piperidines has been researched along with naltrindole* in 14 studies
14 other study(ies) available for piperidines and naltrindole
Article | Year |
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A low pKa ligand inhibits cancer-associated pain in mice by activating peripheral mu-opioid receptors.
Topics: Analgesics, Opioid; Animals; Bone Neoplasms; Cancer Pain; Cell Line, Tumor; Fentanyl; Hydrogen-Ion Concentration; Hyperalgesia; Ligands; Male; Melanoma, Experimental; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Morphinans; Naloxone; Naltrexone; Narcotic Antagonists; Piperidines; Receptors, Opioid, mu | 2020 |
Inhibition of DOR prevents remifentanil induced postoperative hyperalgesia through regulating the trafficking and function of spinal NMDA receptors in vivo and in vitro.
Several studies have demonstrated that intraoperative remifentanil infusions have been associated with opioid-induced hyperalgesia (OIH). Activation of delta opioid receptor (DOR) and augmentation of N-methyl-d-aspartate (NMDA) receptor expression and function may play an important role in the development of OIH. The aim of this study was to investigate whether DOR inhibition could prevent remifentanil-induced hyperalgesia via regulating spinal NMDA receptor expression and function in vivo and in vitro.. A rat model of remifentanil-induced postoperative hyperalgesia was performed with the DOR agonist deltorphin-deltorphin II or the DOR antagonist naltrindole injected intrathecally 10 min before remifentanil infusion. Mechanical and thermal hyperalgesia were measured at -24h, 2, 6, 24 and 48 h after remifentanil infusion. Western blot was applied to detect the membrane and total expression of DOR and NMDA receptor subunits (NR1, NR2A and NR2B) in spinal cord L4-L6 segments. In addition, whole-cell patch-clamp recording was used to investigate the effect of DOR inhibition on NMDA receptor-induced current in spinal cord slices in vitro.. We found that membrane trafficking of DOR, NR1 and NR2B subunits in the spinal cord increased after remifentanil administration and surgery. The DOR antagonist naltrindole could attenuate mechanical and thermal hyperalgesia without affecting baseline nociceptive threshold, reduce membrane expression of DOR and decrease the membrane and total expressions of NR1 and NR2B subunits. Furthermore, the amplitude and the frequency of NMDA receptor-induced current were significantly increased by remifentanil incubation in neurons of the dorsal horn, which was reversed by the application of naltrindole.. The above results indicate that inhibition of DOR could significantly inhibit remifentanil-induced hyperalgesia via modulating the total protein level, membrane trafficking and function of NMDA receptors in the dorsal horn of spinal cord, suggesting that naltrindole could be a potential anti-hyperalgesic agent for treating OIH. Topics: Anesthetics, Intravenous; Animals; Disease Models, Animal; Hot Temperature; Hyperalgesia; Lumbar Vertebrae; Male; Naltrexone; Narcotic Antagonists; Oligopeptides; Pain Threshold; Pain, Postoperative; Piperidines; Posterior Horn Cells; Random Allocation; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Receptors, Opioid, delta; Remifentanil; Spinal Cord; Tissue Culture Techniques; Touch | 2015 |
Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats.
