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Biomedical subjects

T R Raju

Publications and source records attributed to T R Raju.

At least 19 recordsLinked to original sources
PubMed1999

Chronic (-) deprenyl administration alters dendritic morphology of layer III pyramidal neurons in the prefrontal cortex of adult Bonnett monkeys.

Chronic (-) deprenyl (0.2 mg/kg, b.wt; for 25 days) treatment induced alterations in the dendritic morphology of prefrontal cortical neurons in adult Bonnett monkeys were evaluated in the present study. The branching points and intersections in apical and basal dendrites were studied up to a distance of 400 and 200 micrometers, respectively, in Golgi impregnated layer III pyramidal neurons of the prefrontal cortex. Our results revealed a significant (p<0.001) increase in the number of branching points and intersections in both apical and basal dendrites in (-) deprenyl treated monkeys compared to controls. Such an enriched dendritic arborization in prefrontal cortical neurons may be responsible for the enhancement of cognitive functions in Alzheimer disease patients following (-) deprenyl treatment.

Analysis of Variance↗
PubMed1999

Spatial memory impairment in ventral subicular lesioned rats.

The present study examined the effects of ibotenic acid lesions of the ventral subiculum (SUB) on the ability of rats to memorize a rewarded alternation test in a T-maze. Results indicated that rats with ibotenic acid lesions (IL) of the ventral subiculum were impaired in postoperative acquisition of the spatial discrimination task, making more errors than the vehicle treated and normal control rats. In addition, all rats, including the IL group of rats, were able to memorize an acquired spatial behaviour. These findings suggest that the SUB play an important role in spatial information processing in rats.

Animals↗
PubMed1998

Alterations in the density of excrescences in CA3 neurons of hippocampus in rats subjected to self-stimulation experience.

Self-stimulation (SS) rewarding experience induced alterations in the density of excrescences in the apical dendrites of CA3 neurons were studied in adult male Wistar rats. SS experience was provided daily for an hour over a period of 10 days, through bipolar stainless steel electrodes implanted bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. The results revealed a significant (P<0.001) increase in the number of excrescences in both main shaft and sub branches of the apical dendrites in SS experienced group compared to control groups of rats. The increased number of excrescences in CA3 neurons might be due to an enhancement in the synaptic transmission in the mossy fiber pathway following SS experience.

Animals↗
PubMed1998

Long-lasting structural changes in CA3 hippocampal and layer V motor cortical pyramidal neurons associated with self-stimulation rewarding experience: a quantitative Golgi study.

Self-stimulation (SS) rewarding experience induced structural changes in CA3 hippocampal and layer V motor cortical pyramidal neurons in adult male Wistar rats has been demonstrated. In the present study, whether these structural changes are transient or of a permanent nature was evaluated. Self-stimulation experience was provided for 1 h daily over a period of 10 days through bilaterally implanted bipolar electrodes in the lateral hypothalamus and the substantia nigra-ventral tegmental area. Following 10 days of SS experience, the rats were sacrificed after an interval of 30 and 60 days for the quantitative analysis of the dendritic morphology in Golgi stained CA3 hippocampal and layer V motor cortical pyramidal neurons. The results revealed a significant increase in the dendritic branching points and intersections in apical and basal dendrites in both types of neurons in 30 days post-SS group compared to sham control. The total number of apical and basal dendrites were significantly increased in both 30 and 60 days post-SS groups of rats. This study suggests that SS experience induced structural changes are sustainable, even in the absence of rewarding experience.

Analysis of Variance↗
PubMed1998

Chronic (-) deprenyl administration increases dendritic arborization in CA3 neurons of hippocampus and AChE activity in specific regions of the primate brain.

The mechanism by which (-) deprenyl enhances cognitive function in Alzheimer's disease (AD) is not yet understood. (-) Deprenyl (0.2 mg/kg/day) was administered intramuscularly to adult male monkeys (n = 6) for 25 days. Control monkeys (n = 6) received physiological saline by the same route. The activity of acetylcholinesterase (AChE) in different brain regions and the dendritic arborization in CA3 pyramidal neurons of hippocampus were analysed. (-) Deprenyl-treated monkeys showed a significant increase in the AChE activity by 43% (p < 0.001) in the frontal cortex, by 39% (p < 0.025) in the motor cortex, by 66% (p < 0.001) in the hippocampus and by 26% (p < 0.05) in the striatum compared to controls. The branching points and the intersections of both apical and basal dendrites of CA3 hippocampal pyramidal neurons were also significantly increased in (-) deprenyl-treated monkeys. Enhanced AChE activity may increase dendritic arborization in the hippocampus and it may also play a role in improving cognitive functions observed in AD, following (-) deprenyl treatment.

