Biomedical subjects

Tara Sankar Roy

Publications and source records attributed to Tara Sankar Roy.

6 recordsLinked to original sources

PubMed2005

Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.

Neurochemical and behavioral studies indicate that the widely used organophosphorus insecticide, chlorpyrifos (CPF), evokes neurobehavioral teratogenicity with a wide window of vulnerability, ranging from embryonic life through postnatal development. Few studies have detailed morphological damage that corresponds to the operational deficits. We administered 5 mg/kg of CPF sc daily on postnatal days (PN) 11-14, a regimen that is devoid of systemic toxicity, but that elicits long-term cognitive impairment and disruption of cholinergic, catecholaminergic, and serotonergic synaptic function. On PN15 and 20, we conducted quantitative morphologic examinations of neurons and glia in CA1, CA3, and dentate gyrus regions of the hippocampus. Although hippocampal morphology after CPF exposure was normal on gross observation, morphometric analysis revealed a significant overall reduction in the total number of neurons and glia. Superimposed on this basic effect, CPF elicited a delayed-onset increase in the neuron/glia ratio that emerged by PN20, connoting selective gliotoxicity. The alterations in cell numbers were accompanied by significant perikaryal swelling and by enhanced development of astrocytic processes. Layer thickness also showed delayed-onset effects of CPF, with thinning of the CA1 and CA3 layers and enlargement of the dentate gyrus. Our results indicate that there are subtle morphological changes in the juvenile rat brain after neonatal CPF exposure that are detectable only with quantitative analysis and that correlate with regional and cell-specific targets identified earlier in neurochemical studies. The simultaneous targeting of neurons and glia by CPF is likely to play an important role in its developmental neurotoxicant effects.

Animals↗

PubMed2005

Development of the human fetal cochlear nerve: a morphometric study.

Ontogenesis of the human peripheral auditory pathway is relatively less explored. While the distal part of the auditory perception apparatus (i.e. the cochlea) received attention, studies on the neural element carrying information to the brainstem (i.e. the cochlear nerve) are scarce. In the present study, axonal differentiation, maturation and myelination of the distal end of the human cochlear nerve (CN) were assessed using light and electron microscopy. Seven human fetuses of 12, 15, 18, 20, 22, 28 and 38 weeks' gestation (WG) were analyzed. Light microscopy revealed nerve fascicles as early as 12 WG, initially arranged loosely but later compacted by 18 WG. Myelinated fibers were clearly detected at 28 WG. Ultrastructurally, at 12 WG developing Schwann cells were present between the thin unmyelinated axons. At 15 WG, the fascicular arrangement was distinct with blood vessels in the perineurium. The maximum number of axons was found at 20 WG, which subsequently reduced to reach the adult level at 22 WG. The myelinated axons in the CN were first observed on the left side at 20 WG, following which the number and proportion of myelinated axons increased until term, incorporating both small and large axons. The right CN lagged behind in maturation. Axon size also increased with age. Thus, the maturation of the human CN commences during the mid-gestation period and produces exuberant axons that are eventually pruned at a time when axons start to myelinate. During this developmental period the human CN maintains maturational asymmetry, the functional consequences of which remain to be elucidated.

Axons↗

PubMed2005

Asian-Oceanic Pancreatic Association: conception to actuality.

The Asian-Oceanic Pancreatic Association (AOPA) was organized on July 22, 2005 with the purpose of promoting communication, scholarship, and scientific collaboration, as well as the exchange of knowledge in both basic and clinical research and education in Asian and Oceanic countries. The society will host biennial scientific meetings during the Asian Pacific Digestive Week (APDW) and members consist of individuals rather than regional societies. Given the diversity of its members, English was selected as the common language of communication to facilitate the exchange of ideas. The first AOPA symposium, which aimed to describe the pancreatology in various regions, was held in conjunction with the 60th Annual Meeting of the Japan Society of Gastroenterological Surgery (JSGS). The second scientific meeting will be held during APDW 2007.

Asia↗

PubMed2004

Morphologic effects of subtoxic neonatal chlorpyrifos exposure in developing rat brain: regionally selective alterations in neurons and glia.