Opioid agonists have been implicated in neuroprotection from hypoxic injury through regulating mitogen-activated protein kinases and cytokines. We determined the effects of remifentanil in focal brain ischemia and reperfusion (I/R) injury. Mechanisms linked to mitogen-activated protein kinases, including extracellular signaling-regulated kinase (ERK) 1/2, p38 kinases, and c-Jun N-terminal kinase (JNK), and various cytokines were also examined.. Male Sprague-Dawley rats were subjected to an I/R insult consisting of 90 minutes' middle cerebral artery occlusion (MCAO) followed by reperfusion under general anesthesia. Neurological deficit scores and infarct volume were determined after 24 hours of reperfusion. Remifentanil (5 μg/kg/min) was given alone or combined with naltrindole (δ-opioid receptor antagonist; 1 mg/kg), D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH(2) (μ-opioid receptor antagonist; 1 mg/kg), or 5'-guanidinonaltrindole (κ-opioid receptor antagonist; 1 mg/kg). Opioid antagonists were administered 20 minutes before MCAO. Remifentanil infusion was started 10 minutes before MCAO and continued throughout. The control group was without drugs. The expression levels of ERK1/2, p38, and JNK, and also those of tumor necrosis factor-α (TNF-α) and interleukin-6, were determined after 1, 3, and 24 hours of reperfusion.. Remifentanil significantly improved the functional outcome and reduced the infarct volumes (69.0±24.3 mm(3) vs. 108.9±24.8 mm(3)), which were not affected by D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH(2) or 5'-guanidinonaltrindole, but were abolished by naltrindole. The I/R insult enhanced the phosphorylation of ERK 1/2 and the expression of TNF-α, which were significantly reduced by remifentanil. Neither the phosphorylation of p38 and JNK nor the production of interleukin-6 was altered throughout the experiment.. Remifentanil may be neuroprotective against focal I/R injury, possibly through the activation of δ-opioid receptors and attenuation of ERK 1/2 activity and TNF-α production, in the rat brain. Topics: Anesthetics, Intravenous; Animals; Blood Pressure; Blotting, Western; Carbon Dioxide; Dose-Response Relationship, Drug; Infarction, Middle Cerebral Artery; Interleukin-6; Ischemic Attack, Transient; Male; Mitogen-Activated Protein Kinases; Naltrexone; Narcotic Antagonists; Nervous System Diseases; Neuroprotective Agents; Piperidines; Rats; Rats, Sprague-Dawley; Remifentanil; Reperfusion Injury; Tumor Necrosis Factor-alpha | 2012 |
Endogenous opioid and cannabinoid mechanisms are involved in the analgesic effects of celecoxib in the central nervous system.
In this study we analyzed the mechanisms underlying celecoxib-induced analgesia in a model of inflammatory pain in rats, using the intracerebroventricular (i.c.v.) administration of selective opioid and cannabinoid antagonists.. Analgesic effects of celecoxib were prevented by selective μ-(β-funaltrexamine) and δ-(naltrindole), but not κ-(nor-binaltorphimine) opioid antagonists, given i.c.v. 30 min before celecoxib. Similar pretreatment with AM 251, but not SR 144528, cannabinoid CB(1) and CB(2) receptor antagonists, respectively, prevented celecoxib-induced analgesia. The fatty acid amide hydrolase inhibitor, URB 597, also prevented celecoxib-induced analgesia.. Our data provided further evidence for the involvement of endogenous opioids and revealed a new cannabinoid component of the mechanism(s) underlying celecoxib-induced analgesia. Topics: Analgesics; Animals; Carrageenan; Celecoxib; Central Nervous System; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Inflammation; Male; Naltrexone; Pain; Piperidines; Pyrazoles; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Receptors, Opioid, delta; Receptors, Opioid, mu; Sulfonamides | 2012 |
Structural biology: How opioid drugs bind to receptors.
Topics: Animals; Biomimetic Materials; Humans; Morphinans; Naltrexone; Nociceptin Receptor; Opioid Peptides; Piperidines; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Spiro Compounds; Tetrahydroisoquinolines | 2012 |
Novel object recognition as a facile behavior test for evaluating drug effects in AβPP/PS1 Alzheimer's disease mouse model.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the AβPP/PS1 transgenic mouse model is a commonly used experimental model to mimic the pathological and cognitive impairments in AD. As a classic method to evaluate spatial learning and memory, the Morris water maze is widely applied to study the cognitive deficits in rodent AD models. However, the assay procedure is relatively complicated and requires a properly equipped environment. The novel object recognition test is a relatively simple and straightforward method to test working memory in rodents. However, whether the latter can be used as a common tool for evaluating the therapeutic effects of drugs in the AβPP/PS1 transgenic AD mouse model remains unclear. In the present study, we assessed the cognitive impairment of AβPP/PS1 AD mice with the novel object recognition test. In parallel, Morris water maze was performed and compared with the novel object recognition study. Both assays worked equally well in evaluating the cognitive defect of AβPP/PS1 mice. Furthermore, we drew similar conclusions from the novel object recognition assay as from the Morris water maze in assessing the therapeutic effects of two previously reported compounds, donepezil and naltrindole, on AD. We found the novel object recognition to be a facile assay with almost no stress to mice and think it could be used as an ideal primary screening assay to evaluate drug effects on AβPP/PS1 AD model. Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Disease Models, Animal; Donepezil; Drug Evaluation, Preclinical; Female; Humans; Indans; Male; Maze Learning; Mice; Mice, Inbred C57BL; Mice, Transgenic; Naltrexone; Pattern Recognition, Visual; Piperidines; Presenilin-1; Random Allocation | 2012 |
Antinociceptive action of isolated mitragynine from Mitragyna Speciosa through activation of opioid receptor system.
