Copyright (c) 2013 All rights reserved. http://works.bepress.com/kuldip_bedi Recent documents in Kuldip Bedi en-us Tue, 12 Mar 2013 21:50:27 PDT 3600 http://works.bepress.com/kuldip_bedi/26 http://works.bepress.com/kuldip_bedi/26 Sun, 07 Oct 2012 22:40:26 PDT Apolipoprotein E (apoE) is one of the major transporters of cholesterol in the body and is essential for maintaining various neural functions in the brain. Given that hypercholesterolemia is a risk factor in Alzheimer's disease (AD), it has been suggested that altered cholesterol metabolism may be involved in the development of the pathogenesis, including neural degeneration, commonly observed in AD patients. Neurotrophic factors and their receptors, which are known to regulate various neural functions, are also known to be altered in various neurodegenerative diseases. We therefore hypothesized that cholesterol metabolism may itself influence the neurotrophin system within the brain. We decided to investigate this possibility by modulating the amount of dietary cholesterol given to apoE-knockout (apoE-KO) and wild-type (WT) mice, and examining the mRNA expression of various neurotrophin ligands and receptors in their hippocampal formations. Groups of eight-week-old apoE-KO and WT mice were fed a diet containing either "high" (HCD) or "normal" (ND) levels of cholesterol for a period of 12 weeks. We found that high dietary cholesterol intake elevated BDNF mRNA expression in both apoE-KO and WT mice and TrkB mRNA expression in apoE-KO animals. On the other hand, NGF and TrkA mRNA levels remained unchanged irrespective of both diet and mouse type. These findings indicate that altered cholesterol metabolism induced by HCD ingestion combined with apoE deficiency can elicit a differential response in the various neurotrophin ligand/receptor systems in the mouse hippocampus. Whether such changes can lead to neural degeneration, and the mechanisms that may be involved in this, awaits further research.

]]> Zhi-Yu Wang et al. http://works.bepress.com/kuldip_bedi/24 http://works.bepress.com/kuldip_bedi/24 Mon, 10 Jan 2011 15:30:47 PST Effects of early postnatal ethanol exposure on brain-derived neurotrophic factor (BDNF) mRNA expression in the rat hippocampus were investigated. Wistar rats were assigned to either ethanol treatment (ET), separation control (SC) or mother-reared control (MRC) groups. Ethanol exposure was achieved by a vapor inhalation method for 3 hours a day between postnatal days (PND) 10-15. On PND 16, 20, 30, and 60, the expression of BDNF mRNA in the hippocampus was determined using real-time RT-PCR analysis. There was a significant age-related increase in the BDNF mRNA expression between PND 30–60 in MRC animals. The BDNF mRNA expression in ET rats was increased at both PND 16 and 20 and thereafter decreased at PND 60 compared to SC animals. Such age-related fluctuation in the expression of BDNF mRNA differed from that of MRC animals. The exact functional implications, if any, of these ethanol-induced changes in BDNF mRNA expression remain unknown although it can be speculated that they may have an effect on the behaviors known to be influenced by the hippocampal formation.

]]> Takanori Miki et al. http://works.bepress.com/kuldip_bedi/25 http://works.bepress.com/kuldip_bedi/25 Mon, 10 Jan 2011 15:29:52 PST We have previously shown that exposing rats to a relatively high dose of ethanol during early postnatal life can result in an alteration in spatial learning ability. The hippocampal formation is known to be involved in the control of this ability. The purpose of the present study was to determine whether exposure of rats to ethanol during early postnatal life had either immediate or delayed effects on the numbers of pyramidal cells in the CA1-CA3 subregion of the hippocampus. Wistar rats were exposed to a relatively high daily dose of ethanol at postnatal day 10–15 by placing them for 3 h/day in a chamber containing ethanol vapor. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anesthetized and killed at 16 and 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle was used to determine the volumes of the CA1 and CA2+CA3 regions. The physical disector method was used to estimate the numerical density of neurons in each of the subdivisions. The total number of pyramidal cells was calculated by multiplying the appropriate estimates of the numerical density by the volume. There were significant age-related reductions in the total numbers of pyramidal cells at 16–30 days of age irrespective of the groups examined. Ethanol treated rats were found to have slightly but significantly fewer pyramidal cell neurons than either the MRC or SC groups. These observations indicate that pyramidal cells in the hippocampus may be vulnerable to a relatively high dose of ethanol exposure during this short period of early postnatal life.

