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Biomedical subjects

L S Rafales

Publications and source records attributed to L S Rafales.

6 recordsLinked to original sources
PubMed1983

Effects of acrylamide on locomotion and central monoamine function in the rat.

Male rats receiving acrylamide (ACR) in their drinking water (100 ppm) for a six-week period displayed increased psychomotor stimulation to d-amphetamine (d-A; 1.0 mg/kg SC) under several conditions of handling and drug administration. Following behavioral tests a subset of the animals was sacrificed at 15, 50, 80 and 120 minutes following d-A and the brains removed and dissected for determinations of regional brain levels of several monoamine neurotransmitters and metabolites. ACR rats had elevated levels of 5-hydroxyindoleacetic acid (5-HIAA) in the striatum, septal area, and thalamus. The effect was most pronounced at 15 minutes post-drug with ACR rats not demonstrating a depression in 5-HIAA levels present in controls. Increases in accumben's dopamine and norepinephrine levels, evident after d-A, were of lesser magnitude in ACR-exposed rats. Decreases in dihydroxyphenylacetic acid and homovanillic acid, also evident after d-A, persisted for a longer duration in ACR-exposed rats. Light and electron microscopy of spinal cord, striatum, nucleus accumbens and thalamus did not reveal morphologic abnormalities. Sciatic nerves showed histopathological changes characteristic of multi-focal dying-back peripheral nerve degeneration. It was concluded that acrylamide's effect on the psychomotor stimulant properties of d-A may be related to changes in a serotonergic inhibitory system.

Acrylamide↗
PubMed1981

Responsiveness to d-amphetamine in lead-exposed rats as measured by steady state levels of catecholamines and locomotor activity.

Locomotor activity and brain catecholamine concentrations following d-amphetamine challenge were evaluated in lead-exposed rats. Sucklings were exposed to lead via its transfer from maternal drinking solutions (0.02% Pb (Ac)2, 109 ppm Pb) to the maternal milk supply. At 21 days of age half of each exposed litter was weaned to the maternal regimen, the remainder to distilled water. Spontaneous locomotor activity and lead in blood were qualified at 21, 30 and 90 days of age. At 90 days of age rats were also challenged with d-amphetamine sulfate (1.0 mg/kg, SC) and their drug-induced activity recorded for a 2 hours period. One week later the same animals received a similar dose of d-amphetamine and were sacrificed at 0, 0.5, 1, 3, 6, 12, 24 and 48 hours post injection for analysis of whole brain dopamine (DA) and norepinephrine (NE). Catecholamine concentrations did not differ between lead-exposed and control rats in the absence of a d-amphetamine challenge. However, over the 48 hr period following drug challenge, lead-exposed rats had lower whole brain steady state levels of NE than control animals. Similar changes were evident for rats exposed to lead continuously and for those exposed to lead only during the 21 day period from birth to weaning. The spontaneous locomotor activity of lead-exposed and control rats was comparable at all ages tested. However, drug-induced activity was greater in lead-exposed animals than controls. This facilitated drug response was statistically greater than that of controls for continuously lead-exposed rats. Those exposed only during the neonatal period showed similar trends.

Animals↗
PubMed1979

Drug induced activity in lead-exposed mice.

Three interrelated studies were conducted to examine the locomotor activity of lead-exposed mice. The effects of lead were examined as a function of the dose and duration of exposure. Exposure during the first three weeks occurred via the maternal milk supply. Exposure following weaning was achieved via the water supply. Mice received challenges with various pharmaceutical agents, including d-amphetamine, methylphenidate, apomorphine and phenobarbital. The spontaneous activity prior to injection and the drug-induced activity were monitored. Lead-exposed mice usually displayed spontaneous activity which was indistinguishable from that of the control animals. In only one set of observations did lead exposure result in a modest increase in spontaneous activity. The drug-induced activity varied in a complex manner as a function of the magnitude and duration of the lead exposure. Depressed body weight, which was concurrent with high lead exposure (0.5% Pb(Ac)2) was also a significant parameter affecting both the spontaneous and drug-induced activity.

Age Factors↗
PubMedDate not supplied

Behavioral and pharmacological responses following acrylamide exposure in rats.

The onset of acrylamide related toxicity and indications of recovery were evaluated using several behavioral tasks. Rats were chronically housed and tested for the first 15 weeks of the study in running wheels where food and water consumption and activity were continuously monitored. Separate groups of animals were repeatedly tested on at least one additional behavioral task: an operant schedule FR20 GO/NO-GO, spontaneous and drug-induced locomotor activity, drug-induced asymmetric rotation, or splaying of the hindlimbs. Animals were administered acrylamide monomer in their drinking water (100 ppm) for a six week period. Behavioral evaluations were initiated up to six weeks prior to acrylamide exposure and continued up to 12 weeks after termination of the exposure. Operant behavior and spontaneous locomotor activity in an open field were not affected by acrylamide exposure. Nocturnal activity in running wheels was decreased, and hindlimb splay increased by exposure to acrylamide. Subsequent to injections of d-amphetamine locomotor activity in an "open field" was markedly increased following exposure to acrylamide. d-Amphetamine induced asymmetric rotation was also altered following acrylamide exposure. It is suggested that this altered pharmacological response was due to an effect of acrylamide on hepatic mechanisms or on central dopaminergic function.

Acrylamides↗