Cannabinoids and opioids systems share numerous pharmacological properties and antinociception is one of them. Previous findings have shown that mitragynine (MG), a major indole alkaloid found in Mitragyna speciosa (MS) can exert its antinociceptive effects through the opioids system. In the present study, the action of MG was investigated as the antinociceptive agent acting on Cannabinoid receptor type 1 (CB1) and effects on the opioids receptor. The latency time was recorded until the mice showed pain responses such as shaking, licking or jumping and the duration of latency was measured for 2 h at every 15 min interval by hot plate analysis. To investigate the beneficial effects of MG as antinociceptive agent, it was administered intraperitoneally 15 min prior to pain induction with a single dosage (3, 10, 15, 30, and 35 mg/kg b.wt). In this investigation, 35 mg/kg of MG showed significant increase in the latency time and this dosage was used in the antagonist receptor study. The treated groups were administered with AM251 (cannabinoid receptor-1 antagonist), naloxone (non-selective opioid antagonist), naltrindole (δ-opioid antagonist) naloxonazine (μ(1)-receptor antagonist) and norbinaltorpimine (κ-opioid antagonist) respectively, prior to administration of MG (35 mg/kg). The results showed that the antinociceptive effect of MG was not antagonized by AM251; naloxone and naltrindole were effectively blocked; and norbinaltorpimine partially blocked the antinociceptive effect of MG. Naloxonazine did inhibit the effect of MG, but it was not statistically significant. These results demonstrate that CB1 does not directly have a role in the antinociceptive action of MG where the effect was observed with the activation of opioid receptor. Topics: Analgesics; Animals; Cannabinoid Receptor Antagonists; Cannabinoid Receptor Modulators; Male; Mice; Mice, Inbred ICR; Mitragyna; Naloxone; Naltrexone; Narcotic Antagonists; Piperidines; Pyrazoles; Receptors, Cannabinoid; Receptors, Opioid; Secologanin Tryptamine Alkaloids | 2012 |
Remifentanil post-conditioning attenuates cardiac ischemia-reperfusion injury via kappa or delta opioid receptor activation.
Ischemic pre- or post-conditioning of the heart has been shown to involve opioid receptors. Remifentanil, an ultra-short-acting selective mu opioid receptor agonist in clinical use, pre-conditions the rat heart against ischemia-reperfusion injury. This study investigates whether remifentanil post-conditioning is also cardioprotective.. Remifentanil post-conditioning (5-min infusion at 1, 5, 10 or 20 microg/kg/min) or ischemic post-conditioning (three cycles of a 10 s reperfusion interspersed with a 10 s ischemia) was induced in an open-chest rat heart model of ischemia and reperfusion injury, in the presence or absence of nor-binaltorphimine, naltrindole or CTOP, specific kappa, delta and mu opioid receptor antagonists, respectively. The same sequence of experiments was repeated in the isolated heart model using the maximal protective dose of remifentanil from the dose-response studies.. Both ischemic and remifentanil post-conditioning reduced the myocardial infarct size relative to the control group in both models. This cardioprotective effect for both post-conditioning regimes was prevented by the prior administration of nor-binaltorphimine and naltrindole but not CTOP. The sole administration of the antagonists had no effect on the size of myocardial infarction.. These results indicate that remifentanil post-conditioning protects the heart from ischemia-reperfusion injury to a similar extent as of ischemic post-conditioning. This protection involves kappa and delta but not mu opioid receptor activation. This drug has great potential as a clinical post-conditioning modality as it can be given in large doses without prolonged opioid-related side effects. Topics: Analgesics, Opioid; Animals; Blood Pressure; Cardiotonic Agents; Dose-Response Relationship, Drug; Heart Rate; In Vitro Techniques; Ischemic Preconditioning, Myocardial; Male; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Naltrexone; Narcotic Antagonists; Piperidines; Rats; Rats, Sprague-Dawley; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Remifentanil; Somatostatin | 2010 |
Opioid, cannabinoid CB1 and NOP receptors do not mediate APAP-induced hypothermia in rats.