]]> Takanori Miki et al. http://works.bepress.com/kuldip_bedi/23 http://works.bepress.com/kuldip_bedi/23 Tue, 20 Jul 2010 23:25:24 PDT Diet restriction of rodents during adult life is known to cause an increased life span. It has been hypothesised that this increase may be related to effects on the anti-oxidant defence systems. However, it has been suggested that undernutrition during the gestation and pre-weaning may reduce their life span as it is known to have other deleterious effects on a rodent's growth and development. We have now examined the activity levels of some anti-oxidant defence system enzymes and other markers of oxidative stress in mice that have been undernourished from conception until 21 postnatal days of age, followed in some cases by a period of nutritional rehabilitation until 61 days of age. We found that such undernutrition exerted only minimal effects on oxidative stress markers under investigation (ROS enzyme activities, GSH levels, and lipid peroxidation). Only GSH levels were significantly affected by pre-weaning undernutrition. In conclusion, pre-weaning undernutrition may regulate anti-oxidant enzymes at the transcriptional level differently from that at the post-transcriptional, translational, or post-translational levels. The possible effects that these changes at the cellular level, may have on the longevity of the animals remain of great interest and importance.

]]> G. Partadiredja et al. http://works.bepress.com/kuldip_bedi/22 http://works.bepress.com/kuldip_bedi/22 Mon, 10 Aug 2009 23:39:41 PDT Maternal alcohol ingestion during pregnancy adversely affects the developing fetus, often leading to fetal alcohol syndrome (FAS). One of the most severe consequences of FAS is brain damage that is manifested as cognitive, learning, and behavioral deficits. The hippocampus plays a crucial role in such abilities; it is also known as one of the brain regions most vulnerable to ethanol-induced neurotoxicity. Our recent studies using morphometric techniques have further shown that ethanol neurotoxicity appears to affect the development of the dentate gyrus in a region-specific manner; it was found that early postnatal ethanol exposure causes a transitory deficit in the hilus volume of the dentate gyrus. It is strongly speculated that such structural modifications, even transitory ones, appear to result in developmental abnormalities in the brain circuitry and lead to the learning disabilities observed in FAS children. Based on reports on possible factors deciding ethanol neurotoxicity to the brain, we review developmental neurotoxicity to the dentate gyrus of the hippocampal formation.

]]> Takanori Miki et al. http://works.bepress.com/kuldip_bedi/21 http://works.bepress.com/kuldip_bedi/21 Mon, 10 Aug 2009 23:39:40 PDT It has been hypothesised that the increased life span commonly observed in rodents that have had their diet restricted after weaning may be related to its effects on the anti-oxidant defence systems. However, undernutrition during the gestation and pre-weaning period is known to have long-term deleterious effects on a rodent's growth and development, and it has been suggested that this may reduce their life span. We have now examined some of the anti-oxidant defence system in rats that have been undernourished from conception until 21 postnatal days-of-age, followed in some cases by a period of nutritional rehabilitation until 62 days of age. We found that such undernutrition could modulate the mRNA expression of Cu/ZnSOD and catalase in some brain regions. However, only catalase showed any undernutrition-induced change of enzyme activity level. There was some evidence that undernourished (but not control) rats had an age-related increase in the level of lipid peroxidation between 21 and 62 days of age, although the group × age interaction was not statistically significant. There was no significant change in the level of reduced glutathione induced by the pre-weaning period of undernutrition. If ROS and the extent of oxidative damage are truly implicated in the determination of life span, our results indicate that this is unlikely to be markedly affected by the relatively small changes we have observed in the anti-oxidant defence systems induced by undernutrition of rats from conception until weaning.