Acetylcholinesterase↗
PubMed1998

Corticosterone attenuates zinc-induced neurotoxicity in primary hippocampal cultures.

Primary hippocampal cultures derived from newborn rats were exposed to zinc chloride at 50, 75, 100, 150 and 200 microM concentrations. Neuronal injury was assessed morphologically and by the lactate dehydrogenase (LDH) efflux assay. Zinc exposure increased LDH efflux in a concentration-dependent manner. Exposure to 100 microM zinc for 24 h resulted in beading of neurites and swelling of neuronal soma. When cultures were co-exposed to zinc at 100 microM and corticosterone in the range of 10-5 to 10-7 M, degeneration of neurons caused by zinc was attenuated. Our study suggests that corticosterone can protect neurons from zinc-induced neurotoxicity at low doses.

Analysis of Variance↗
PubMed1998

Reactive astrogliosis in neonatal rat spinal cord after exposure to cerebrospinal fluid from patients with amyotrophic lateral sclerosis.

Previous studies have proposed the presence of circulating toxic factor(s) in the cerebrospinal fluid (CSF) of patients with amyotrophic lateral sclerosis (ALS). In the present study we show that there is an increased number of astrocytes intensely immunoreactive for glial fibrillary acidic protein (GFAP) in the gray matter of the spinal cords of neonatal rats exposed to ALS CSF. There is also increased expression of GFAP in the astrocytes of the white matter of neonatal rat spinal cords exposed to ALS CSF. Western blot analysis also confirmed the increased expression of GFAP. Accordingly, our study provides for the first time a clear evidence for the pathological response of glia to the circulating toxic factor(s) in the CSF of ALS patients.

Amyotrophic Lateral Sclerosis↗
PubMed1998

(-)-Deprenyl attenuates spinal motor neuron degeneration and associated locomotor deficits in rats subjected to spinal cord ischemia.

We have evaluated potential neuroprotection offered by (-)-deprenyl on degenerating motor neurons of the spinal cord when subjected to transient ischemia. Thirty-six healthy adult male Wistar rats were trained for a motor function test in a staircase maze and randomly but equally (n = 6) grouped into normal control, sham control, ischemia (IS), IS rats treated with vehicle (IV), and rats treated with low (0.1 mg/kg) and high (1.0 mg/kg) doses of (-)-deprenyl. (-)-Deprenyl was given intraperitoneally 30 min after the induction of ischemia and thereafter everyday for 14 days. Spinal cord ischemia was produced at the lumbar level in conscious rats by occluding the abdominal aorta just below the branching point of the left renal artery for 30 min. Analysis of the motor performance in all groups of rats revealed a significant (P < 0.001) increase in the time taken to cross the run way of the maze, in i.s. and i.v. rats compared to all other groups of rats. In addition, qualitative and quantitative examination of spinal motor neurons at the lumbar level showed a significant (P < 0.001) decrease in the number of healthy motor neurons in i.s. and i.v. rats compared to controls. Postischemic administration of (-)-deprenyl, at both doses, significantly prevented motor neuron degeneration and the associated locomotor deficits in IS rats.

Animals↗
PubMed1998

Self-stimulation of lateral hypothalamus and ventral tegmentum increases the levels of noradrenaline, dopamine, glutamate, and AChE activity, but not 5-hydroxytryptamine and GABA levels in hippocampus and motor cortex.

Self-stimulation (SS) rewarding experience induced structural changes have been demonstrated in the hippocampal and motor cortical pyramidal neurons. In the present study, we have evaluated whether these changes are accompanied by neurochemical alterations in the hippocampus and motor cortex in SS experienced rats. Self-stimulation experience was provided one hour daily over a period of 10 days through stereotaxically implanted bipolar stainless steel electrodes, bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. Self-stimulation experience resulted in a significant (P < 0.001) increase in the levels of noradrenaline, dopamine, glutamate and AChE activity but not 5-hydroxytryptamine and GABA levels in hippocampus and motor cortex. Such alterations in the levels of neurotransmitters may enhance the cognitive functions in the SS experienced rats.

