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Biomedical subjects

L D Reid

Publications and source records attributed to L D Reid.

At least 55 records · Page 3Linked to original sources
PubMed1985

Endogenous opioid peptides and regulation of drinking and feeding.

Considerable work across the last 10 yr has implicated the endogenous opioid peptides in the regulation of ingestion. The opioid antagonists, such as naloxone and naltrexone, reduce intake of water, flavored water, and food. Naloxone's effects are pharmacologically specific, ie, its effects are dose-related and stereoselective. Further, a variety of antagonists produce similar effects. A primary site of action of naloxone, with respect to intake, is in the central nervous system. Naloxone's effects are also behaviorally specific, ie, its effects seem particularly related to palatability functions. The effects of opioid agonists, in small doses, enhance intake of some nutrients, but these effects are not opposite those of the antagonists. Benzodiazepines enhance drinking and eating and apparently interact with opioid systems. These observations combine with those directly measuring features of the endogenous opioid peptides to support a conclusion that opioid peptides are part of a system for regulating ingestion.

Animals↗
PubMed1983

Opioid antinociception and positive reinforcement are mediated by different types of opioid receptors.

Fentanyl (FEN) and diprenorphine's (DIPR) potentials for analgesia and reinforcement were assayed using rats. Analgesia was measured by the classic tail-flick test. The test germane to opioid reinforcement involved measuring pressing rates for direct electrical stimulation of the lateral hypothalamus and ventral tegmental area. FEN, as does morphine and heroin, produced strong analgesia and enhanced pressing rates for brain stimulation. DIPR produced no analgesia and antagonized FEN's analgesia. DIPR, at doses antagonizing FEN's analgesia, enhanced pressing for brain stimulation. DIPR's enhancement of pressing was antagonized by naloxone (100 micrograms/kg). When FEN and DIPR were given concurrently, pressing for brain stimulation was not reduced and was greater than after FEN alone was given. These data support a conclusion that different types of receptors are associated with opioid analgesia and reinforcement.

Analgesics↗
PubMed1983

The opioid peptide dynorphin, circadian rhythms, and starvation.

Dynorphin, an opioid peptide whose functions are unknown, is found in brain, pituitary, and peripheral organs. Specific radioimmunoassays were used to measure dynorphin in the hypothalamus and pituitary, during the day and at night, as a function of food and water deprivation. Immunoreactive dynorphin was increased in the hypothalamus and decreased in the pituitary at night. Water deprivation led to more than 50 percent reduction in daytime levels of pituitary dynorphin and concomitant increases in hypothalamic dynorphin.

Animals↗
PubMed1983

Assaying addiction liability of opioids.

A number of procedures are available to assess an opioid's capacity to be positively reinforcing, but each has limitations that could lead to the false conclusion of no addiction potential. The recently developed conditioned place preference (CPP)-test, however, overcomes some of these limitations. Diprenorphine can be used to establish a CPP indicating it has an unsuspected capacity to elicit positive affect. Since diprenorphine antagonizes opioid analgesia and elicits signs of positive affect, the conclusion is confirmed that opioid analgesia and opioid's capacity to be positively reinforcing are separable.

Animals↗
PubMed1983

Addictive agents and intracranial stimulation (ICS): novel antagonists and agonists of morphine and pressing for ICS.

Rats fixed with chronically indwelling bipolar electrodes pressed for intracranial stimulation (ICS) of the lateral hypothalamus during daily sessions. The effects of two antagonists of morphine (Win 44,441 and naloxone) were then assessed. Naloxone (10 mg/kg) produced its characteristic reduction in pressing. Win 44, 441 produced a reliable increase in pressing at doses as small as 1 mg/kg. Large doses of morphine (10 mg/kg) produced its characteristic effects: depression in pressing when given 1 hr before the test session and facilitation when given 3 hr before the test session. Win 44,441 antagonized morphine's depressive effects. Other compounds (Win 44,156, Win 42,156), having similar structure to Win 44,441 but having agonist and mixed agonist-antagonist activity with respect to analgesia, also facilitated pressing for ICS. All three compounds' effects on pressing for ICS were antagonized by naloxone. It is inferred that opioids' facilitatory effects on pressing for ICS are separable from opioids' other capabilities such as production of analgesia.