The widely used organophosphate insecticide, chlorpyrifos (CPF), elicits neurobehavioral teratogenesis with exposure windows ranging from the embryonic neural tube stage through postnatal development. To explore the morphologic changes occurring in late-stage exposure, newborn rats were given 5 mg/kg of CPF s.c. daily on postnatal days (PN) 11-14, a regimen that is devoid of systemic toxicity, but that elicits long-term cognitive impairment. On PN15 and 20, we examined the septal nucleus, striatum and somatosensory cortex. Across all three regions, CPF elicited a significant decrease in the number of glial cells. Superimposed on this basic pattern, there were region-specific alterations in the number and type of neurons, and neuronal perikaryal dimensions. In the septal nucleus, the CPF group exhibited an increase in the number of neurons on PN20, representing a delay in the normal maturational decline; there was a parallel decrease in the glial/neuronal ratio. In the striatum, the number of neurons per unit area was reduced in the CPF group, accompanied by perikaryal hypertrophy, as evidenced by an increase in the average neuronal cell diameter. In the somatosensory cortex, the distribution of cell sizes indicated a decrease in the proportion of small, nonpyramidal cells. Thus, there are subtle morphological changes in the juvenile rat brain after neonatal CPF exposure that are detectable with quantitative analysis and that correlate with later emergence of behavioral alterations. Furthermore, the current findings support the hypothesis that CPF interferes with gliogenesis, a relatively late event in brain development; accordingly, the vulnerable period for adverse effects of CPF is likely to extend into childhood or adolescence.

Analysis of Variance↗

PubMed2003

Variant human pancreas: aberrant uncinate process or an extended mesenteric process.

Variations in the morphology of pancreas are not very common. We observed a rare variant of the uncinate process of the pancreas that extended in the mesentery of the small intestine. After its origin from the lower part of the head of the pancreas, the mesenteric process (MP) passed over the third part of the duodenum to enter the mesentery of the jejunum and ileum and extended up to the level of the pelvic brim. The branches of the superior mesenteric vessels were embedded in the extended MP of the pancreas. This aberrant extension of the pancreas was drained by a narrow duct, which joined the main pancreatic duct inside the head. We did not observe a separate uncinate process arising from the head. On histology normal acini and endocrine cells were observed in the extension. This variant is important as symptoms of pancreatic disease from such extensions may be confused with other commonly encountered acute or chronic abdominal conditions.

Cadaver↗

PubMed2002

Prenatal nicotine exposure evokes alterations of cell structure in hippocampus and somatosensory cortex.

Offspring of women who smoke during pregnancy show behavioral abnormalities, including increased incidence of attentional deficit, learning disabilities, and cognitive dysfunction. Animal models indicate that nicotine elicits changes in neural cell replication and differentiation, leading to deficits in synaptic neurochemistry and behavioral performance, many of which first emerge at adolescence. We evaluated cellular morphology and regional architecture in the juvenile and adolescent hippocampus and the somatosensory cortex in rats exposed to nicotine prenatally. Pregnant rats were given nicotine throughout gestation via minipump infusion of 2 mg/kg/day, a regimen that elicits nicotine plasma levels comparable with those found in smokers. On postnatal days 21 and 30, brains were perfusion-fixed, coronal slices were taken between the anterior commissure and median eminence, and the morphology of the dorsal hippocampus and somatosensory cortex was characterized. In the hippocampal CA3 region and dentate gyrus, we found a substantial decrease in cell size, with corresponding decrements in cell layer thickness, and increments in cell packing density. Smaller, transient changes were seen in CA1. In layer 5 of the somatosensory cortex, although there was no significant decrement in the average cell size, there was a reduction in the proportion of medium-sized pyramidal neurons, and an increase in the proportion of smaller, nonpyramidal cells. All regions showed elevated numbers of glia. Taken together with previous work on neurochemical and functional defects, these data demonstrate that prenatal nicotine exposure compromises neuronal maturation, leading to long-lasting alterations in the structure of key brain regions involved in cognition, learning, and memory.

Animals↗