Biomedical subjects

D J Calcagnetti

Publications and source records attributed to D J Calcagnetti.

40 records · Page 3Linked to original sources

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↗

PubMedDate not supplied

Olfactory bulbectomy disrupts the expression of cocaine-induced conditioned place preference.

The role of the olfactory sense in the expression of cocaine-induced conditioned place preference (CPP) was examined in adult male rats (n = 35) of the N/Nih strain. Consistent with the scientific literature, rats were observed to significantly (p < 0.05) increase (double) the seconds spent in their least-preferred chamber following cocaine-chamber pairings. Subsequently, groups of rats underwent one of three treatments: 1) olfactory bulbectomy (BULBX), 2) sham surgery (SHAM), or 3) sham surgery plus intranasal zinc sulfate perfusion (ZnSO4). Zinc sulfate was used to produce a temporary loss of olfaction. In a separate behavioral measure of olfactory acuity, both BULBX and ZnSO4-treated rats performed at an equally deficient level, in contrast to SHAM-treated rats that were not rendered anosmic. A second conditioned place preference test revealed that the ZnSO4-perfused and SHAM groups did not differ from their original postcocaine preference measurements. In contrast, the BULBX group spent significantly fewer seconds in the cocaine-paired chamber. After a 14-day interval, a third preference test revealed that SHAM and ZnSO4-treated rats displayed an equivalent preference for the cocaine-paired chamber (at 2.7 times above baseline). Interestingly, the seconds spent in the cocaine-paired chamber by BULBX rats did not differ from their baseline (e.g., precocaine exposure). These results suggest that bulbectomy disrupts the expression of cocaine-induced place preference. Interpretations of data from BULBX rats involving the production of an anhedonic condition and the relevance of olfactory bulbectomy as an animal model of anhedonic depression are discussed.

Animals↗

PubMedDate not supplied

[D-Ala2,Leu5,Cys6]enkephalin: short-term agonist effects and long-term antagonism at delta opioid receptors.

Four experiments were conducted. Two examined the in vivo short-term effects (less than 35 min) and two examined the in vivo long-term effects (greater than 2 days) of the synthetic enkephalin analogue, [D-Ala2,Leu5,Cys6]enkephalin (DALCE). In the short term, DALCE was found to produce analgesia and transient immobility after intracerebroventricular (ICV) administration. We found a dose-related increase in paw-lick latency for rats placed on a hotplate (52 degrees C). In the second experiment, we determined that immobility was attenuated by pretreatment with naltrexone methobromide (QNTX, 0.1 microgram), and the delta selective antagonist, 16-methyl cyprenorphine (M80, 5 micrograms). QNTX and M80 significantly attenuated DALCE-induced immobility by more than 50% of control. Paw-lick latency was then measured on the hotplate to assess analgesia. Pretreatment with M80 reliably attenuated the DALCE-induced analgesia. Whereas QNTX failed to reliably attenuate paw-lick latency on the first trial, it was as effective as M80 on the second trial. We suggest that the short-term agonist effects of DALCE are produced by actions at mu and delta opioid receptors as would be predicted from prior in vitro studies showing moderate to high affinity, respectively, at these receptors. In the third experiment, DALCE was shown to display long-term behavioral antagonism that was selective for the delta receptor. Rats were injected ICV with 6.7 micrograms of DALCE and tested 48 hr later. Analgesia was measured by injecting 15% formalin subcutaneously followed 20 min later by an ICV injection of one of three selective opioid agonists (DAGO, DPDPE or U50488H).(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMedDate not supplied

Differential effects of selective opioid peptide antagonists on the acquisition of pavlovian fear conditioning.

Pretreatment with opioid antagonists enhances acquisition of Pavlovian fear conditioning. The present experiments attempted to characterize the type of opioid receptor responsible for this effect using a procedure that assessed the fear of rats to a chamber previously associated with electric shock (1 mA, 0.75 s). Freezing, a species-typical immobility, was employed as an index of fear. Two mu opioid antagonists, CTOP (40 ng) and naloxonazine (10 micrograms), enhanced conditioning. On the other hand, the kappa antagonist nor-binaltorphimine reduced conditioning. Two delta antagonist treatments (16-methyl cyprenorphine and naltrindole) had no reliable effect on acquisition. Thus the enhancement of conditioning appears to be mediated by mu receptors. Previous research has shown that the conditional fear produced by these procedures caused an analgesia that is also mediated by mu receptors. It is argued that the enhancement effect occurs because of an antagonism of this analgesia and that the analgesia normally acts to regulate the level of fear conditioning.

Animals↗