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E B Geller

Publications and source records attributed to E B Geller.

At least 19 recordsLinked to original sources
PubMed2004

GABAA receptors modulate cannabinoid-evoked hypothermia.

Cannabinoids evoke hypothermia by stimulating central CB(1) receptors. GABA induces hypothermia via GABA(A) or GABA(B) receptor activation. CB(1) receptor activation increases GABA release in the hypothalamus, a central locus for thermoregulation, suggesting that cannabinoid and GABA systems may be functionally linked in body temperature regulation. We investigated whether GABA receptors modulate the hypothermic actions of [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenyl-carbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one] (WIN 55212-2), a selective cannabinoid agonist, in male Sprague-Dawley rats. WIN 55212-2 (2.5 mg/kg im) produced a rapid hypothermia that peaked 45-90 min postinjection. The hypothermia was attenuated by bicuculline (2 mg/kg ip), a GABA(A) antagonist. However, SCH 50911 (1-10 mg/kg ip), a GABA(B) blocker, did not antagonize the hypothermia. Neither bicuculline (2 mg/kg) nor SCH 50911 (10 mg/kg) by itself altered body temperature. We also investigated a possible role for CB(1) receptors in GABA-generated hypothermia. Muscimol (2.5 mg/kg ip), a GABA(A) agonist, or baclofen (5 mg/kg ip), a GABA(B) agonist, evoked a significant hypothermia. Blockade of CB(1) receptors with SR141716A (2.5 mg/kg im) did not antagonize muscimol- or baclofen-induced hypothermia, indicating that GABA-evoked hypothermia does not contain a CB(1)-sensitive component. Our results implicate GABA(A) receptors in the hypothermic actions of cannabinoids and provide further evidence of a functional link between cannabinoid and GABA systems.

Animals↗
PubMed2001

Possible mechanism of hypothermia induced by intracerebroventricular injection of orphanin FQ/nociceptin.

Orphanin/nociceptin (OFQ/N), a 17-amino-acid peptide, is an endogenous peptide, the receptor for which is similar to mu-, delta- and kappa-opioid receptors ( approximately 65% homology). Reports indicate that OFQ/N can block the antinociception induced by mu-, delta- and kappa-opioid agonists in the rat and in the mouse, indicating that there is a functional interaction between opioid receptors and OFQ/N receptors in the nervous system. It is well known that activation of the mu- and kappa-opioid receptors results in hyperthermia and hypothermia, respectively, in Sprague-Dawley rats. The present studies were designed to examine effects of OFQ/N on body temperature (Tb) and explore whether the mechanism of T(b) change induced by OFQ/N involved the opioid system. The results show that (1) i.c.v. injection of a high dose of OFQ/N (9-18 micro g) produces hypothermia in adult rats; (2) OFQ/N (1.8 micro g, i.c.v., t=+30 s after morphine) can decrease morphine-induced hyperthermia; (3) neither the opioid receptor antagonist, naloxone (10 mg/kg, s.c., t=-15 s before OFQ/N) nor the kappa-opioid receptor antagonist nor-BNI (1 micro g/5 microl, i.c.v., t=-30 s before OFQ/N) reduces the hypothermia induced by i.c.v. injection of OFQ/N at dose of 18 micro g (P>0.05); (4) 60 micro g/5 microl AS oligo (i.c.v. treatment on days 1, 3 and 5) against OFQ/N receptors significantly reduces the hypothermia induced by i.c.v. injection of 9 micro g OFQ/N (P<0.01). These results suggest that the hypothermia induced by i.c.v. injection of a high dose of OFQ/N (9 or 18 micro g) is mediated, at least partially, by its own receptor, independent or downstream of opioid receptors in the rat brain and that OFQ/N probably acts as a physiological antagonist to reduce morphine-induced hyperthermia.

Animals↗
PubMed2001

Effect of central and peripheral administration of a nitric oxide synthase inhibitor on morphine hyperthermia in rats.

