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Biomedical subjects

H H Samson

Publications and source records attributed to H H Samson.

133 records · Page 8Linked to original sources
PubMedDate not supplied

The effects of local application of ethanol in the n. accumbens on dopamine overflow and clearance.

The actions of ethanol on extracellular dopamine levels in the n. accumbens were examined in both anesthetized and unanesthetized rats using either in vivo voltammetry or microdialysis. In the voltammetry studies, ethanol was microinjected directly into the accumbens. For the microdialysis studies, the ethanol was injected systemically. The voltammetry studies failed to find any direct effect of local ethanol on extracellular dopamine levels. However, exposure to high ethanol concentrations directly injected into the n. accumbens showed the rise rate and the return to baseline rate to a n. accumbens KCl-stimulated dopamine release. In the microdialysis studies, increased levels of extracellular dopamine in the n. accumbens were found in unanesthetized rats, similar to those reported in the literature. However, in the anesthetized rats, the extracellular dopamine levels were not increased, even with similar local ethanol levels measured in the dialysate. Taken together, the data suggest that the actions of ethanol to increase extracellular dopamine levels in the n. accumbens are most likely not an effect of ethanol at the level of the accumbens but rather an action which increases neural activity within the mesoaccumbens pathway, perhaps via actions at the ventral tegmental area.

Anesthesia↗
PubMedDate not supplied

Ethanol-induced microcephaly in neonatal rats: relation to dose.

Neonatal rats were exposed to several different doses of ethanol during the first part of the brain growth spurt (postnatal days 5, 6, 7 and 8) and examined for decreased brain weights at 18 days of age. The occurrence of reduced brain weight was found to require a dose of at least 6.0 g ethanol/kg body weight/day. Above this dose, the extent of brain weight reduction was related to increased dose, provided death from overdose did not occur. Measured blood ethanol levels suggested that blood levels below 100 mg/100 ml failed to result in significant brain weight reductions. The possibility that blood ethanol levels below this point may impair brain growth in more subtle ways remains to be determined.

Alcohol Drinking↗
PubMedDate not supplied

Oral ethanol reinforcement: interactive effects of amphetamine, pimozide and food-restriction.

Twelve male Long Evans rats, trained to lever press using 10% (v/v) oral ethanol reinforcement, were maintained with ad lib access to food and water in the home cage. After stabilization of responding, the rats were randomly divided into two groups: Group P received pimozide (PIM) injections (0.1 to 0.5 mg/kg) and Group A received d-amphetamine (DEX) injections (0.05 to 0.5 mg/kg). Following the sequence of either PIM or Dex injections, all rats were given four different combinations of PIM + DEX injections. The lower doses of amphetamine did not affect responding, but 0.5 mg/kg significantly reduced responding. All PIM doses except the lowest reduced responding. The combined PIM + DEX doses all reduced responding, in some cases further than either constituent dose alone. Next, all rats were reduced to 80% of their free feeding weights by food restriction, and tested with 0.25 mg/kg DEX, 0.1 mg/kg PIM, and 0.1 PIM + 0.25 DEX. As a result of food restriction, baseline responding increased significantly. The 0.25 mg/kg DEX dose tended to increase responding even above this baseline increase, while both PIM and PIM + DEX reduced responding.

Animals↗
PubMedDate not supplied

n-Propanol induced microcephaly in the neonatal rat.

Neonatal rats were reared using an artificial feeding technique from postnatal day 5 through 18. On days 5, 6, 7 and 8 some animals received n-propanol in their milk formula with the remaining animals serving as controls. The propanol was given in doses similar to that of ethanol which is known to result in microcephaly using this procedure. Following the 4 day alcohol exposure, all animals received the plain milk formula until day 18, when they were decapitated and various organ weights measured. Brain weights and brain/body weight ratios were significantly decreased in the alcohol exposed group. Biochemical analysis showed the alcohol exposed group had a decreased amount of DNA in all brain areas examined. Cholesterol levels were decreased in the forebrain and cerebellar samples of the alcohol group, while protein levels were decreased only in the forebrain samples. The results suggest that exposure to n-propanol during a portion of the brain growth spurt of the neonatal rat inhibits brain development. The biochemical measures of brain growth imply n-propanol interferes with the development of the brain in a manner similar to ethanol.

1-Propanol↗
PubMedDate not supplied

Ethanol induced microcephaly in the neonatal rat: occurrence without withdrawal.

Neonatal rats exposed to ethanol with an artificial rearing technique on postnatal days 4--8 have been found to have up to 20% decrease in brain weight when examined on postnatal day 18. Following the four day ethanol exposure these animals went through a moderate to severe abstinence syndrome. Since the appearance of any detectable brain growth differences were not found until after the withdrawal period, it was possible that the microcephaly was a result of withdrawal and not ethanol exposure. To test this hypothesis, neonatal rats were exposed to ethanol for either the four day exposure period used in the previous work, or until determination of brain growth impairment at day 11. This last group of animals were administered a daily dose of ethanol such that they did not have an observable abstinence syndrome. Examination of brain weights on day 11 revealed no differences in the extent of the observed microcephaly between the ethanol exposure conditions, suggesting that withdrawal per se was not responsible for the production of the brain growth retardation.

Animals↗
PubMedDate not supplied

Ethanol and tertiary butanol induced microcephaly in the neonatal rat: comparison of brain growth parameters.

Neonatal rats were reared using an artificial feeding technique from postnatal day 4 through 18. On Postnatal Days 4 through 7, corresponding to the onset of the brain growth spurt, some animals were administered either ethanol or tertiary butanol in the milk formula, with the remaining animals serving as controls. The alcohol dosages were equated to each other by membrane to buffer partition coefficients. Following the 4 day alcohol exposure, all animals were given the plain milk formula until Day 18, when they were decapitated and various organ weights measured. The only significant weight differences between alcohol-exposed animals and controls were absolute brain weights and brain weight/body weight ratios, which were decreased in both alcohol groups. Biochemical analysis of the brains showed similar DNA levels for the ethanol, tertiary butanol, and control group forebrain samples. Both alcohol groups had significantly lower DNA levels than the control group for the hindbrain samples. Cholesterol levels and cholesterol/DNA ratios indicated that ethanol, but not tertiary butanol, impaired myelination and/or arborization. Total protein and protein/DNA ratios suggested that ethanol interfered with protein production and/or incorporation. The tertiary butanol animals did not show this deficit. The results imply that while exposure to either alcohol during the brain growth spurt can lead to microcephaly, the ethanol-induced alteration of myelin formation and protein production in neonatal brain tissue may be due to additional properties of ethanol.

Animals↗