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PubMed1982

Striatal glutamatergic function: modifications following specific lesions.

The effects of specific lesions of the striatum: (a) hemidecortication; (b) striatal injection of (+/-) ibotenate; and (c) 6-hydroxydopamine injections into the substantia nigra, were investigated on specific [3H]glutamate binding to striatal membranes. One month after decortication, there was a substantial reduction of calcium-dependent, stimulated glutamate release from striatal slices, indicating effective loss of glutamatergic fibres. Striatal glutamate binding increased by approximately 30% and this supersensitivity could be attributed solely to an increased receptor density. Ibotenate lesions which destroy target neurones for the glutamatergic fibres (sparing terminals), reduced glutamate binding in the striatum, as did nigral 6-OHDA lesions which delete striatal dopaminergic terminals. This finding supports the concept of there being glutamate receptors on pre-synaptic dopamine terminals in the striatum, involved in regulation of dopamine release. 6-OHDA lesions also result in a supersensitivity of the dopamine receptors localized on the cortico-striatal afferent terminals, as evidenced by the enhanced ability of dopamine to inhibit the K+-evoked, calcium-dependent release of endogenous striatal glutamate.

Animals↗
PubMed1977

Cerebral necrosis following radiotherapy of extracranial neoplasms.

We have examined 6 patients with delayed cerebral necrosis following irradiation of extracranial neoplasms. Four of the 6 patients received 1,760 rets (or less) tumor dose. The initial symptoms attributable to radiation necrosis appeared 4 to 31 months after irradiation and were those of a focal supratentorial mass. Cerebral angiography delineated an avascular frontal or temporal lesion in all 6 patients; in 1 case a magnification study revealed narrowing, irregularity, and occlusion of small cortical vessels. Four of our 6 patients underwent craniotomy with partial or complete surgical extirpation of necrotic brain tissue. Two operated patients are alive and without disabling neurological symptoms 30 and 25 months, respectively, after the operation. The characteristic neuropathological features of delayed radiation necrosis of brain suggest that vascular injury rather than neuronal or glial damage is of primary pathogenetic significance.

Adult↗
PubMed1979

The effect of the sequence of contralateral cortical and collicular lesions on the rate of relearning a visual discrimination by cats.

Visual field deficits which follow ablation of the posterior two-thirds of one cerebral hemisphere in the cat have been shown to be ameliorated by ablation of the contralateral superior colliculus. The present study was designed to determine whether the sequence in which contralateral cortical and collicular lesions are made is a significant factor affecting the rate of monocular relearning through the eye ipsilateral to the cortical lesion. Nine adult cats had the optic chiasm sectioned, were trained to criterion monocularly on a dark-light discrimination, and were divided into two groups. Four cats (Group S) had one superior colliculus ablated, followed one month later by ablation of the contralateral two-thirds of the neocortex. Five cats (Group C) had the same lesions in the reverse order. One month after the second brain lesion, each cat was retrained monocularly through each eye on the dark-light discrimination for food reward in a Y-maze. Through the eye ipsilateral to the cortical lesion, all cats in Group S relearned to criterion more rapidly than cats previously reported with only unilateral neocortical lesions. Four of the five cats in Group C were severely retarded in relearning and two of these cats failed to relearn. The results show that when chiasm-sectioned cats are trained monocularly in a Y-maze on a dark-light discrimination, ablation of the superior colliculus prior to ablation of the contralateral neocortex facilitates relearning through the eye ipsilateral to the cortical ablation. When ablation of the superior colliculus follows the neocortical lesion, learning occurs but is not facilitated by the additional lesion.

Animals↗
PubMed1992

Cortical and striatal structure and connectivity are altered by neonatal hemidecortication in rats.

The cortical cytoarchitecture, cortical thickness, corticostriatal connections, cortical dendritic arborization, and striatal patch-matrix compartmentalization were compared in rats with neonatal (1 day of age) or adult hemidecortication. Neonatal hemidecortication produced few changes in cytoarchitecture of the remaining hemisphere and did not preclude the development of a patch-matrix compartmentalization in either striatum. There was a significant modification of contralateral cortical-striatal connections, however, as there were extensive crossed connections from layer II/III of the prefrontal cortex in the neonatal hemidecorticates, which contrasts with connections from layer V in the normal brain. Adult hemidecorticates had no crossed corticostriatal connections. Neonatal hemidecortication also led to an increase in cortical thickness relative to adult operates or controls and the neonatal hemidecorticates, and led to an increase in dendritic arborization in layer II/III pyramidal cells of the somatosensory and motor cortex but not in the visual or temporal cortex. The results suggest that the behavioral sparing of sensorimotor and some prefrontal functions after neonatal hemidecortication could be supported, in part, by the anatomical changes in the prefrontal and sensorimotor connectivity and dendritic arborization.

Animals↗
PubMed1985

Neonatal hemidecortication and bilateral cutaneous stimulation in rats.