Acetylcholinesterase↗
PubMed1998

Role of monoamine oxidase type A and B on the dopamine metabolism in discrete regions of the primate brain.

The role of monoamine oxidase (MAO) type A and B on the metabolism of dopamine (DA) in discrete regions of the monkey brain was studied. Monkeys were administered (-)-deprenyl (0.25 mg/kg) or clorgyline (1.0 mg/kg) or deprenyl and clorgyline together by intramuscular injections for 8 days. Levels of DA and its metabolites, dihydroxy phenylacetic acid (DOPAC) and homovanillic acid (HVA) were estimated in frontal cortex (FC), motor cortex (MC), occipital cortex (OC), entorhinal cortex (EC), hippocampus (HI), hypothalamus (HY), caudate nucleus (CN), globus pallidus (GP) and substantia nigra (SN). (-)-Deprenyl administration significantly increased DA levels in FC, HY, CN, GP and SN (39-87%). This was accompanied by a reduction in the levels of DOPAC (37-66%) and HVA (27-79%). Clorgyline administration resulted in MAO-A inhibition by more than 87% but failed to increase DA levels in any of the brain regions studied. Combined treatment of (-)-deprenyl and clorgyline inhibited both types of MAO by more than 90% and DA levels were increased (57-245%) in all brain regions studied with a corresponding decrease in the DOPAC (49-83%) and HVA (54-88%) levels. Our results suggest that DA is metabolized preferentially, if not exclusively by MAO-B in some regions of the monkey brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Facilitation of acquisition and performance of operant and spatial learning tasks in self-stimulation experienced rats.

Adult male Wistar rats were implanted bilateraly with bipolar electrodes in substantia nigra-ventral tegmental area (SN-VTA) to experience intracranial self-stimulation (ICSS) for 15 min per day over a period of 10 days. These rats were then assessed for the acquisition and performance of the operant and the spatial learning tasks. ICSS experienced rats showed rapid acquisition of both the operant and the spatial learning tasks. Both the lever press performance for 7 sessions in the operant learning task and mean number of alternations per session in the spatial learning task were significantly higher (p < .001) in ICSS experienced rats compared with controls. The results suggest that prior ICSS experience facilitates the acquisition and performance in both the operant and the spatial learning tasks, which may be due to the structural and neurochemical alterations in the hippocampus induced by ICSS experience.

Analysis of Variance↗
PubMed1997

Entorhinal cortex lesioning protects hippocampal CA3 neurons from stress-induced damage.

The role of the entorhinal cortex (EC) in stress-induced damage in terms of dendritic branching points and intersections of hippocampal CA3 neurons has been investigated. Following bilateral electrolytic lesions of the EC, the rats were subjected to restraint stress, 6 h per day for 21 days. Chronic restraint stress resulted in the atrophy of hippocampal CA3 neurons and the lesioning of the EC prior to stress significantly (P < 0.001) reduced this dendritic atrophy. These results show that the neuronal vulnerability to chronic stress can be attenuated by entorhinal glutamatergic denervation.

Animals↗
PubMed1997

Developmental expression of synaptophysin, synapsin I and syntaxin in the rat retina.

Expression of synaptophysin, synapsin I and syntaxin was studied immunocytochemically in the developing rat retina using indirect immunoperoxidase technique. In the inner plexiform layer (IPL), syntaxin immunoreactivity appeared at postnatal day 1 (P1) whereas synaptophysin and synapsin I staining were first observed at P2. In the outer plexiform layer (OPL), synaptophysin appeared at P4, while synapsin I and syntaxin appeared at P8. In the case of synaptophysin, a punctate pattern of staining was observed from the time of its appearance (P4) in the OPL and from P12 onwards in the IPL. Synapsin I and syntaxin immunoreactivity in the OPL were of a low intensity throughout the development and in the adult stage. These findings are discussed in relation to synaptogenesis in the rat retina.

Animals↗
PubMed1997

Selective reduction of monoamine oxidase A and B in the frontal cortex of subordinate rats.