]]> G. Partadiredja et al. http://works.bepress.com/kuldip_bedi/20 http://works.bepress.com/kuldip_bedi/20 Thu, 19 Feb 2009 17:05:07 PST Fetal alcohol syndrome is a major cause of mental retardation. We investigated possible long-lasting effects of alcohol on the hippocampus using a model for human third trimester brain development. Treatment of neonatal rats with an ethanol vapor atmosphere of 39.4 +/- 2.6 mg ethanol/liter of air for 3 h a day from postnatal day 4 through 9 produced daily blood ethanol levels of 351 +/- 14 mg/dL. Separation control animals were removed from their mothers in parallel with the ethanol vapor treatment, while suckle controls were left to develop normally.We prepared hippocampal slices from these animals between postnatal days 45 and 60 and recorded extracellular responses to Schaffer collateral stimulation. The maximum population spike in the CA1 pyramidal region and population excitatory postsynaptic potentials in the stratum radiatum did not differ significantly between groups. However, slices prepared from ethanol-treated rats as opposed to separation and suckle controls required larger stimulus currents to produce normal postsynaptic responses. In addition, the ratio of the population excitatory postsynaptic potential (pEPSP) slope to the presynaptic volley was significantly reduced in ethanol-treated rats. Ethanol vapor-treated rats and separation control rats did not exhibit any significant changes in long-term potentiation or paired-pulse potentiation compared with normal suckle controls. These results suggest that early postnatal ethanol treatment produces a long-lasting reduction in synaptic efficacy but not plasticity.

]]> Frederick P. Bellinger et al. http://works.bepress.com/kuldip_bedi/19 http://works.bepress.com/kuldip_bedi/19 Thu, 19 Feb 2009 17:05:06 PST Adult neural progenitors have been isolated from diverse regions of the CNS using methods which primarily involve the enzymatic digestion of tissue pieces; however, interpretation of these experiments can be complicated by the loss of anatomical resolution during the isolation procedures. We have developed a novel, explant-based technique for the isolation of neural progenitors. Living CNS regions were sectioned using a vibratome and small, well-defined discs of tissue punched out. When cultured, explants from the cortex, hippocampus, cerebellum, spinal cord, hypothalamus, and caudate nucleus all robustly gave rise to proliferating progenitors. These progenitors were similar in behaviour and morphology to previously characterised multipotent hippocampal progenitor lines. Clones from all regions examined could proliferate from single cells and give rise to secondary neurospheres at a low but consistent frequency. Immunostaining demonstrated that clonal cortical progenitors were able to differentiate into both neurons and glial cells, indicating their multipotent characteristics. These results demonstrate it is possible to isolate anatomically resolved adult neural progenitors from small amounts of tissue throughout the CNS, thus, providing a tool for investigating the frequency and characteristics of progenitor cells from different regions.

