Receptor Agonists In Rats Research Articles

Reversal of phencyclidine effects by a group II metabotropic glutamate receptor agonist in rats.

Glutamatergic abnormalities have been associated with several psychiatric disorders, including schizophrenia and addiction. Group II metabotropic glutamate receptors were targeted to normalize glutamatergic disruptions associated with an animal model of schizophrenia, the phencyclidine model. An agonist of this group of receptors, at a dose that was without effects on spontaneous activity and corticolimbic dopamine neurotransmission, attenuated the disruptive effects of phencyclidine on working memory, stereotypy, locomotion, and cortical glutamate efflux. This behavioral reversal occurred in spite of sustained dopamine hyperactivity. Thus, targeting this group of receptors may present a nondopaminergic therapeutic strategy for treatment of psychiatric disorders.

Decrease in gastric sensitivity to distension by 5-HT1A receptor agonists in rats.

Using an in vivo model for evaluation of gastric sensitivity in awake rats, we aimed to determine whether 5-hydroxytryptamine 1A (5-HT1A) agonists modify pain threshold and gastric compliance specifically through 5-HT1A receptors. Isobaric gastric distensions were performed with a barostat using steps of 5 mm Hg in male rats equipped with a gastric balloon and electrodes implanted in the neck muscles. Gastric distension at 15 or 20 mm Hg induced a typical posture associated with contractions of the neck muscles. Rats received drugs 30 min before gastric distension. The 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), administered intraperitoneally (0.5 mg/kg) increased gastric pain threshold and gastric tone. These effects were reproduced when administered centrally (0.05 mg/kg) and blocked by intracerebroventricular administration of the 5-HT1A antagonist WAY 100635. Flesinoxan (4 mg/kg, intraperitoneally), another 5-HT1A agonist reproduced the effects of 8-OH-DPAT on pain threshold and gastric tone and the alpha2-receptor antagonist yohimbine did not modify the action of 8-OH-DPAT. Our results indicate that activation of 5-HT1A receptors at the level of the central nervous system increases gastric tone and decreases gastric sensitivity to distension.

Priming of 6-hydroxydopamine-lesioned rats with l-DOPA or quinpirole results in an increase in dopamine D 1 receptor-dependent cyclic AMP production in striatal tissue

Priming with a dopamine agonist greatly enhances the behavioral effectiveness of dopamine D 1 receptor agonists in rats with 6-hydroxydopamine lesions of the nigrostriatal pathway. The present study investigated the influence of priming on cyclic AMP production in striatal slices. Stimulation of dopamine D 1 receptors with dopamine or the dopamine D 1 receptor agonist, 1-phenyl-6-Cl-7,8-diol-2,3,4,5-tetrahydro-(1H)-3-benzazepine (SKF 81297), increased cyclic AMP production in the lesioned striatum of rats primed with l-3,4-dihydroxyphenylalanine ( l-DOPA) by 329% and 405%, respectively, whereas in drug-naive rats the increase was 183% and 187%, respectively. Priming with quinpirole produced similar results. It is suggested that priming with either l-DOPA or a dopamine D 2 receptor agonist results in increased effectiveness of dopamine D 1 signal transduction, apparently not only related to previous stimulation of D 1 receptors.

Antiarrhythmic effects of μ-opiate receptor agonists in rats with epinephrine-induced arrhythmias: Role of the vegetative nervous system

The μ-opiate receptor agonists DAGO and DALDA preinjected intravenously in a dose of 0.1 mg/kg prevented the occurrence of arrhythmias in rats injected with epinephrine. Their antiarrhythmic activity was not modified by atropine or hexamethonium. It is concluded that the vegetative nervous system plays no substantial role in mediating the antiarrhythmic effects of DAGO and DALDA, and that these effects are most likely associated with stimulation of cardiac opiate receptors.

Opposite modulation of cocaine-seeking behavior by D1- and D2-like dopamine receptor agonists.

