of Npy 1-enk Dyn and Ntmentioning

confidence: 97%

Time‐course of neuropeptide changes in peri‐ischemic zone and amygdala following focal ischemia in rats

Cheung

Diab

Cechetto

1995

J of Comparative Neurology

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“…Interestingly, this enzyme can be detected in the cerebrospinal fluid of patients in advanced stages of Alzheimer disease (32). In some in vivo injury paradigms, neuronal degeneration is accompanied by an increase in astrocyte GS (33)(34)(35)(36). This increase has been attributed to reactive astrocytosis that occurs in response to neural insults and might be part of an endogenous mechanism for neuroprotection.…”

Section: Discussionmentioning

confidence: 97%

Glutamine synthetase protects against neuronal degeneration in injured retinal tissue

Gorovits

Avidan

Avisar

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

127

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The neurotransmitter glutamate is neurotoxic when it is accumulated in a massive amount in the extracellular f luid. Excessive release of glutamate has been shown to be a major cause of neuronal degeneration after central nervous system injury. Under normal conditions, accumulation of synaptically released glutamate is prevented, at least in part, by a glial uptake system in which the glia-specific enzyme glutamine synthetase (GS) plays a key role. We postulated that glial cells cannot cope with glutamate neurotoxicity because the level of GS is not high enough to catalyze the excessive amounts of glutamate released by damaged neurons. We examined whether elevation of GS expression in glial cells protects against neuronal degeneration in injured retinal tissue. Analysis of lactate dehydrogenase eff lux, DNA fragmentation, and histological sections revealed that hormonal induction of the endogenous GS gene in retinal glial cells correlates with a decline in neuronal degeneration, whereas inhibition of GS activity by methionine sulfoximine leads to increased cell death. A supply of purified GS enzyme to the culture medium of retinal explants or directly to the embryo in ovo causes a dose-dependent decline in the extent of cell death. These results show that GS is a potent neuroprotectant and that elevation of GS expression in glial cells activates an endogenous mechanism whereby neurons are protected from the deleterious effects of excess glutamate in extracellular f luid after trauma or ischemia. Our results suggest new approaches to the clinical handling of neuronal degeneration.Glutamate neurotoxicity plays an important role in the process of neuronal degeneration after trauma or focal ischemia (for reviews, see refs. 1 and 2). Glutamate, a neurotransmitter that mediates normal excitatory synaptic transmission by interaction with postsynaptic receptors, is neurotoxic when present in excessive amounts. Injured neurons release massive amounts of glutamate, which induce neuronal cell death by continuous overexcitation of postsynaptic receptors. In this way, the initial trauma is amplified and causes the damage to spread to neighboring cells. Under normal conditions, the synaptically released glutamate is taken up into glial cells, where it is converted into glutamine by the glia-specific enzyme glutamine synthetase [GS; L-glutamate:ammonia ligase (ADPforming); EC 6.3.1.2]; glutamine reenters the neurons and is hydrolyzed by glutaminase to form glutamate, thus replenishing the neurotransmitter pool (3, 4). This biochemical pathway fails, however, to prevent glutamate neurotoxicity after insult. We hypothesized that GS is a limiting factor in this process and that its level in glial cells is not high enough to catalyze the excessive amounts of glutamate released by damaged cells. If this is the case, an increase in GS expression should have neuroprotective benefits.To examine the neuroprotective potential of GS, it is necessary to employ an experimental system in which expression of GS can be modulated. The ...

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“…It has been suggested that GS activity can be used as a biochemical marker of reactive gliosis (Sandberg et al, 1985). We have previously reported a transient increase of GS activity in a model of gliosis secondary to a neurotoxic lesion in the rat hippocampus (Condorelli et al, 1988).…”

Section: Introductionmentioning

confidence: 98%

Glial fibrillary acidic protein messenger RNA and glutamine synthetase activity after nervous system injury

Condorelli

Dell’Albani

Kaczmarek

et al. 1990

J of Neuroscience Research

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The level of the mRNA for glial fibrillary acidic protein (GFAP), the major protein of the intermediate filaments of astroglial cells, and the activity of glutamine synthetase (GS), an enzyme selectively localized in astrocytes, were measured at different times after a unilateral mechanical lesion in the rat cerebral cortex. A rapid and early increase (6 hours post-lesion) in GFAP mRNA was observed; GFAP mRNA level reached a peak at 1-3 days and then decreased. Moreover, an astrocytic activation in cortical zones far from the injury site and in the contralateral hemisphere was detected. No change of GS activity was observed in the same model of brain injury, showing that this astroglial marker is not modified during the reactive gliosis obtained with this experimental model. GFAP mRNA has also been detected in the rat sciatic nerve; however, its level was not modified after nerve transection, suggesting a different regulation of GFAP expression in the peripheral nervous system.

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Effect of Cortico‐Striate Pathway Lesion on the Activities of Enzymes Involved in Synthesis and Metabolism of Amino Acid Neurotransmitters in the Striatum

Cited by 64 publications

References 35 publications

Time‐course of neuropeptide changes in peri‐ischemic zone and amygdala following focal ischemia in rats

Time‐course of neuropeptide changes in peri‐ischemic zone and amygdala following focal ischemia in rats

Glutamine synthetase protects against neuronal degeneration in injured retinal tissue

Glial fibrillary acidic protein messenger RNA and glutamine synthetase activity after nervous system injury

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