PubMed Health⌕ Search

Biomedical subjects

S R Overmann

Publications and source records attributed to S R Overmann.

15 recordsLinked to original sources
PubMed1987

Neurobehavioral and somatic effects of perinatal PCB exposure in rats.

Developing rats were exposed to PCBs via provision of diets containing 0.02 (no PCB added), 2.5, 26, or 269 ppm Aroclor 1254 to sperm-positive female rats from mating to weaning of their pups. Provision of the 269 ppm diet decreased the number of impregnated rats that delivered a litter and lowered pup birth weight, and most pups died within 7 days of birth. Pregnancy success, pup birth weight, and dam body weight and food intake were not altered in the 2.5 and 26 ppm conditions. Preweaning pup growth was reduced in the 26 ppm condition and slightly reduced in the 2.5 ppm condition. The ontogeny of negative geotaxis, auditory startle, and air righting was delayed in pups from the 26 ppm condition. Pups in the 2.5 ppm condition had slightly delayed development of auditory startle. PCB exposure did not affect the duration of forepaw suspension or age at eye opening. Maximal electroshock seizure tests on postweaning rats showed that perinatal PCB exposure decreased seizure severity of both the 2.5 and 26 ppm groups as indicated by increased durations of forelimb and hindlimb flexion and decreased duration of hindlimb extension. PCB exposure increased pup liver weights at birth and dam and pup liver weights at weaning. Spleen and thymus weights were lower in PCB-exposed pups, while brain weights were unaffected. Analytical determination of PCB levels in brain showed greater maternal transfer of PCBs during lactation than during gestation. Elevated PCB levels were detectable in brains of perinatally exposed adult rats. The results indicate that perinatal PCB exposure of rats alters neurobehavioral and somatic ontogeny.

Animals↗
PubMed1984

Morphometric effects of preweaning lead exposure on the hippocampal formation of adult rats.

We previously observed that lead exposure beginning at parturition reduced or retarded neuropil development and synaptogenesis in specific regions of the hippocampal formation in 15-day-old rats. To determine if morphologic effects of perinatal lead exposure persist into adulthood, the hippocampus of rats exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate was analyzed by light and electron microscopy at 90-97 days of age. Preweaning lead exposure did not cause obvious hippocampal cytotoxicity, edema, damaged vasculature or altered numerical density (number per unit area) of dentate granule or hippocampal pyramidal neurons. However, lead exposure increased the area of the hilar portion of stratum pyramidale, increased the number of blood vessels per section in the dentate stratum granulosum and tended to increase the number of glial cells per section in the non-hilar CA3 stratum pyramidale. Effects of early postnatal lead exposure on synaptic profiles in the suprapyramidal mossy fiber zone (MFZ) were limited to the proximal (close to the dentate gyrus) region of the extrahilar zone. Both numerical density and areal density (proportion of neuropil covered) of complex invaginated (Ci) profiles, typical of mature mossy fiber boutons, were increased by lead exposure in the deep (close to stratum pyramidale) subfield of the proximal portion of the suprapyramidal MFZ. Lead exposure tended to increase the mean cross-sectional area of Cl profiles in the superficial (distant from stratum pyramidale) subfield of the proximal portion, and reduced the cross-sectional area of complex noninvaginated (CN) synaptic profiles in some subfields. Although lead exposure reduced or delayed neuropil development in selected late developing hippocampal regions examined at 15 days of age, it appeared to allow normal growth or to induce compensatory hypertrophy in these same regions in the adult.

Animals↗
PubMed1982

Morphometric effects of postnatal lead exposure on hippocampal development of the 15-day-old rat.

Neurotoxic sequelae of developmental lead exposure suggest that the hippocampus may be affected. Therefore, rats received low-level exposure via the milk of dams drinking 0.2% lead acetate beginning at parturition, and mid-dorsal sections of the hippocampus and dentate gyrus (DG) from 15-day-old pups were examined by light and electron microscopy. Lead exposure did not reduce body weight nor produce obviously abnormal vascularity or signs of cytotoxicity in the hippocampal formation, and total numbers per section of dentate granule cells or CA3 pyramidal cells were not reduced. On the other hand, lead exposure reduced neuropil development as evidenced both by reduced areas of the dentate hilus and dentate infrapyramidal stratum moleculare and by increased number of hilar CA3 pyramidal cells per unit area. Also, lead exposure reduced numbers of several types of synaptic profiles per unit area in the suprapyramidal mossy fiber zone. Complex invaginated (CI) profiles, assumed to be mature mossy fiber boutons, were characterized by multiple membrane densities and deep invaginations around dendritic spines of pyramidal cells. Complex noninvaginated (CN) boutons exhibited bag-like profiles with multiple membrane densities. Smaller, less numerous, simple (S) profiles contacted either dendritic trunks (ST) or spines (SS). Lead exposure reduced the numerical density of any of the profiles in the deep (close to stratum pyramidale) part of the proximal (close to DG) region of the suprapyramidal mossy fiber zone, but did not alter the numerical density of any of the profiles in the superficial (distal to stratum pyramidale) parts of either proximal or distal (close to CA1) regions. Average size of CN profiles in the distal region was increased by lead exposure. The pattern of effects suggests that low-level lead exposure during development preferentially affects later developing structures within the hippocampal formation, rather than affecting mature structures.