Animals↗
PubMed1983

Morphine and acceptability of putative reinforcers.

Rats were given the opportunity to take one of five concentrations of saccharin solutions. Intake across concentrations generated a preference-aversion curve. Morphine, 2 mg/kg, increased intake of saccharin solutions when rats were 12-hr water deprived or were not deprived. These effects with morphine are opposite to those of naloxone and strengthen the idea that there is opioid involvement in incentive motivation.

Aging↗
PubMed1983

Endophinergic modulation of acceptability of putative reinforcers.

A series of experiments was conducted in order to gain additional insight into how endogenous opioids may modulate taste reactivity and, thus, hedonic processes. Using a wide range of saccharin concentrations ranging from mildly preferred to aversive, it was demonstrated that naloxone reduced preference for saccharin over water. This reduction was not dependent upon concentration of saccharin and resulted in a downward displacement of the preference/aversion curve. Naltrexone was shown to result in a greater decrease in intake in animals drinking a mildly aversive quinine solution, as compared to animals drinking tap water. In conclusion, endogenous opioids may serve to broaden the range of food-related stimuli which are avidly accepted, perhaps by inhibiting any aversive component associated with ingestion.

Animals↗
PubMed1982

Naloxone modifies sugar-water intake in rats drinking with open gastric fistulas.

The effects of the opiate antagonist naloxone (NX) on fluid preference and intake were determined in rats drinking with chronically indwelling gastric fistulas. The subjects were tested both after 22.5 hr fluid deprivation, and no deprivation, with open fistulas (sham drinking), as well as with closed fistulas. Following an injection of either saline or NX (0.5-10.0 mg/kg, administered SC), or no injection, the subjects were given the choice to drink water or 10% sucrose, in a two-bottle test, for 1 hr/day. With open fistulas, and following fluid deprivation, the animals sham drank both sucrose and water, but had a strong preference for sucrose. When not fluid deprived, the same animals sham drank sucrose almost exclusively. NX significantly reduced sucrose intake by the sham drinking animals, in both the deprived and not deprived conditions, but did not modify fluid preference. These data support the idea that NX modifies affective reactivity to palatable solutions, and that NX's antidipsogenic actions are not due to feedback from post-absorptional events.

Animals↗
PubMed1982

A temporal analysis of naloxone's suppressant effect on drinking.

Licking activity was monitored in water deprived rats following various doses of naloxone. It was found that naloxone, at doses ranging from 0.01 to 10.0 mg/kg, had very little effect on initial drinking. However, naloxone did slow sustained drinking after 2 to 6 min into the bout, dependent upon dose. We takes these results to mean that naloxone is interfering with those processes which serve to sustain continued drinking throughout a drinking bout.

Animals↗
PubMed1981

Intracerebral administration of naloxone and drinking in water-deprived rats.

In 24-hr water-deprived rats, naloxone, at various doses (0, 12.5, 25, 50 micrograms/rat), was administered prior to a 15-min drinking period. Infusions were made bilaterally into each lateral ventricle, frontal cortex, lateral preoptic area, lateral hypothalamus, and caudate nucleus. Naloxone reliably reduced water consumption at 50 micrograms/rat when infused into the lateral ventricles and lateral hypothalamic areas. When comparable doses of naloxone were given by peripheral injection, no effect on drinking was observed. There appeared to be a trend developing for greater sensitivity to naloxone when infusions were made into a particular part of the hypothalamus. These data support the idea that naloxone reduces drinking by acting at central opiate receptors.

Animals↗
PubMed1981

Naloxone reduces fluid intake in rats with open gastric fistulas.

Water-deprived rats, fixed with chronically indwelling gastric fistulas, drank with the fistulas open (sham drinking) for 20 min. The subjects were given three doses of naloxone (0.0, 1.0, and 10 mg/kg, SC) 15 min before the opportunity to sham drink. The mean water intakes on days of 0.0, 1.0 and 10 mg/kg of naloxone were 43.3, 36.3 and 23.1 g, respectively. Naloxone clearly reduced fluid intake in rats engaged in sham drinking. This finding, that naloxone reduces fluid intake when post-ingestional absorption is prevented, lends support to the idea that naloxone modified central neural regulatory processes. The results of these experiments do not support the hypothesis that the endorphins are involved exclusively with drive-reduction.