]]> Hiram Chipperfield et al. http://works.bepress.com/kuldip_bedi/18 http://works.bepress.com/kuldip_bedi/18 Thu, 19 Feb 2009 17:05:06 PST Recent reports have suggested that proper maturation of synapses in the hippocampus requires activation of NMDA receptors. We previously demonstrated that neonatal ethanol exposure results in a lasting reduction in synaptic strength in the hippocampus. To determine if this reduction was due to ethanol’s effects on NMDA receptors, we investigated long-term changes in synaptic properties resulting from administration of NMDA receptor antagonists to neonatal animals. Rats were injected daily from PND 4–9 with either the noncompetitive NMDA receptor antagonist MK-801, the competitive NMDA receptor antagonist CPP, or the AMPA receptor antagonist NBQX. Control rats were either injected daily with physiological saline during the same period or left to develop normally. Hippocampal slices were prepared from nembutalanesthetized animals between PND 35 and PND 40. The maximum pEPSP and PS values were not significantly different between controls and NMDA antagonist-treated animals. However, slices from animals injected with NMDA receptor antagonists required higher stimulus currents to attain comparable pEPSPs. The ratio of the slope of the pEPSP to the amplitude of the presynaptic volley was also reduced, as were pEPSP responses to specific stimulus currents. None of these effects were observed in slices prepared from animals treated with the AMPA receptor antagonist NBQX. Glutamate receptor antagonism did not produce lasting changes in long-term potentiation or paired-pulse facilitation. These results indicate activation of NMDA receptors during development is necessary for proper development of synapses.

]]> Frederick P. Bellinger et al. http://works.bepress.com/kuldip_bedi/16 http://works.bepress.com/kuldip_bedi/16 Thu, 19 Feb 2009 17:05:05 PST We have previously shown that undernutrition during early life causes a permanent deficit in the total number of dentate granule cells. However, it is unknown whether this deficit is due to neuronal cell death and/or to fewer cells being born during the period of neurogenesis. We have therefore used stereological methods combined with specific labeling techniques to examine the numbers of apoptotic cells in specific regions of the hippocampal formation. Rats were undernourished by restricting their daily food intake to about half that eaten by well-fed controls. Control and undernourished rats were killed on postnatal day 21, and their brains fixed in 4% paraformaldehyde. Serial sections through the hippocampal formation were labeled with the TUNEL technique to distinguish apoptotic cells. All care and animal handling procedures were approved by the institutional Animal Ethics Committee in line with Australian NHMRC procedures. There were about 21,500 and 57,000 TUNEL-positive cells in the dentate gyrus granule cell layer of control and undernourished rats, respectively. The difference between these values was statistically significant. In the CA3+CA2 region, there were about 22,000 and 19,500 TUNEL-positive cells in control and undernourished rats, respectively. The difference between these values was not statistically significant. Furthermore, it was observed that the majority of the TUNEL-positive cells in the dentate gyrus were located close to the border between the dentate gyrus granule cells and hilus of the hippocampal formation. Our results show that undernutrition during gestation and lactation can result in an increase in the level of TUNEL-positive apoptotic cells in the rat dentate gyrus.

]]> Sani Jahnke et al. http://works.bepress.com/kuldip_bedi/17 http://works.bepress.com/kuldip_bedi/17 Thu, 19 Feb 2009 17:05:05 PST The hippocampal formation has been shown to be particularly vulnerable to the neurotoxic effects of chronic ethanol consumption. It was hypothesized that this damage was due to the disruption of the expression of neurotrophic factors and certain other proteins within the hippocampus. By using real-time reverse transcription-polymerase chain reaction (RT-PCR) techniques, this study aimed to determine whether chronic ethanol consumption could alter the mRNA expression level of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and oligodendrocyte myelin glycoprotein (OMgp) in the hippocampus. Wistar male rats received an unrestricted access to a liquid diet containing 5% (v/v) ethanol as the sole source of fluid from 10 to 29 weeks of age. Control rats had unlimited access to a liquid diet containing an isocaloric amount of sucrose. We found that chronic ethanol consumption did not cause significant changes in the levels of mRNA for BDNF and GDNF. However, OMgp mRNA showed a significant deficit in ethanol-treated animals. It is suggested that this deficit may be related to the demyelination that is commonly observed in human alcoholics and that this may contribute to the functional and cognitive deficits. Copyright © 2007 Elsevier