The effect of central and peripheral administration of a nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on morphine hyperthermia was studied in male Sprague-Dawley rats. The first series of experiments examined the effect of subcutaneous (s.c.) administration of L-NAME on the hyperthermia induced by morphine given s.c. in doses of 4 and 15 mg/kg. L-NAME, at a s.c. dose of 50 mg/kg, per se, had no influence on body temperature (T(b)). Coadministration of L-NAME (50 mg/kg, s.c.) with the higher dose of morphine (15 mg/kg, s.c.) caused a significant suppression of morphine hyperthermia during the first 30 min and then produced hypothermia. In contrast, s.c. injection of L-NAME (50 mg/kg, s.c.) failed to alter the hyperthermic response induced by the lower dose of morphine (4 mg/kg). In the second series of experiments, we investigated the effect of intracerebroventricular (i.c.v.) administration of L-NAME on the hyperthermia induced by morphine given s.c. L-NAME, itself, given i.c.v. at a dose of 1 mg did not evoke any change in T(b). Intracerebroventricular administration of L-NAME (1 mg) blocked the hyperthermia induced by 15 mg/kg morphine during the first 30 min and induced a slight hypothermia but did not alter the hyperthermia induced by 4 mg/kg morphine. The results indicate that either central or peripheral NO synthesis is required for the production of hyperthermia induced by 15 mg/kg of morphine. However, NO synthesis does not seem to be involved in the hyperthermic process induced by 4 mg/kg of morphine.

Animals↗
PubMed2001

Administration of mu-, kappa- or delta2-receptor agonists via osmotic minipumps suppresses murine splenic antibody responses.

Previously, our laboratory has shown that morphine given by implantation of a 75-mg slow-release pellet for 48 h suppresses murine splenic antibody responses to sheep red blood cells (SRBCs) in a plaque-forming cell (PFC) assay. However, the use of slow-release pellets for such studies is limited, as these pellets are only available in fixed doses and similar pellets for kappa and delta agonists have not been developed. In the present study, we investigated the feasibility of administering opioids via Alzet osmotic minipumps to assess their immunomodulatory effects. Groups of mice received minipumps dispensing morphine sulfate, which has primary activity at the mu opioid receptor; U50,488H, which is a kappa-selective agonist; deltorphin II, which is a delta2-selective agonist; or DPDPE, which has greater selectivity for delta1 than delta, receptors. Morphine, U50,488H and deltorphin II were all immunosuppressive, with biphasic dose-response curves exhibiting maximal (approximately 50%) suppression of the PFC response at doses of 0.5 to 2 mg/kg/day 48 h after pump implantation. Further, immunosuppression by morphine sulfate, U50,488H or deltorphin II was blocked by simultaneous implantation of a minipump administering the opioid receptor-selective antagonists CTAP (1 mg/kg/day), nor-binaltorphimine (5 mg/kg/day), or naltriben (3 mg/kg/day), respectively. DPDPE was inactive at doses lower than 10 mg/kg/day. We conclude that osmotic minipumps are a practical and useful way of administering opioids to study their effects on the immune system, and give further evidence that immunosuppression induced in vivo by opioid agonists is mediated not only via mu, but also via kappa and delta2 opioid receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2000

Blockade of lipopolysaccharide-induced fever by a mu-opioid receptor-selective antagonist in rats.

The endogenous opioid system has been found to be involved in fever caused by pyrogens. In the present study, we have investigated the role of the mu-opioid receptor in the brain in fever induced by lipopolysaccharide. Rats were microinjected with 1 microg of the mu-opioid receptor-selective antagonist, cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP), into the preoptic anterior hypothalamus. Thirty minutes later, lipopolysaccharide (50 microg/kg) was injected intraperitoneally (i.p.). CTAP reduced by 1 degrees C the fever induced by lipopolysaccharide. However, it did not affect lipopolysaccharide fever when it was given 3 h after lipopolysaccharide injection. These data indicate that mu-opioid receptors within the preoptic anterior hypothalamus mediate the initiation of lipopolysaccharide fever and suggest that the opioid system is involved in the pathogenesis of fever in rats.

Amino Acid Sequence↗
PubMed2000

Morphine increases susceptibility to oral Salmonella typhimurium infection.