Animals↗
PubMed1981

Morphine antagonists and consummatory behaviors.

Opiate antagonists were tested for their effects upon either drinking or eating in eight experiments. Naloxone, nalorphine, and the active isomer of WIN 44,441 all reduce drinking. Neither an analog of nalorphine that does not cross the blood-brain barrier, nor the inactive isomer of WIN 44,441 is effective in reducing water intake. These data provide support for the conclusion that these antagonists ahve stereospecific effects within the central nervous system. Naloxone suppresses drinking following procedures inducing osmotic, volemic, or hormonal thirst. Naloxone suppresses eating following procedures inducing glucoprivation but does not alter eating elicited by tail-pressure. Collectively, these data lead to the conclusion that endorphins play a role in the organization of ingestive behavior following challenges to homeostasis.

Angiotensin II↗
PubMed1981

Opiate antagonists and sexual behavior in female hamsters.

Mating or administration of morphine to female hamsters reliably decreases lateral displacement, a sensitive index of female sexual responsitivity. Morphine's effects are antagonized by naloxone. We asked whether endogenous opiates are significantly involved in the mating-induced inhibition of sexual responsitivity by testing whether naloxone or naltrexone attenuated the mating-induced decreases in lateral displacement. Naloxone (4 mg/kg) increased lateral displacement in only one of three tests in females before mating. Naloxone did not attenuate the mating-induced decreases in lateral displacement or lordosis behavior in either ovariectomized, hormonally supplemented or intact females. Large doses of naltrexone produced no reliable effects on sexual behavior during estrus in unmated females, nor did it attenuate the mating-induced decreases in sexual responding, regardless of the time of day of mating. Naloxone often increases the variability of sexual responding. We conclude that naloxone-sensitive mechanisms do not play a critical role in the expression of sexual behavior in female hamsters.

Animals↗
PubMed1980

Naloxone reduces fluid intake: effects of water and food deprivation.

Food and fluid deprived and nondeprived male rats showed 36% and 46% decreases, respectively, in sucrose consumption 15-min after injection with 2 mg/kg of naloxone in one hr tests. The magnitude of this decrease was not correlated with an index of naloxone's ability to produce a sickness, as measured by the conditioned taste aversion test. Tests with animals scheduled to drink water in a 15-min daily session showed naloxone had similar effects in reducing water intake in 23-hr and 47-hr water deprived rats. Morphine, when self-administered, produced an increase in water intake during 6-hr sessions. The data support the idea that naloxone disrupts a component of normal regulation of ingestion.

Animals↗
PubMed1979

Morphine and naloxone's effects on sexual behavior of the female golden hamster.

The effects of morphine and naloxone were observed after administration to female golden hamsters (Mesocricetus auratus). Large doses of morphine, 80 mg/kg, consistently produced sedation and behavioral depression of responses to nociceptive stimuli. Smaller doses of morphine (e.g., 10 mg/kg), that produced few other behavioral changes, suppressed a measure of female sexual responding. The suppressive effects on sexual behavior were reversed by 4 mg/kg of naloxone. Morphine administered intracerebroventricularly had little effect on sexual responding, even at doses which produced other side effects. Doses of 4 and 8 mg/kg of naloxone in opioid-naive subjects did not reliably alter sexual responding up to 2 hr after administration. These observations lead to the suggestion that morphine produces effects which are incompatible with full sexual functioning in female hamsters.

Animals↗
PubMed1975

Intracranial self-stimulation effects along the route of the nigro-striatal bundle.

Recent evidence suggesting a possible dopaminergic nigro-striatal substrate of self-stimulation led us to map this route for both self-stimulation and stimulus-bound motor effects. The results of 128 electrode placements show that the route of the nigro-striatal projection supports strong self-stimulation effects from the substantia nigra to the ento-peduncular nucleus. Beyond this level, such effects disappear. Our results indicate that the striatum itself is neutral with regard to reinforcement, and suggest that such apparent neutrality cannot be ascribed to motor or other artifacts. These findings require a reappraisal of the hypothesis of a dopaminergic self-stimulation system, although they are not in conflict with the idea that dopaminergic manipulations may affect self-stimulation through some more general regulatory influence on operant responding.

Animals↗