Acetaminophen (APAP) produces antinociception and hypothermia. Because the antinociceptive effect in rats is partially dependent on opioid and cannabinoid CB1 receptor activation, we determined if activation of these receptors also contributes to the hypothermic effect of APAP. Rats injected with APAP (100, 250, 375 or 500 mg/kg, i.p.) displayed dose-related hypothermia. For combined administration, the hypothermic effect of APAP (400 mg/kg, i.p.) was not altered by pretreatment with: naltrexone (10 mg/kg, s.c.), a non-selective opioid antagonist; naltrindole (1 mg/kg, s.c.), a delta opioid antagonist; nor-binaltorphimine (10 mg/kg, i.p.), a kappa opioid antagonist; SR 141716A (3 mg/kg, i.m.), a cannabinoid CB1 receptor antagonist; or JTC-801(1 mg/kg, i.p.), a nociceptin/orphanin FQ peptide (NOP) receptor antagonist. The demonstration that APAP produces hypothermia independent of opioid, cannabinoid CB1 or NOP receptor activation is contrary to its antinociceptive effect, which requires opioid and cannabinoid CB1 receptor activation. Topics: Acetaminophen; Aminoquinolines; Animals; Benzamides; Body Temperature; Hypothermia, Induced; Male; Naltrexone; Nociceptin Receptor; Piperidines; Pyrazoles; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Receptors, Opioid; Rimonabant | 2009 |
Kappa-opioid receptor-mediated effects of the plant-derived hallucinogen, salvinorin A, on inverted screen performance in the mouse.
Salvinorin A is a pharmacologically active diterpene that occurs naturally in the Mexican mint Ska Maria Pastora (Salvia divinorum) and represents the first naturally occurring kappa-opioid receptor agonist. The chemical structure of salvinorin A is novel among the opioids, and thus defines a new structural class of kappa-opioid-receptor selective drugs. Few studies have examined the effects of salvinorin A in vivo, and fewer still have attempted to assess the agonist actions of this compound at mu-opioid, delta-opioid, and kappa-opioid receptors using selective antagonists. In the mouse, salvinorin A disrupted climbing behavior on an inverted screen task, indicating a rapid, but short-lived induction of sedation/motor incoordination. Similar effects were observed with the mu-agonist remifentanil and the synthetic kappa-agonist U69,593. When behaviorally equivalent doses of all three opioids were challenged with antagonists at doses selective for mu-opioid, delta-opioid, or kappa-opioid receptors, results suggested that the motoric effects of remifentanil were mediated by mu-receptors, whereas those of salvinorin A and U69,593 were mediated via kappa-receptors. Despite similar potencies and degrees of effectiveness, salvinorin A and U69,593 differed with regard to their susceptibility to antagonism by the kappa-antagonist nor-binaltorphamine. This later finding, coupled with the novel chemical structure of the compound, is consistent with recent findings that the diterpene salvinorin A may bind to the kappa-receptor in a manner that is qualitatively different from that of more traditional kappa-agonists such as the benzeneacetamide U69,593. Such pharmacological differences among these kappa-opioids raise the possibility that the development of other diterpene-based opioids may yield important therapeutic compounds. Topics: Analgesics, Opioid; Animals; Behavior, Animal; Benzeneacetamides; Diterpenes; Diterpenes, Clerodane; Hallucinogens; Male; Mice; Naloxone; Naltrexone; Narcotic Antagonists; Piperidines; Psychotropic Drugs; Pyrrolidines; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Remifentanil | 2005 |
Localization of opioid receptor antagonist [3H]-LY255582 binding sites in mouse brain: comparison with the distribution of mu, delta and kappa binding sites.