This study examined the effect of morphine on oral infection with virulent Salmonella typhimurium. Animals were treated with a 75-mg slow-release morphine pellet followed by inoculation with salmonellae. Morphine markedly sensitized mice to oral infection, as assessed by survival, mean survival time, and colony culture. By 24 h after Salmonella inoculation, morphine-treated mice had a 105-fold difference in number of organisms in the Peyer's patches, compared with controls. The opioid antagonist naltrexone significantly blocked Salmonella colonization in Peyer's patches and reduced Salmonella burden in other organs, indicating that morphine acts at least in part via an opioid receptor-mediated pathway. The data show that morphine markedly potentiates Salmonella infection at the gastrointestinal portal of entry and enhances subsequent dissemination of Salmonella organisms. The results have implications for potentiating gastrointestinal opportunistic infections in intravenous drug abusers and in opioid-medicated postsurgical patients.

Animals↗
PubMed1998

CCK(B) receptors in the periaqueductal grey are involved in electroacupuncture antinociception in the rat cold water tail-flick test.

Cholecystokinin octapeptide (CCK-8) (0.25-2.0 ng), the CCK(A) receptor antagonist L-364,718 (60-100 ng) or the CCK(B) receptor antagonist L-365,260 (0.3125-1.25 ng) was administered into the periaqueductal grey (PAG) of male SD rats. The antinociceptive effect induced by electroacupuncture (EA) stimulation of different frequencies was then measured by the cold water tail-flick (CWT) test. The results showed that (1) microinjection of CCK-8 into the PAG can significantly block the antinociceptive effect induced by all frequencies of EA stimulation. The effectiveness of the blockade was 100 > 2 Hz. In addition, CCK-8 blocks the antinociception seen following termination of the electrical stimulation at 100 Hz; (2) microinjection of L-365,260 (1.25 ng) into the PAG significantly increased the 100 Hz EA antinociceptive effect but not the 2 Hz EA antinociceptive effect and microinjection of L-364,718 into PAG did not affect either 2 or 100 Hz EA antinociception. These results demonstrate that CCK-8 in the PAG can antagonize the antinociceptive effect induced by EA stimulation, and the CCK effect is likely to be mediated by the CCK(B) receptor, but not the CCK(A) receptor.

Animals↗
PubMed1998

Effect of a mu-selective opioid antagonist on CCK-8-induced changes in thermoregulation in the rat.

We examined the effects of I.C.V. injection of CCK-8 alone and in combination with CTAP, a mu-selective antagonist, on brain surface temperature (Tb), oxygen consumption (VO2), and heat exchange (Q) in unrestrained male S-D rats at an ambient temperature of 20 +/- 0.5 degrees C. CCK-8 (300 ng, I.C.V.) produced hyperthermia (deltaTb: 0.86 +/- 0.22 degrees C) lasting for 30-60 min, which was associated with an increase in VO2 (1.42 +/- 0.28 ml/g/h). There was an increase in Q (1.87 +/- 1.2 cal/g/h) beginning 15 min after injection and lasting for 60 min. The CCK-8-induced hyperthermia was attenuated by a postinjection increase in Q. During the 60-120 min postinjection period, VO2 and Q returned to baseline followed by the return of Tb to preinjection levels. CCK-8-induced increases in Tb, Q, and VO2 were blocked by pretreatment with CTAP (0.75 nmol, I.C.V.) 15 min earlier. CTAP alone did not significantly affect deltaTb, deltaVO2, and deltaQ. These results suggest that, within the thermoneutral zone, the thermoregulatory effects of CCK-8 in the rat involve participation of mu-opioid receptors.

Analysis of Variance↗
PubMed1997

Interaction of cholecystokinin and somatostatin with a selective mu-opioid agonist and mu- and kappa-antagonists in thermoregulation.