]]> Hanayo Okamoto et al. http://works.bepress.com/kuldip_bedi/15 http://works.bepress.com/kuldip_bedi/15 Thu, 19 Feb 2009 17:05:05 PST Stereology is a group of mathematical and statistical methods that allows the extrapolation of three-dimensional structural information from two-dimensional sections (or slices). This allows researchers to derive important quantitative structural information, such as the volume, surface area or numbers of particular particles (e.g. cells) within defined regional boundaries. The need for such quantitative information in biology is of particular importance when evaluating the influence of various experimental treatments on specific organs, tissues and cells in the body. Knowledge of such changes has given important insights into the neural substrates that may be responsible for the functional and behavioral consequences of a disparate range of experimental treatments. Here, we describe some of these methods as applied to quantifying the total numbers of cells in defined regions of the hippocampal formation. The methods used for this evaluation were, first, the Cavalieri principle, which was used to determine the volumes of the various subdivisions of the rat hippocampus, and, second, the ‘physical disector’ method, which was used to estimate the numerical density of neurons within each subdivision. Once these values were derived, it was but a simple task to multiply them together to obtain estimates for the total numbers of cells in the given hippocampal region. We found that 16- and 30-day-old normal male rats had 176 800 and 152 700 pyramidal cells in the CA1 region, respectively. This decrease in the neuronal number was statistically significant. However, in the CA2 + CA3 region, there were approximately 169 300 and 149 600 pyramidal cells in 16- and 30-day-old normal male rats, respectively, which was not significantly different. In the dentate gyrus, there were approximately 36 700 neurons in the hilus region and 483 000 granule cells in the granule cell layer, irrespective of the age of the rats. There were no significant differences between these estimates of hilus neurons and granule cells.

]]> Takanori Miki et al. http://works.bepress.com/kuldip_bedi/14 http://works.bepress.com/kuldip_bedi/14 Thu, 19 Feb 2009 17:05:04 PST The effects of maternal deprivation (MD) during early postnatal life on the brain-derived neurotrophic factor (BDNF) level were investigated in the present study. Wistar rats were assigned to either maternal deprivation or mother-reared control (MRC) groups. MD manipulation was achieved by separating rat pups from their mothers for 3 h a day during postnatal days (PND) 10–15. At 16, 20, 30, and 60 days of age, the level of BDNF mRNA in the hippocampal formation of each group was determined using real-time PCR analysis. Early postnatal maternal deprivation of rat pups resulted in a significant increase in body weight at 60 days of age. The expression of BDNF mRNA in the hippocampus was significantly decreased at 16 days of age, and increased at 30 and 60 days of age. These data indicate that even a brief period of maternal deprivation during early postnatal life can affect hippocampal BDNF expression.

]]> Hiromi Kuma et al. http://works.bepress.com/kuldip_bedi/13 http://works.bepress.com/kuldip_bedi/13 Thu, 19 Feb 2009 17:05:04 PST In the developing nervous system, cell death is an important component of refining axonal projections. In the developing rat inferior olive, previous studies have demonstrated cell death as temporally incongruent with both initial axon–target interactions and subsequent axon collateral regression. Furthermore, these studies identified a late rise in neuron numbers that is concurrent with climbing fibre regression. As axonal regression has not previously been associated with increasing neuron numbers, and since immature neurons and glia have similar morphological characteristics, it was decided to reassess the timing of cell death within the inferior olive in animals in which neurons and glia had been differentially stained. Glia were identified by the presence of glial cytoskeletal proteins, S100, or glial fibrillary acidic protein, and stereological counts were made of both neurons and glia in the inferior olive from rats of ages 0, 5, 10, 15, and 30 days. The number of inferior olivary neurons was approximately 22,000 between birth and day 10, which decreased to about 17,500 by day 30 (P < 0.05). In contrast, the number of glia rose from about 5,000 at birth to approximately 15,000 by day 10 (P < 0.001), after which there was no further increase. The changes in neurons and glia caused the neuron-to-glia ratio to fall to approximately 1.5 by the time of functional maturation within the olive. These results confirm that there is neuronal death in the inferior olive but that it is temporally correlated with both climbing fibre regression and functional maturation of the olivocerebellar projection.

