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Biomedical subjects

P M Adams

Publications and source records attributed to P M Adams.

48 records · Page 3Linked to original sources
PubMed1975

Effects of stereotactic cingulumotomy on a sequential motor task in man.

The effect of bilateral cingulumotomy on sequential tapping behavior was investigated in 6 patients, Contrary to previous clinical studies and predictions derived from data on cingulate lesions in the rat, a consistent decrement in postoperative performance was not found. Temporal integration of behavior in man, as measured in terms of accuracy of sequential motor performance, does not appear to be critically dependent upon the integrity of the cingulum bundle at the level of interruption investigated in the present study.

Adult↗
PubMed1975

Effect of chronic marijuana administration of stages of primate sleep-wakefulness.

The effects of the repeated administration of delta-9-tetrahydrocannabinol on sleep-wakefulness patterns were studied in adult male squirrel monkeys. The percent time spent in slow wave sleep was reduced with chronic treatment and failed to return to base line levels after 30 days of recovery. The amount of time spent in Stage 1 or drowsy state increased with repeated treatment and remained elevated through recovery. Changes observed in other stages of sleep-wakefulness were sensitive to repeated treatment with marijuana but were found to return to base line levels during recovery.

Administration, Oral↗
PubMedDate not supplied

Perinatal diazepam exposure: behavioral and neurochemical consequences.

In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.

Animals↗
PubMedDate not supplied

Toxic exposure to ethylene dibromide and mercuric chloride: effects on laboratory-reared octopuses.

The effects of acute and chronic exposure to either ethylene dibromide (EDB) or mercuric chloride (MC) were studied in laboratory-reared Octopus joubini, O. maya and O. bimaculoides. The advantages of using octopuses were that the responses were immediate, highly visible and sensitive. All species demonstrated signs of toxicity to acute and chronic exposure to EDB and to MC. A dosage-sensitive relationship for the loss and subsequent recovery of locomotor response and of chromatophore expansion was found for each species after acute exposure. For each species the LC50 for chronic exposure occurred within 12 hr at 100 mg/l for EDB and within 3 hr at 1,000 mg/l for MC. This study demonstrated the potential usefulness of laboratory-reared octopuses in evaluating the toxicity of marine environmental pollutants.

Animals↗
PubMedDate not supplied

The effects of thyroid hormone level and action in developing brain: are these targets for the actions of polychlorinated biphenyls and dioxins?

Alterations in thyroid hormone level or responsivity to thyroid hormone have significant neurologic sequelae throughout the life cycle. During fetal and early neonatal periods, disorders of thyroid hormone may lead to the development of motor and cognitive disorders. During childhood and adult life, thyroid hormone is required for neuronal maintenance as well as normal metabolic function. Those with an underlying disorder of thyroid hormone homeostasis or mitochondrial function may be at greater risk for developing cognitive, motor, or metabolic dysfunction upon exposure to substances which alter thyroid hormone economy. Polychlorinated biphenyls (PCBs) and dioxins have been argued to interfere with thyroid hormone action and thus may affect the developing and mature brain. Animal models provide useful tools for studying the effects of thyroid hormone disorders and the effects of environmental endocrine disruptors. The congenitally hypothyroid, hyt/hyt, mouse exhibits abnormalities in both the cognitive and motor systems. In this mouse and other animal models of thyroid hormone disorders, delayed somatic and reflexive development are noted, as are permanent deficits in hearing and locomotor and adaptive motor behavior. This animal's behavioral abnormalities are predicated on anatomic abnormalities in the nervous system. In turn, these abnormalities are correlated with differences in neuronal structural proteins. In normal mice, the expression of mRNAs coding for these proteins occurs temporally with the onset of autonomous thyroid hormone production. The hyt/hyt mouse has a mutation in the thyroid stimulating hormone receptor (TSHr) gene which renders it incapable of transducing the TSH signal in the thyrocyte to produce thyroid hormone. Some behavioral and possibly some biochemical abnormalities in mice exposed to PCBs are similar to those seen in the hyt/hyt mouse. In addition to direct effects on brain development and neuronal maintenance, thyroid hormone is necessary for maintaining metabolic functioning through its influence on mitochondria. Because the brain is particularly sensitive to inadequate energy generation, disorders of thyroid hormone economy also indirectly impair brain functioning. Alterations in thyroid hormone level result in differing expression of mitochondrial genes. Mutations in these mitochondrial genes lead to well-recognized syndromes of encephalomyopathy, myopathy, and multisystem disorder. Hence, PCBs and dioxins, by possibly altering the thyroid hormone milieu, may alter the functioning of mitochondria in the generation of adenosine triphosphate (ATP). The use of animal models of thyroid hormone deficiency for behavioral, anatomic, histologic, and molecular comparison will help elucidate the mechanisms of action of these putative endocrine-disrupting compounds. The study of thyroid hormone disorders provides a template for relating thyroid hormone mediated effects on the brain to these compounds.

Animals↗
PubMedDate not supplied

Effects of perinatal chlordiazepoxide exposure on rat preweaning and postweaning behavior.

The effects of perinatal chlordiazepoxide (CDZ) exposure were studied in 3 to 30 day old F344 rats. Pregnant primaparous rats were treated daily on days 1-21 of pregnancy with CDZ (1 mg/kg) or saline (IP). Lactating females were treated with CDZ or saline in order to expose pups on postnatal days 1-21. Behavioral measures on all litters included: cliff avoidance (postnatal days 4-10), swimming (postnatal days 6-10), open field activity (postnatal days 14 and 21) and active avoidance (beginning postnatal day 30). Neonates perinatally exposed to CDZ were significantly slower in cliff avoidance development as measured by latency to meet criterion. Swimming development was impaired by both prenatal and postnatal CDZ exposure. Open field activity was minimally affected on day 14 but only for males exposed postnatally to CDZ. Postnatal CDZ exposure significantly affected active avoidance performance as reflected in faster response latencies and an increased number of avoidance responses to reach criterion for extinction. Only the postnatally exposed male pups were significantly affected on the avoidance behavior. These results are consistent with the suggestion that CDZ is a potential behavioral teratogen.

Animals↗
PubMedDate not supplied

Active avoidance behavior in the F1 progeny of male rats exposed to cyclophosphamide prior to fertilization.

The acquisition and extinction of a one-way active avoidance task was studied in 30 day old F1 progeny of male rats previously exposed to either acute or chronic treatment with cyclophosphamide (CP) prior to breeding with normal females. Chronic treatment (10 mg/kg/day x 5 days x 5 weeks) was given to adult F344 males followed by subsequent breeding with normal females (CP-S). Separate groups of males were given a single CP injection (10 mg/kg) and breeding with normal females was done at 7-9, 14-16 and 28-30 days following the CP treatment. F1 progeny of males exposed to chronic CP or to a single CP treatment when bred 7-9 (females only) and 14-16 days post exposure (males and females) took significantly longer to reach the criterion for extinction. These progeny also responded significantly faster during extinction than progeny of the saline treated males. These findings support our earlier evidence of behavioral anomalies induced in the F1 progeny of male rats exposed to CP prior to breeding and that this effect reflects damage in post-meiotic germ cells.

Animals↗