We examined the effects of intracerebroventricular (i.c.v.) injections of cholecystokinin-octapeptide (CCK-8) and somatostatin (SST) and the interactions of these neuropeptides with the selective opioid antagonists, CTAP (mu) and nor-BNI (kappa) and the mu-agonist, PL017, on body temperature (Tb) of the rat at normal ambient temperature (21 +/- 0.5 degrees C). CCK-8 produced short-lasting (15-60 min), dose-related increases in Tb in a dose range of 20 to 900 ng but did not change the Tb at lower doses (0.1-2 ng). Lower doses of SST (1 and 2 micrograms) produced hyperthermia (30-60 min) and a higher dose of SST (10 micrograms) caused hypothermia (30-45 min). PL017 (1 microgram, i.c.v.), alone and in combination with CCK-8, produced hyperthermia. The CCK-8 (300 ng)-induced hyperthermia was blocked by pretreatment of rats with CTAP (1 microgram, i.c.v.), suggesting that the higher doses of CCK-8 increase Tb through the interaction with mu-receptors or the enhancement of release of endogenous opioids acting on the mu-receptor. The hyperthermia elicited by a lower dose of SST (1 microgram) was prevented by pretreatment with CTAP but not with nor-BNI (1 microgram, i.c.v.). Pretreatment with nor-BNI blocked the higher dose (10 micrograms) of SST-induced hypothermia. PL017 or CTAP did not prevent the hypothermic effect of that dose of SST. These results indicate that a lower dose of SST (1 microgram) stimulates the mu-receptor (directly or indirectly) and a higher dose (10 micrograms) interacts with the kappa-receptor in regulation of Tb. Thus, the effects of both CCK-8 and SST on Tb appear to involve the endogenous opioid system.

Animals↗
PubMed1997

Body temperature and analgesic effects of selective mu and kappa opioid receptor agonists microdialyzed into rat brain.

Opioids administered by i.c.v. injection produce body temperature (Tb) changes and analgesic responses in rats. The present study was undertaken to investigate the effects on Tb and analgesia of highly selective mu and kappa opioid receptor agonists and antagonists delivered directly into the preoptic anterior hypothalamus (POAH) and periaqueductal gray (PAG) by the intracerebral microdialysis method. Microdialyzed into the POAH, the mu receptor agonist Tyr-Pro-N-MePhe-D-Pro-NH2 induced dose-related hyperthermia that could be prevented or antagonized by the mu receptor antagonist cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 or by naloxone, but not by the kappa receptor antagonist nor-binaltorphimine. The kappa receptor agonist dynorphin A(1-17), microdialyzed into the POAH, induced dose-related hypothermia that was prevented or antagonized by nor-binaltorphimine but not cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2. Neither Tyr-Pro-N-MePhe-D-Pro-NH2 nor dynorphin A(1-17) microdialyzed into the PAG produced significant changes in Tb. However, these agonists microdialyzed into the PAG produced analgesic responses that did not occur after administration into the POAH. These results support the hypothesis that the hyperthermic response to opioids is mediated by the mu receptor and the hypothermic response is mediated by the kappa receptor in rats. The POAH is a primary functional area in Tb, but not in analgesic, responses to opioids, whereas the PAG is a sensitive area for analgesic, but not for Tb, responses to opioids.

Analgesics, Opioid↗
PubMed1997

Substance P release in the rat periaqueductal gray and preoptic anterior hypothalamus after noxious cold stimulation: effect of selective mu and kappa opioid agonists.

Intracerebral microdialysis was used to measure changes in the extracellular level of substance P (SP) released from the periaqueductal gray (PAG) and the preoptic anterior hypothalamus (POAH) of freely moving Sprague-Dawley rats after noxious cold stimulation. Artificial cerebrospinal fluid was perfused into the dialysis probe in the PAG or POAH and samples were collected every 30 min for 4 hr. SP-like immunoreactivity in the samples was measured by radioimmunoassay. In the PAG, SP base-line release was 0.43 +/- 0.08 fmol/fraction. SP release was increased to 1.3 +/- 0.4 fmol/fraction during the first collection period after noxious cold. Pretreatment with the selective mu opioid receptor agonist PL017 (0.8-3.4 nmol) or the kappa opioid receptor agonist dynorphin A1-17 (4.6-9.2 nmol), administered into the PAG by microinjection, produced dose-related inhibition of the cold-evoked SP release. Naloxone (10 mg/kg s.c.) administration 10 min before these opioid agonists reduced the inhibition of SP release. In the POAH, SP base-line release was 0.45 +/- 0.06 fmol/fraction and noxious cold did not cause any significant change in SP release. Microdialysis of SP (271 fmol-271 pmol/microl/min, for 30 min) into the PAG, but not the POAH, induced dose-related analgesia (35-68% MPA) in the cold-water tail-flick test. However, microdialysis of SP into the POAH or PAG failed to induce any significant change in body temperature. These data suggest that 1) SP released from the PAG acts as a neuromodulator to transmit nociceptive information; 2) opioid receptor agonists can suppress this information by inhibiting SP release; 3) SP evoked by noxious cold may have a role in triggering the antinociceptive function of the PAG; and 4) SP does not appear to act as a neuromodulator for thermoregulatory responses in the POAH.