]]> J J. Cunningham et al. http://works.bepress.com/kuldip_bedi/12 http://works.bepress.com/kuldip_bedi/12 Thu, 19 Feb 2009 17:05:03 PST Previous in vitro studies have shown that X-irradiation during early postnatal life can change the environment of CNS tissue in later adult life such that it becomes more supportive of neurite regeneration from adult dorsal root ganglion (DRG) neurons than non-irradiated tissue. The question arises whether or not x-irradiation during adult life can alter the CNS environment such that it also becomes more supportive of neurite regeneration. This was investigated by exposing portions of the spinal cord of adult rats to 10, 20 or 40 Gray of X-irradiation and later using this tissue to prepare cryosections suitable for use as a substrate in a cryoculture assay. Fixed cryocultures were immunolabelled using anti-glial fibrillary acidic protein (GFAP) to visualise the tissue sections and anti-growth associated protein (GAP-43) to visualise the regenerating neurites. Tissue sections from sham-irradiated animals and from those irradiated with 10 Gray did not support the regeneration of neurites. However, sections of spinal cords from rats treated with either 20 or 40 Gray of X-irradiation 4 or 32 days prior to sampling were found to support a certain degree of neurite regeneration. It is concluded that X-irradiation of adult CNS tissue can alter its environment such that it becomes more supportive of neurite regeneration and it is speculated that this change may be the result of alterations in the glial cell populations in the post-irradiated tissues.

]]> Danny Pinjuh et al. http://works.bepress.com/kuldip_bedi/11 http://works.bepress.com/kuldip_bedi/11 Thu, 19 Feb 2009 17:05:03 PST Axonal regeneration of retinal ganglion cells (RGCs) into a normal or pre-degenerated peripheral nerve graft after an optic nerve pre-lesion was investigated. A pre-lesion performed 1–2 weeks before a second lesion has been shown to enhance axonal regeneration in peripheral nerves (PN) but not in optic nerves (ON) in mammals. The lack of such a beneficial pre-lesion effect may be due to the long delay (1–6 weeks) between the two lesions since RGCs and their axons degenerate rapidly 1–2 weeks following axotomy in adult rodents. The present study examined the effects of the proximal and distal ON pre-lesions with a shortened delay (0–8 days) on axonal regeneration of RGCs through a normal or pre-degenerated PN graft. The ON of adult hamsters was transected intraorbitally at 2 mm (proximal lesion) or intracranially at 7 mm (distal lesion) from the optic disc. The pre-lesioned ON was re-transected at 0.5 mm from the disc after 0, 1, 2, 4, or 8 days and a normal or a pre-degenerated PN graft was attached onto the ocular stump. The number of RGCs regenerating their injured axons into the PN graft was estimated by retrograde labeling with FluoroGold 4 weeks after grafting. The number of regenerating RGCs decreased significantly when the delay-time increased in animals with both the ON pre-lesions (proximal or distal) compared to control animals without an ON pre-lesion. The proximal ON pre-lesion significantly reduced the number of regenerating RGCs after a delay of 8 days in comparison with the distal lesion. However, this adverse effect can be overcome, to some degree, by a pre-degenerated PN graft applied 2, 4, or 8 days after the distal ON pre-lesion enhanced more RGCs to regenerate than the normal PN graft. Thus, in order to obtain the highest number of regenerating RGCs, a pre-degenerated PN should be grafted immediately after an ON lesion.

