Morphological evidence of an altered process of synaptic transcytosis in adult rats exposed to ethanol.

Aims: The effects of ethanol exposure on synaptic structure were investigated in the nucleus of solitary tract (NST) in rats, using the horse-radish peroxidase (HRP) method.

Methods: Eight-week-old experimental rats were allowed free access to a liquid diet containing ethanol for 3 weeks, while controls were given an isocaloric diet. Some of the control and experimental animals were given an injection of wheat germ agglutinin conjugated with HRP (WGA-HRP) into the vagus nerve toward the end of the treatment period.

A high cholesterol diet given to apolipoprotein E-knockout mice has a differential effect on the various neurotrophin systems in the hippocampus.

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.

Early postnatal ethanol exposure induces fluctuation in the expression of BDNF mRNA in the developing rat hippocampus.

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) 1015.

Ethanol neurotoxicity and dentate gyrus development.

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.

Rats exposed to cocaine during late gestation and early postnatal life show deficits in hippocampal pyramidal and granule cells in later life.

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.

Undernutrition during early life increases the level of apoptosis in the dentate gyrus but not in the CA2+CA3 region of the hippocampal formation.

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.

Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption.

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.

Dose determination of haloperidol, risperidone and olanzapine using an in vivo dopamine D2-receptor occupancy method in the rat.

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.

Ethanol prevents NMDA receptor reduction by maternal separation in neonatal rat hippocampus.

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.

Application of the physical disector to the central nervous system: estimation of the total number of neurons in subdivisions of the rat hippocampus.

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.

Early maternal deprivation induces alterations in brain-derived neurotrophic factor expression in the developing rat hippocampus.

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 3h a day during postnatal days (PND) 10-15.

Effects of age and alcohol exposure during early life on pyramidal cell numbers in the CA1-CA3 region of the rat hippocampus.

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.

X-irradiation of adult spinal cord increases its capacity to support neurite regeneration in vitro.

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.

Effects of alcohol exposure during early life on neuron numbers in the rat hippocampus. I. Hilus neurons and granule cells.

We previously showed that 16-day-old rats exposed to a relatively high dose of ethanol at 10-15 postnatal days of age have fewer neurons in the hilus region of the hippocampus compared with controls. Dentate gyrus granule cell numbers, however, showed no statistically significant changes attributable to the ethanol treatment. It is possible that some of the changes in brain morphology, brought about as a result of the exposure to ethanol during early life, may not be manifested until later in life.

Current concepts in central nervous system regeneration.

A dictum long-held has stated that the adult mammalian brain and spinal cord are not capable of regeneration after injury. Recent discoveries have, however, challenged this dogma. In particular, a more complete understanding of developmental neurobiology has provided an insight into possible ways in which neuronal regeneration in the central nervous system may be encouraged.

Axonal regeneration of retinal ganglion cells after optic nerve pre-lesions and attachment of normal or pre-degenerated peripheral nerve grafts.

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 effect of the timing of prenatal X-irradiation on Purkinje cell numbers in rat cerebellum.

Exposure of the developing brain to X-irradiation in utero is known to cause various deleterious consequences. We have previously reported the effects of prenatal X-irradiation on the development of the cerebral cortex in rats. We have now extended this study to examine the effects of such X-irradiation on the development of the cerebellum.

Heparan sulfates isolated from adult neural progenitor cells can direct phenotypic maturation.

Multipotent progenitor stem cells that generate both neurons and glia are components of the hippocampus, subventricular zone and olfactory system of adult mammalian nervous system. The lineage choices any stem cell makes are known to be greatly dependent on the constitution of the extracellular matrix to which they are exposed during their development. Here, the adult rat hippocampus was used as a source of cells for clonal culture in order to investigate the effects of the extracellular glycosaminoglycan heparan sulfate (HS).

Neonatal ethanol exposure reduces AMPA but not NMDA receptor levels in the rat neocortex.

Fetal alcohol syndrome (FAS) is the leading cause of mental retardation in western society. We investigated possible changes in glutamate receptor levels in neonatal animals following ethanol exposure using radioligand binding and western blot analysis. We used a vapor chamber to administer ethanol to neonatal Wistar rats 3 h a day from postnatal day (PND) 4-9.

Long-lasting synaptic modification in the rat hippocampus resulting from NMDA receptor blockade during development.

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.

Adult Rat Dorsal Root Ganglion Neurons Extend Neurites on Predegenerated But Not on Normal Peripheral Nerves In Vitro.

The abilities of embryonic and adult rat sensory neurons to regenerate were compared when cultured on cryostat sections of normal and lesioned sciatic nerve tissues. Differences in neurite growth, visualized by GAP-43 immunolabelling, were most pronounced on substrata consisting of longitudinal sections of normal versus predegenerated sciatic nerve. Adult dorsal root ganglion (DRG) neurons grew only on the lesioned nerves.