Animals↗
PubMed1981

Motor development, tissue weights and seizure susceptibility in perinatally lead-exposed rats.

Motor impairments and seizures are frequent neurologic sequelae of excess lead exposure in children. To evaluate the relative significance of such symptoms in an animal model, Long-Evans rats were lead-exposed from parturition to weaning by adulteration of the dams' drinking water with 0.02% or 0.2% lead acetate. Ontogeny of swimming ability from 6 through 24 days of age was not altered by postnatal lead exposure. Rotorod performance was tested on 21, 30, 60, 90, 150 and 440 days of age and was maximal in rats 30 through 150 days of age, with the poorest performance by 440-day-old rats. Rotorod performance was decreased by both levels of lead exposure and this effect was most evident at 60 and 150 days of age. Both levels of lead exposure increased kidney weights of dams at weaning and the 0.2% lead acetate exposure decreased hematocrit of dams. Kidney weights of lead-exposed pups were not increased at 10 days of age, but pups in the 0.2% lead acetate group had increased kidney weights at 20, 90 and 150 days of age. Hematocrit values of pups in the 0.2%, but not in the 0.02%, lead acetate exposure group were decreased at 20 days of age. No effects of lead exposure on hematocrits were found at 10, 90 or 150 days of age. Wet weight of brain, cerebellum, adrenals, spleen and thymus were not altered at any age by postnatal lead treatment. In a second study, Sprague-Dawley rats exposed to lead via dams drinking 0.2% lead acetate throughout gestation and lactation. Pre- and postnatal lead exposure did not alter the ontogeny of electro-shock seizure thresholds in rats tested on 8 through 20 days of age. The results suggest that the lead exposure levels used were at or near a no-effect level for several common neurobehavioral tasks and that kidney weight may be a more discriminative index of excess lead exposure than some simple neurobehavioral indices.

Animals↗
PubMedDate not supplied

Hippocampal potentials evoked by stimulation of olfactory basal forebrain and lateral septum in the rat.

Electrophysiological characteristics of olfactory-hippocampal relations were examined because recent anatomical studies have described a substantial olfactory input to the hippocampus via the entorhinal cortex. Potentials evoked in the dorsal hippocampus of anesthetized rats by stimulation of the prepyriform cortex, pyriform cortex, diagonal band, lateral olfactory tract, anterior commissure, olfactory tubercle and anterior olfactory nucleus had similar characteristics, although latencies differed. For example, latencies were twice as long after stimulation of the obliquely oriented portion of the diagonal band than after stimulation of the prepyriform cortex. A relatively low-amplitude, initially negative wave was recorded in the subiculum, CA1 and CA2, and a relatively high-amplitude, initially positive wave was recorded in CA4 and the dentate gyrus. In CA3 negative potentials were observed at dorsal recording sites and positive potentials were recorded at more ventral sites. Peak latencies were usually two to four msec shorter for the negative than for the positive wave. Laminar distributions of responses evoked in the hippocampus by stimulation of the prepyriform cortex and diagonal band were evaluated by driving eight electrodes mounted on one carrier through the brain and were found to be strikingly similar. Maximal amplitudes of the negative wave were recorded at the level of stratum moleculare of CA1 and the subiculum, and peak amplitudes of the positive wave were associated with the hilus of the dentae gyrus. Transition from negative to positive waveforms occurred approximately at the hippocampal fissure. Although the negative and positive waves were usually elicited together, they also were separable in that only negative waves were recorded along some tracks and only positive waves along others. Also, various stimulation sites in the prepyriform cortex elicited stable high-amplitude positive waves accompanied by negative waves of varying amplitude. It is suggested that branches of the perforant path are involved in generation of the two waves and that activity in a number of olfactory structures may influence the hippocampus, probably via the perforant pathway. Thus, hippocampal potentials following prepyriform or diagnonal band stimulation were not abolished by transection of the fornix-fimbria. Dorsolateral septal stimulation evoked hippocampal responses with characteristics and distribution distinctly different from those evoked by stimulation of olfactory areas. The findings suggest that lateral septal stimulation may activate the hippocampus antidromically.

Animals↗