Biomedical subjects

B V Seri

Publications and source records attributed to B V Seri.

4 recordsLinked to original sources

PubMed1996

Thiamine administration during chronic alcohol intake in pregnant and lactating rats: effects on the offspring neurobehavioural development.

A number of mechanisms may be involved in the pathogenesis of thiamine deficiency in the alcoholic. Among these mechanisms are inadequate dietary intake of thiamine, impaired intestinal transport of the vitamin and decreased conversion of thiamine to the active coenzyme. The present study was undertaken to further investigate the mechanism by which alcohol can interfere with thiamine deficiency in the brain. Thus, the neurobehavioural development of rat pups (E) nursed by 12% ethanol/water-drinking mothers, or pups (E-T) nursed by mothers drinking 12% ethanol/water + thiamine hydrochloride mixture, was monitored from the 1st to 45th postnatal days. Appropriate pair-fed saccharose (S) and ad libitum controls (C) were assessed. Histological studies were performed at the age of 45 days on the hippocampal CA3 pyramidal neurons of the offspring from each treatment. Exposing rat pups to ethanol during pregnancy and lactation showed a significant impairment of neurobehavioural development, more cornered pyramidal cells in the hippocampal field CA3, reduced cell number and cell size. The results point out long-lasting effects of maternal alcohol exposure in the offspring. Both functional and structural studies showed that neurotoxic effects of developmental alcohol exposure were not reversed by thiamine administration. However, adverse effects of undernutrition following developmental alcohol exposure were suppressed by thiamine administration. From this work, we suggest that inadequate dietary intake of thiamine and impaired intestinal transport of the vitamin are not critical mechanisms leading to thiamine deficiency in chronic alcoholism. The most prevalent mechanism contributing to ethanol-induced thiamine deficiency in chronic alcoholics would be the alteration of thiamine metabolism, and particularly the reduction of the vitamin conversion to its metabolically active form TPP (thiamine pyrophosphate).

Animals↗

PubMed1995

Psychomotor functions in developing rats: ontogenetic approach to structure-function relationships.

The functional development of the central nervous system (CNS) in the rat was studied from the 10th to the 45th postnatal day, through the ontogeny of psychomotor and sensory functions, by a battery of behavioral tests. The ontogenetic development of 10 different functions was described. The results showed that novelty-induced functions matured progressively in an adult-like pattern of functioning in the 3rd postnatal week. Indeed, exploratory activity was low at the 10th day, increased significantly to reach highest values from 20th to 30th postnatal day, then declined at the 45th postnatal day. No habituation was exhibited by 10- and 15-day-old rats; it appeared at the age of 20 days. Emotional reactivity induced by the novelty of surroundings clearly appeared from the 20th postnatal day, when the features of adult animal were reached. It appeared also that reflex and automatic motor functions came to maturity by the age of 3 wk, while voluntary motor functions continued to improve until the 30th day. Thus, the latency of the hind paw lifting reflex occurrence significantly decreased from the 10th to the 20th postnatal day, when the most improved values were reached. The wire-grasping times increased from the 10th to the 25th postnatal day in an exponential fashion. Locomotor activity developed significantly from the 10th to the 15th day, when the mature locomotion pattern was exhibited. The coordination of complex movements and motor initiative appeared only after the 20th postnatal day. The latencies of execution of crawling along the wire and of leap onto the ground decreased significantly from the 20th to the 45th day. These studies reveal the presence of the caudal to rostral sequence of CNS development, predicting a spatio-temporal functional maturation of nuclei and centers in the rat's CNS. The building of the time-sequence of regional maturation of the brain integrated activities was attempted.

Aging↗

PubMed1993

Functional development of central nervous system in the rat: ontogeny of nociceptive thresholds.

The functional development of central nervous system (CNS) in the rat has been studied from the 10th to the 45th postnatal day, through a sensory function: nociception. Baseline pain responsiveness has been assessed with the tail-flick procedure. The mean tail-flick latency clearly decreases from the 10th to the 25th day, and remains stationary from this age to 45 days. The maturational processes underlying these reductions of tail-flick latencies in developing rats are discussed.

Aging↗

PubMedDate not supplied

Comparative effects of developmental thiamine deficiencies and ethanol exposure on the morphometry of the CA3 pyramidal cells.

Maternal alcoholism and thiamine deficiency are frequently considered to be the causal agents of the central nervous system (CNS) damage associated with mental retardation in the offspring. For further understanding of pathological mechanisms underlying CNS damage in both disorders, histological studies were undertaken in developing rats to compare the hippocampus CA3 pyramidal cells measurements and density between three patterns of thiamine deficiency and chronic alcohol exposure. Female rats were given thiamine-deficient diet during different periods of gestation and lactation to obtain pre-, peri-, and postnatal thiamine-deficient pups. Twelve percent ethanol/water drinking fluid was given to mothers throughout gestation and lactation to obtain ethanol-exposed pups. Thiamine was administered during developmental ethanol exposure to assess the extent of interference between ethanol and thiamine metabolism. Nondrug-treated dams were allowed ad lib access to food and water during gestation and lactation to yield control pups. Hippocampus histology was performed in 45-day-old rats, and the CA3 pyramidal cells measurements and density assessed and compared between all treatment groups. It appears that the mean nuclear size of pyramidal cells in the field CA3 was significantly reduced in all the treatments compared to the control. While the mean nuclear size decreased more severely in development ethanol exposure than in the three patterns of thiamine deficiency, no significant difference was noted when pre-, peri-, and postnatal thiamine-deficient rats were compared. However, thiamine administration during developmental ethanol exposure partially restored the mean nuclear size. In contrast, comparisons between ethanol-exposed pups and the three patterns of thiamine-deficient pups, exhibited similar intensity in the deficit of CA3 pyramidal cells. Cell loss generated by ethanol treatment was not suppressed by thiamine administration. Common and separate mechanisms underlying the effects of alcohol intoxication and thiamine deficiency on cell death and cell atrophy were suggested.

Animals↗