Biomedical subjects
Publications and source records attributed to Z Amit.
The construction of a double channel swivel for infusing two fluids separately into an unrestrained animal is described. The swivel is constructed of readily available, inexpensive materials and does not require any machining of parts. These swivels have been found to last for 720 hr without leakage.
Several lines of evidence suggest that the endogenous opioid peptides endorphins may play a role in the defensive response of the organism to stress. The present paper summarizes these findings as well as evidence linking endorphins to the anterior pituitary polypeptide hormone adrenocorticotropin (ACTH). Evidence is presented that endorphins may function as trophic hormones in peripheral target organs such as the adrenal medulla and the pancreas. As such they may be part of the physiological mechanisms that mediate adrenaline and glucagon release in response to stress. Endorphins (enkephalins) are also suggested to play a role in the control of the pituitary gland during stress. In such capacity they may act as hormone-releasing or inhibiting factors. Finally, endorphins appear to play a role in the behavioral concomitants of stress. In such capacity endorphins are suggested to function as modulators of neural systems that mediate the elaboration and expression of the reactive/affective components of stress. Speculations on the mode of interaction between endorphins and ACTH in the global response to stress are discussed.
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Male Wistar rats were presented with an everyday free choice between water and a morphine-sucrose solution. Following a 5-day baseline period animals were injected with either zimelidine (10 or 20 mg/kg, i.p.), a neuronal serotonin uptake inhibitor, or Ringer's solution (2 ml/kg, i.p.) for 5 consecutive days. Treatment with zimelidine was shown to significantly attenuate morphine drinking suggesting that an increased availability of serotonin may interfere with the positive reinforcing properties of morphine. The results are also discussed in terms of a possible interaction with brain norepinephrine. The possibility that the reinforcing effects of both morphine and ethanol are subserved by common mechanisms is suggested.
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Chronic administration of the long acting opiate antagonist naltrexone potentiated the analgesic effects of foot-shock stress in the hot-plate test in rats. No changes in pain responsiveness were noted in naltrexone-treated rats that were not subjected to the foot-shock treatment. The results suggest that chronic opiate receptor may lead to the development of supersensitivity in endogenous opiate systems that mediate the analgesic effects of stress.
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For 11 consecutive days, naive rats were maintained in operant chambers where they were given the opportunity to self-administer acetaldehyde (1,2, or 5% v/v), ethanol (2 or 10% v/v), or pH control solutions directly into the cerebral ventricles. Only the animals that had access to the 2 and 5% acetaldehyde solutions showed rates of lever pressing significantly higher than controls. It is suggested that acetaldehyde rather than ethanol itself may mediate the positive reinforcing effects of ethanol in the brain.
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Laboratory rats were pretreated with either morphine (9 mg/kg IP), diazepam (4 mg/kg 1P) or Ringer's solution 2, 3 1/2, and 2 hr, respectively, prior to ingestion of a novel tasting saccharin solution followed immediately by a single injection of one of these agents. Animals pretreated with Ringer's solution followed by an injection of either morphine or diazepam showed a conditioned taste aversion (CTA) as determined by a significant reduction in the mean saccharin intake on a subsequent test trial. Although the drug pretreatments alone produced no conditioned avoidance behavior, the diazepam pretreatment completely blocked the development of both diazepam and morphine-evoked CTAs while the morphine pretreatment prevented a CTA induced by itself but not by diazepam. The results were discussed in terms of the attenuating effects of the pretreatments on the relative saliency of the subsequent conditioning drug injection.
The role of 5-hydroxytryptamine (5-HT) uptake blockade in the mediation of the positive reinforcing peroperties of ethanol in male wistar rats was investigated. It was demonstrated that treatment with zimelidine (H102/09) a 5-HT uptake inhibitor, specifically attenuated ethanol consumption. In an attempt to extinguish the ethanol drinking response, ethanol preferring animals in a second experiment, were provided with ethanol as the only source of fluid in combination with zimelidine treatment. Animals treated in such a manner subsequently reduced their ethanol consumption when presented with a free-choice between ethanol and water. These results were attributed to an increased availability of central 5-HT, suggesting that central 5-HT mechanisms may in some way be involved in the mediation of the positive reinforcing properties of ethanol.
This experiment was undertaken to examine whether the attenuation of ethanol consumption following treatment with zimelidine (H102/09) could be due to an invasion of surplus serotonin into norepinephrine neurons. In an attempt to prevent this proposed invasion by serotonin, ethanol preferring animals were pre-treated with desmethylimipramine (DMI), a norepinephrine reuptake inhibitor, prior to treatment with zimelidine. The results demonstrated that those animals treated in such a manner consumed significantly more ethanol than those animals treated with zimelidine alone. Based on these results it is suggested that the observed attenuation of ethanol consumption following zimelidine treatment, could be partially due to a serotonin-induced functional depletion of norepinephrine.
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