In humans, a dominant somatosensory consequence of extensive unilateral neocortex damage is "simultaneous extinction," which is an interhemispheric perceptual interaction that is operationally distinguishable from neglect. A tactile stimulus presented on the contralateral side of the body is detected when presented singly, but is completely masked during bilateral stimulation. Analogous tests designed to calibrate somatosensory asymmetries in rats were used to determine the long-term effects of hemidecortication sustained on postnatal Day 1. These data were compared with that observed in adult operated rats at a comparable postoperative period. In one respect the neonatal brain was more vulnerable than the adult brain. That is, unlike adult operated rats which were tested at 3 postoperative months, a sensory asymmetry appeared to be permanent in the neonatally operated rats, at least for the duration of testing (3-9 months). Further analysis suggested that in another way the neonates were more resistant to the effects of hemidecortication than were the adults. Neonatally operated rats appeared to be capable of processing input from both sides of the body simultaneously, even during markedly asymmetrical input. In other words, the early occurrence of brain damage may have spared them from a condition reminiscent of "simultaneous extinction." Finally, the adult operated and neonatally operated rats both displayed a subtle motor abnormality. Thus, depending on the test used, the neonatal operation yielded more severe, less severe, or comparable behavior deficits.

Animals↗
PubMed1987

Evidence for reactive synaptogenesis in the ventrolateral thalamus and red nucleus of the rat: changes in high affinity glutamate uptake and numbers of corticofugal fiber terminals.

High affinity glutamate uptake into corticofugal fiber terminals was measured in the ventrolateral thalamus and red nucleus at varying time intervals after lesions were made by kainic acid in the contralateral interpositus nucleus of the cerebellum in rats. Under similar conditions the density of cortical fiber terminals was estimated using the Fink-Heimer impregnation technique. 1. Glutamate uptake steadily increased in the ventrolateral thalamus up to 60 days after lesions in the contralateral cerebellum. 2. Similar changes were noted in the red nucleus. 3. The changes were dependent on the integrity of corticofugal fibers to the thalamus and red nucleus. 4. No changes in uptake of gamma-aminobutyric acid were noted. 5. Saturation curves for glutamate uptake suggested a change in the maximal number of transport sites. 6. Fink-Heimer degeneration studies showed an increase in cortical terminals in the ipsilateral ventrolateral thalamus and in both rostral and caudal regions of the red nucleus following lesions in the contralateral interpositus nucleus. The data are consistent with an increase in the number of cortical fiber terminals in reaction to loss of cerebellar input to the ventrolateral thalamus and red nucleus. This study correlates anatomical and biochemical evidence for collateral sprouting in a model based on electrophysiologic data in the red nucleus and extends the model to include the thalamus.

Animals↗
PubMed1987

Hemidecortication selectively alters release of glutamate in perfusates collected from cerebral cortex of unrestrained rats.

The effect of hemidecortication on the in vivo release of amino acids was examined in different areas of the cerebral cortex of the freely-moving rat. After one side of the cortex was lesioned by aspiration, four guide tubes for push-pull perfusion were implanted chronically on the contralateral side so as to rest above the frontal, parietal, temporal and occipital areas of the cortex. After 10-14 days elapsed, each of these regions was perfused with an artificial cerebrospinal fluid (CSF) at a rate of 25.0 microliter/min. Two types of assays were undertaken to determine the release of either newly synthesized amino acids from [14C]glucose precursor or the actual endogenous content in samples of perfusate. The separation of the [14C]amino acids was performed by thin layer chromatography, whereas endogenous amino acids were separated by HPLC with electrochemical detection and quantitated in the range of 1.0-10.0 picomoles. When compared to the control group, samples collected in the hemidecorticate rat showed no significant differences in the new synthesis of glutamate, aspartate, glutamine, glycine, and GABA from the precursor. On the other hand, the analysis of the endogenous amino acid neurotransmitters revealed that the levels of glutamic acid and glutamine declined in samples obtained from the parietal and frontal cortex, respectively. These results implicate further the potential role of glutamic acid as a neurotransmitter of interhemispheric connections in the cerebral cortex.

Animals↗
PubMed1987

Impact of neodecortication on colon motor response to a meal in the rat.

The colon motor response to a meal consisting of 100 mM of sodium oleate was assessed before and after neodecortication in male Sprague-Dawley rats. Recording probes were anchored surgically in the ascending and descending colon. Pressure changes were recorded on a dynograph using a low-compliance perfusion system. A motility index took into account the amplitude, duration, and frequency of contractions. Neodecortication increased the motility index of the distal colon in the fasting state. However, removal of the cerebral cortex did not affect significantly the colon motor response to a meal. Meal stimulation increased the motility index before and after neodecortication. These findings suggest that resting colonic motor activity is increased after neodecortication, probably through the loss of an inhibitory influence of the central nervous system; and the cerebral cortex is not required for the colon response to a meal in the rat.

Animals↗