Agonist stimulation of opioid receptors increases feeding in rodents, while opioid antagonists inhibit food intake. The pan-opioid antagonist, LY255582, produces a sustained reduction in food intake and body weight in rodent models of obesity. However, the specific receptor subtype(s) responsible for this activity is unknown. To better characterize the pharmacology of LY255582, we examined the binding of a radiolabeled version of the molecule, [(3)H]-LY255582, in mouse brain using autoradiography. In mouse brain homogenates, the K(d) and B(max) for [(3)H]-LY255582 were 0.156 +/- 0.07 nM and 249 +/- 14 fmol/mg protein, respectively. [(3)H]-LY255582 bound to slide mounted sections of mouse brain with high affinity and low non-specific binding. High levels of binding were seen in areas consistent with the known localization of opioid receptors. These areas included the caudate putamen, nucleus accumbens, claustrum, medial habenula, dorsal endopiriform nucleus, basolateral nucleus of the amygdala, hypothalamus, thalamus and ventral tegmental area. We compared the binding distribution of [(3)H]-LY255582 to the opioid receptor antagonist radioligands [(3)H]-naloxone (mu), [(3)H]-naltrindole (delta) and [(3)H]-norBNI (kappa). The overall distribution of [(3)H]-LY255582 binding sites was similar to that of the other ligands. No specific [(3)H]-LY255582 binding was noted in sections of mu-, delta- and kappa-receptor combinatorial knockout mice. Therefore, it is likely that LY255582 produces its effects on feeding and body weight gain through a combination of mu-, delta- and kappa-receptor activity. Topics: Animals; Autoradiography; Binding Sites; Brain; Cyclohexanes; Mice; Mice, Knockout; Molecular Structure; Naloxone; Naltrexone; Narcotic Antagonists; Piperidines; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Tritium | 2005 |
The antinociceptive effect of Delta9-tetrahydrocannabinol in the arthritic rat.
Our study addressed the hypothesis that spinal release of endogenous opioids underlies Delta9-tetrahydrocannabinol (Delta9-THC)-induced antinociception in Freund's adjuvant-induced arthritic and nonarthritic rats. The paw-pressure test was used to assess the antinociceptive effects of Delta9-THC versus those of morphine, and opioid and cannabinoid receptor-selective antagonists were used to characterize the involved receptors. Cerebrospinal fluid was collected after Delta9-THC injection (i.p.) for the measurement of endogenous opioid peptides. Our results indicate that morphine or Delta9-THC is equally potent and efficacious in both nonarthritic and arthritic rats. Delta9-THC-induced antinociception is attenuated by the kappa opioid receptor antagonist, nor-binaltorphimine, in arthritic rats only. Delta9-THC induces increased immunoreactive dynorphin A (idyn A) levels in nonarthritic rats while decreasing idyn A in arthritic rats. We hypothesize that the elevated idyn A level in arthritic rats contributes to hyperalgesia by interaction with N-methyl-D-aspartate receptors, and that Delta9-THC induces antinociception by decreasing idyn A release. Topics: Animals; Arthritis, Experimental; Cannabinoid Receptor Antagonists; Dose-Response Relationship, Drug; Dronabinol; Dynorphins; Enkephalin, Leucine; Enkephalin, Methionine; Freund's Adjuvant; Injections, Intradermal; Injections, Intraperitoneal; Male; Morphine; Mycobacterium; Naloxone; Naltrexone; Narcotic Antagonists; Pain; Pain Measurement; Piperidines; Pyrazoles; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Receptors, Opioid; Rimonabant | 2004 |
In vitro and ex vivo effects of a selective nociceptin/orphanin FQ (N/OFQ) peptide receptor antagonist, CompB, on specific binding of [3H]N/OFQ and [35S]GTPgammaS in rat brain and spinal cord.