]]> Si-Wei You et al. http://works.bepress.com/kuldip_bedi/9 http://works.bepress.com/kuldip_bedi/9 Thu, 19 Feb 2009 17:05:02 PST In humans, the offspring of maternal cocaine misusers are known to have subtle cognitive and motor impairments in later life. It was therefore hypothesized that such exposure in animals would also affect the morphological structure of the brain. This possibility was investigated by exposing rats to cocaine between embryonic day 15 and postnatal day 6. Samples of the cocaine-exposed and control rats were killed for examination at 22 and 150 postnatal days of age. Stereological procedures (the Cavalieri principle together with the physical disector method) were utilized to estimate the total number of pyramidal and granule cells in defined regions of the hippocampal formation. At 22 days of age, the control offspring had about 373 000 pyramidal cells whereas the cocaine-treated animals only had about 310 000 cells in the CA1 + CA2 + CA3 region. By 150 days of age the values were about 396 000 and 348 000, respectively. The differences between age-matched groups were statistically significant. There were about 626 000 and 687 000 dentate gyrus granule cells in the 22-day-old control and cocaine-treated groups, respectively. By postnatal day 150 the control rats had about 832 000 granule cells whilst the cocaine-treated rats had about 693 000. There was a significant main effect of age as well as group–age interaction in this measure. These results show that even moderate exposure to cocaine during the late gestation and early postnatal period in rats is a potent teratogen and can markedly influence the development of neurons in the hippocampal formation.

]]> Zul Izhar Mohd Ismail et al. http://works.bepress.com/kuldip_bedi/10 http://works.bepress.com/kuldip_bedi/10 Thu, 19 Feb 2009 17:05:02 PST Ninety-day-old hooded male rats were anaesthetised with an intraperitoneal injection of a mixture of xylazine and ketamine and had their right eyes removed. Groups of non-enucleated control and enucleated rats were killed at either 150 or 390 days of age by intracardiac perfusion with fixatives. Stereological methods were used to estimate the synapse-to-neuron ratios within the stratum griseum superficiale (SGS) layers of both the ipsi- and contra-lateral superior colliculi. The enucleation had no significant effects on this ratio irrespective of the side or age of the brains examined. This experiment shows that a constant synapse-to-neuron ratio may be maintained within the SGS layer of the rat superior colliculus despite the inevitable loss of synaptic contacts due to the anterograde transneuronal degeneration initiated by the enucleation.

]]> S A. Smith et al. http://works.bepress.com/kuldip_bedi/8 http://works.bepress.com/kuldip_bedi/8 Thu, 19 Feb 2009 17:05:01 PST The purpose of the present study was to determine antipsychotic doses that achieve 80% striatal dopamine D2-receptor occupancy for haloperidol, risperidone and olanzapine in rats. Wistar rats were treated with normal saline vehicle (controls), haloperidol (0.25 and 0.5 mg/kg/day), risperidone (3, 5 and 6 mg/kg/day) and olanzapine (5 and 10 mg/kg/day) for 7 days via osmotic minipumps. Striatal and cerebellar tissue were collected and in vivo dopamine D2-receptor occupancies were determined using 3H-raclopride. The doses required to achieve dopamine D2-receptor occupancy of 80% in 11- and 24-week old rats were: haloperidol 0.25 mg/kg/day, risperidone 5 mg/kg/day and olanzapine 10 mg/kg/day. Copyright © 2007 Elsevier

]]> Dineshree V. Naiker et al. http://works.bepress.com/kuldip_bedi/7 http://works.bepress.com/kuldip_bedi/7 Thu, 19 Feb 2009 17:05:01 PST We measured the effects of ethanol on glutamate receptor levels in the hippocampus of neonatal Wistar rats using a vapor chamber model. Two control groups were used; a normal suckle group and a maternal separation group. Levels of NMDA receptors were not significantly altered in ethanol-treated animals compared to the normal suckle control group, as shown by [3H]MK-801 binding and Western blot analysis. However, MK-801 binding and NR1 subunit immunoreactivity were greatly reduced in the hippocampus of separation control animals. Neither ethanol treatment nor maternal separation altered levels of GluR1 or GluR2(4). These results have serious implications for the importance of maternal contact for normal brain development. Copyright © 2007 Elsevier

]]> Frederick P. Bellinger et al.