Animals↗
PubMed1996

Antisense confirmation of mu- and kappa-opioid receptor mediation of morphine's effects on body temperature in rats.

Previous studies showed that parenterally administered morphine at 4-16 mg/kg markedly increased body temperature in the rat, but higher doses of morphine (> or = 30 mg/kg, subcutaneously, sc) caused a profound decrease in body temperature. Based on the use of selective opioid agonists and antagonists, we postulated that these effects were due to morphine's actions on mu and kappa receptors, respectively. In the present study, we sought to determine whether an antisense (AS) oligodeoxynucleotide (oligo) against cloned mu or kappa opioid receptors could affect morphine-induced body temperature changes. AS oligos were directed against nucleotides 1-18 of the coding region of the mu receptor and 4-21 of the coding region of the kappa receptor. Male SD rats were surgically implanted with intracerebroventricular (icv) cannulae. Rats received icv injections of vehicle or oligo in the animal colony room on days 1, 3 and 5. Either AS oligo or missense (MS) oligo was infused in a volume of 5 microliters over 30 s to freely moving animals. On day 6, the rats were tested. The results showed that icv treatment with an AS oligo against mu opioid receptors, but not an MS oligo against the mu opioid receptor or an AS oligo against the kappa opioid receptor, significantly attenuated the hyperthermia normally produced by a relatively low dose of morphine administered sc. In addition, treatment with an AS oligo against kappa receptors, but not an MS oligo against kappa opioid receptor or an AS oligo against the mu opioid receptor, significantly blocked the hypothermia induced by a high dose of morphine. This study confirms our earlier postulate that morphine at 4 mg/kg, sc, induces an increase in body temperature primarily via mu opioid receptors in the brain and a high dose (30 mg/kg) of morphine administered sc produces a decrease primarily through kappa opioid receptors in the brain.

Animals↗
PubMed1996

Use of a mu-antisense oligodeoxynucleotide as a mu opioid receptor noncompetitive antagonist in vivo.

We examined whether mu-antisense (AS) oligodeoxynucleotide (oligo) treatment can be used in a manner similar to the mu-selective irreversible antagonist beta-funaltrexamine (beta-FNA) for in vivo pharmacology. Rats were injected intracerebroventricularly (icv) with a mu-AS or a missense (MS) oligo on days 1, 3, 5, 7, and 9 and were tested for the antinociceptive effect of sc injection of morphine on days 2, 4, 6, 8, and 10 in the cold water tail-flick (CWT) test. In another set of experiments, rats were also tested for the antinociceptive action of morphine twenty-four hours after icv injection of beta-FNA. Both beta-FNA and mu-AS produced rightward shifts in the dose-effect curves of morphine. In addition, pretreatment with 2.5 micrograms or more of beta-FNA or the mu-AS oligo for 5-9 days (but not for 1-3 days) reduced the maximal analgesic effect of morphine. The approximate fraction of functional receptor remaining for morphine was determined with the method of Furchgott to be 49.5% following 2.5 micrograms of beta-FNA; that after 5 days of the mu-AS oligo treatment was 50.8%. The results suggest that the mu-AS oligo can be used in the same manner as highly selective, irreversible mu opioid receptor ligands. Thus, properly designed AS oligos against receptors are of particular benefit when irreversible antagonists are not available. AS oligos represent a new class of selective and powerful pharmacological antagonists.

Animals↗
PubMed1996

Electrical stimulation at traditional acupuncture sites in periphery produces brain opioid-receptor-mediated antinociception in rats.