1. A novel selective nociceptin/orphanin FQ (N/OFQ) peptide receptor antagonist, 1-[(3R,4R)-1-cyclooctylmethyl]-3-hydroxymethyl-4-piperidyl)-3-ethyl-1,3-dihydro-2H-benzimidazol-2-one (CompB), inhibited specific binding of [(3)H]N/OFQ to crude membranes from the rat brain and spinal cord in a concentration-dependent manner and their K(i) values were 7.11 and 4.02 nM, respectively. Rosenthal analysis indicated that there was a significant increase in the K(d) value for [(3)H]N/OFQ binding in the brain and spinal cord in the presence of CompB (10 nM). 2. There was a dose-dependent increase in K(d) values for [(3)H]N/OFQ binding in the brain and spinal cord following i.v. injection of CompB at relatively low doses (0.69-6.88 micro mol kg(-1)), compared with the control values. In the spinal cord, enhancement with each dose was constantly greater and the duration of enhancement (6.88 micro mol kg(-1)) was significantly longer. 3. The degree of increase in K(d) values for [(3)H]N/OFQ binding after i.v. injection of CompB (6.88 micro mol kg(-1)) was significantly larger in the lumbar region of the spinal cord compared to other regions. 4. CompB (0.1, 0.3 micro M) shifted the concentration-effect curves of N/OFQ-stimulated [(35)S]GTPgammaS binding in the brain and spinal cord to the right. 5. The i.v. injection of CompB (6.88 micro mol kg(-1)) significantly suppressed the N/OFQ-stimulated [(35)S]GTPgammaS binding in the rat spinal cord and shifted the concentration-effect curve to the right, while it produced little inhibitory effect in the brain. The present study has shown that CompB may exhibit pharmacological effects through a predominant blockade of N/OFQ peptide receptors in the spinal cord under in vivo conditions. Topics: Animals; Benzimidazoles; Binding, Competitive; Brain; Dose-Response Relationship, Drug; Guanosine Triphosphate; Injections, Intravenous; Male; Naltrexone; Narcotic Antagonists; Nociceptin Receptor; Opioid Peptides; Peptide Fragments; Piperidines; Radioligand Assay; Rats; Rats, Sprague-Dawley; Receptors, Opioid; Spinal Cord | 2003 |
Involvement of the opioid system in the anxiolytic-like effects induced by Delta(9)-tetrahydrocannabinol.
Recent studies have shown that several pharmacological actions induced by cannabinoids, including antinociception and reward, involve the participation of the endogenous opioid system.. The present study was designed to examine the possible involvement of the different opioid receptors in the anxiolytic-like responses induced by Delta(9)-tetrahydrocannabinol (THC).. The administration of a low dose of THC (0.3 mg/kg) produced clear anxiolytic-like responses in the light-dark box, as previously reported. The effects of the pretreatment with the CB(1) cannabinoid receptor antagonist, SR 141716A (0.5 mg/kg), or the micro -opioid receptor antagonist, beta-funaltrexamine (5 mg/kg), the delta-opioid receptor antagonist, naltrindole (2.5 mg/kg) and the kappa-opioid receptor antagonist, nor-binaltorphimine (2.5 mg/kg) were evaluated on anxiolytic-like responses induced by THC.. SR 141716A completely blocked the anxiolytic-like response induced by THC, suggesting that this effect is mediated by CB(1) cannabinoid receptors. The micro -opioid receptor antagonist beta-funaltrexamine and the delta-opioid receptor antagonist naltrindole, but not the kappa-opioid receptor antagonist nor-binaltorphimine, abolished THC anxiolytic-like effects, suggesting an involvement of micro - and delta-opioid receptors in this behavioural response.. These results demonstrate that the endogenous opioid system is involved in the regulation of anxiety-like behaviour by cannabinoids and provide new findings to clarify further the interaction between these two neuronal systems. Topics: Animals; Anti-Anxiety Agents; Anxiety; Behavior, Animal; Darkness; Dronabinol; Endorphins; Light; Male; Mice; Naltrexone; Narcotic Antagonists; Piperidines; Pyrazoles; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Rimonabant | 2002 |