We have previously shown that subordination causes a reduction in the levels of 5-hydroxytryptamine and dopamine selectively in the frontal cortex [6]. These monoamines are catabolised mainly by the enzyme monoamine oxidase (MAO) which exists in two isoforms; MAO-A and MAO-B. The present study was carried out to determine whether there is any change in the activity of these two iso-enzymes induced by subordination and if any such alteration is confined to the frontal cortex. The animal model of dominance-subordination used was a worker-parasite paradigm in male Wistar rats. The enzyme activities were measured in five brain regions, the frontal cortex, entorhinal cortex, hippocampus, hypothalamus and striatum, using kynuramine as the substrate. Clorgyline and L-deprenyl were used in vitro to block the activities of MAO-A and MAO-B, respectively. There was a significant (P < 0.001) reduction in the activity of MAO-A as well as MAO-B selectively in the frontal cortex of the subordinate animals. This finding may suggest a reduced neurotransmitter turnover in the serotonergic and dopaminergic neurons terminating in the frontal cortex.

Animals↗
PubMed1997

An isocratic assay for norepinephrine, dopamine, and 5-hydroxytryptamine using their native fluorescence by high-performance liquid chromatography with fluorescence detection in discrete brain areas of rat.

A rapid and simple isocratic chromatographic procedure for simultaneous determination of norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) using their native fluorescence by high-performance liquid chromatography coupled to fluorescence detection (HPLC-FD) is described. Since the present procedure does not involve sample prepurification, the recovery of monoamines was more than 97% (n = 12) and within a given run, coefficient of variation was less than 3.1% (n = 12). Accordingly, use of an internal standard is not mandatory. In a single chromatographic run, levels of NE, DA, and 5-HT can be determined in less than 30 min. The minimum concentration of monoamines which could be detected by this method was found to be 250 pg for NE and DA and 100 pg for 5-HT. The validity of the method was confirmed by the estimation of levels of monoamines in the hypothalamus and striatum of rat brain following treatment with clorgyline, a monoamine oxidase inhibitor.

Amines↗
PubMed1997

Loss of hippocampal CA1 neurons and learning impairment in subicular lesioned rats.

30-Day-old male Wistar rats were tested for acquisition and retention of operant conditioned behavior after bilateral subicular lesions made either electrolytically or chemically (ibotenic acid). The acquisition of operant learning was carried out in lesioned rats by assessing the number of sessions required to learn the operant task, whereas the retention test was performed after lesions by assessing performance on a previously learnt operant task. The acquisition of pedal press operant learning was significantly delayed in both types of lesioned rats, without any impairment in the retention of the previously learned task after lesioning. In these animals the cell densities were quantified in cresyl violet-stained sections in different subfields of hippocampus. Following the lesion of subiculum, selective degeneration of CA1 cells without the involvement of other hippocampal subfields was observed. This might be due to the loss of target area (subiculum) through which hippocampus is connected with neocortical and subcortical structures. This, in turn, might have resulted in behavioral deficits. The data suggest that the subiculum might be involved in the acquisition of new information rather than in retention.

Animals↗
PubMed1997

Regeneration of the olfactory tract following neonatal lesion in rats.

Neuronal regeneration following early postnatal olfactory tract transection (OTS) was investigated in newborn Wistar rats. Olfactory tract lesioned rats were sacrificed at different time periods and the brains processed for Nissl staining. This was used to study the neural cell architecture; fiber tracts (myelinated fibers) were examined with Luxol Fast Blue staining. In addition, a neuronal tracing technique (i.e., retrograde labeling) was employed to study the reestablishment of connections with the target sites following transection of the tract. Degeneration of the olfactory tract was evident at the 7th day following lesion. Regeneration of the tract was not apparent even up to 60 days following transection. However, by 240 days, the olfactory tract had regenerated and the tract fibers had reestablished connection. This was confirmed by retrograde labeling of mitral cells of the olfactory bulb with Fast Blue (FB) injected into the piriform cortex, the target site of these neurons. In this study, we show that mammalian olfactory tract can regenerate spontaneously if the olfactory tract is lesioned neonatally. The results suggest that the olfactory tract is an excellent model to investigate some issues related to central nervous system regeneration.

Amidines↗