Previous studies in rats measuring latency to tail flick with radiant heat have shown that the antinociceptive effect induced by electrical stimulation of different frequencies at traditional acupuncture sites is mediated via different opioid receptors in the spinal cord. The present study was designed to observe (1) whether electrical stimulation at such sites could produce antinociceptive effects in the cold water tail-flick (CWT) test; (2) whether the antinociceptive effects could be blocked by s.c. injection of the opioid receptor antagonist naloxone and (3) whether i.c.v. injection of selective antagonists for mu (cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2, CTAP), delta (naltrindole) or kappa (nor-binaltorphimine) opioid receptors would block the antinociceptive effect produced by electrical stimulation. Sprague-Dawley rats were stimulated at frequencies of 2, 30 or 100 Hz with acupuncture needles inserted into acupoints Zusanli and Sanyinjiao in the hind leg for 30 min. Antinociception was assayed in the CWT. The results showed that (1) a significant, frequency-related increase in threshold in the CWT was observed in all electrical stimulation groups as compared with the placebo group and the antinociceptive effect lasted about 30 min poststimulation; (2) naloxone (s.c.) antagonized the antinociceptive effect induced by 2 Hz, 30 Hz or 100 Hz electrical stimulation and (3) either CTAP or naltrindole (i.c.v.) almost completely blocked the antinociceptive effect induced by 2 Hz or 30 Hz electrical stimulation, but was less effective in blocking antinociception induced by 100 Hz electrical stimulation; nor-binaltorphimine (i.c.v.) greatly reduced antinociception induced by 30 Hz or 100 Hz electrical stimulation, but not by 2 Hz electrical stimulation. These results indicate that the antinociception induced by 2 Hz electrical stimulation is mediated by both mu and delta opioid receptors; the antinociception induced by 100 Hz electrical stimulation is mediated primarily by the kappa receptor; and the antinociception induced by 30 Hz electrical stimulation is mediated by all three opioid receptor types. Thus, the antinociceptive effect induced by peripheral electrical stimulation, as measured by the CWT, involves opioid receptors in the rat brain.

Acupuncture Therapy↗
PubMed1996

Outcome of temporal lobe epilepsy surgery predicted by statistical parametric PET imaging.

UNLABELLED: PET is useful in the presurgical evaluation of temporal lobe epilepsy. The purpose of this retrospective study is to assess the clinical use of statistical parametric imaging in predicting surgical outcome. METHODS: Interictal 18FDG-PET scans in 17 patients with surgically-treated temporal lobe epilepsy (Group A-13 seizure-free, group B = 4 not seizure-free at 6 mo) were transformed into statistical parametric imaging, with each pixel representing a z-score value by using the mean and s.d. of count distribution in each individual patient, for both visual and quantitative analysis. RESULTS: Mean z-scores were significantly more negative in anterolateral (AL) and mesial (M) regions on the operated side than the nonoperated side in group A (AL: p < 0.00005, M: p = 0.0097), but not in group B (AL: p = 0.46, M: p = 0.08). Statistical parametric imaging correctly lateralized 16 out of 17 patients. Only the AL region, however, was significant in predicting surgical outcome (F = 29.03, p < 0.00005). Using a cut-off z-score value of -1.5, statistical parametric imaging correctly classified 92% of temporal lobes from group A and 88% of those from Group B. CONCLUSION: The preliminary results indicate that statistical parametric imaging provides both clinically useful information for lateralization in temporal lobe epilepsy and a reliable predictive indicator of clinical outcome following surgical treatment.

Adult↗
PubMed1995

Antisense oligodeoxynucleotides against mu- or kappa-opioid receptors block agonist-induced body temperature changes in rats.

PL017 and dynorphin A1-17 were shown previously to cause a marked increase and a profound decrease in body temperature (Tb), respectively. In this study, we examined whether an antisense (AS) oligodeoxynucleotide (oligo) against cloned mu or kappa opioid receptors could block PL017- or dynorphin A-induced body temperature changes. Treatment with an AS oligo against mu receptors, but not sense (S) oligo, missense (MS) oligo or artificial cerebrospinal fluid (aCSF), abolished PL017-induced hyperthermia. In addition, treatment with an AS oligo against kappa receptors, but not S oligo, MS oligo or aCSF, greatly attenuated dynorphin A-induced hypothermia. This study further supports the notion that mu and kappa receptors mediate Tb regulation.

Animals↗