Activation of the mesolimbic dopamine system is known to trigger relapse in animal models of cocaine-seeking behavior. We found that this "priming" effect was selectively induced by D2-like, and not by D1-like, dopamine receptor agonists in rats. Moreover, D1-like receptor agonists prevented cocaine-seeking behavior induced by cocaine itself, whereas D2-like receptor agonists enhanced this behavior. These results demonstrate an important dissociation between D1- and D2-like receptor processes in cocaine-seeking behavior and support further evaluation of D1-like receptor agonists as a possible pharmacotherapy for cocaine addiction.

Survey on the pharmacodynamics of the new antipsychotic risperidone

This review reports on the pharmacodynamics of the new antipsychotic risperidone. The primary action of risperidone is serotonin 5-HT2 receptor blockade as shown by displacement of radioligand binding (Ki: 0.16 nM), activity on isolated tissues (EC50: 0.5 nM), and antagonism of peripherally (ED50: 0.0011 mg/kg) and centrally (ED50: 0.014 mg/kg) acting 5-HT2 receptor agonists in rats. Risperidone is at least as potent as the specific 5-HT2 receptor antagonist ritanserin in these tests. Risperidone is also a potent dopamine D2 receptor antagonist as indicated by displacement of radioligand binding (Ki: 1.4 nM), activity in isolated striatal slices (IC50: 0.89 nM), and antagonism of peripherally (ED50: 0.0057 mg/kg in dogs) and centrally acting D2 receptor agonists (ED50: 0.056-0.15 mg/kg in rats). Risperidone shows all effects common to D2 antagonists, including enhancement of prolactin release. However, some central effects such as catalepsy and blockade of motor activity occur at high doses only. Risperidone is 4-10 times less potent than haloperidol as a central D2 antagonist in rats and it differs from haloperidol by the following characteristics: predominant 5-HT2 antagonism; LSD antagonism; effects on sleep; smooth dose-response curves for D2 antagonism; synergism of combined 5-HT2/D2 antagonism; pronounced effects on amphetamine-induced oxygen consumption; increased social interaction; and pronounced effects on dopamine (DA) turnover. Risperidone displays similar activity at pre- and postsynaptic D2 receptors and at D2 receptors from various rat brain regions. The binding affinity for D4 and D3 receptors is 5 and 9 times weaker, respectively, than for D2 receptors; interaction with D1 receptors occurs only at very high concentrations. The pharmacological profile of risperidone includes interaction with histamine H1 and alpha-adrenergic receptors but the compound is devoid of significant interaction with cholinergic and a variety of other types of receptors. Risperidone has excellent oral activity, a rapid onset, and a 24-h duration of action. Its major metabolite, 9-hydroxyrisperidone, closely mimics risperidone in pharmacodynamics. Risperidone can be characterized as a potent D2 antagonist with predominant 5HT2 antagonistic activity and optimal pharmacokinetic properties.

Sensitization to 5-HT 1C receptor agonist in rats observed following withdrawal from chronic ethanol

Anxiogenic action of m-chlorophenylpiperazine (mCPP), a 5-HT 1C receptor agonist, was studied in naive rats and in ethanol-tolerant rats following withdrawal from chronic ethanol administration. The purpose of this investigation was to determine whether a sensitization to mCPP develops during withdrawal from chronic ethanol. Male Long-Evans hooded rats were fed a liquid diet containing 4.5% ethanol or dextrin (as control) for four days. Twelve hours (acute withdrawal) or 4 days (protracted withdrawal) after the last dose of ethanol, rats were injected with saline or mCPP (0.08–5.0 mg/kg) and were tested in the elevated plus-maze 15 min postinjection. A reduction in percent open-arm activity, indicative of anxiogenic behavior, was observed in ethanol-treated rats injected with saline. Administration of mCPP further reduced the percent open-arm entries and time in ethanol-withdrawn rats. An eightfold reduction in maximum effective dose of mCPP was observed during acute ethanol withdrawal as compared to that in naive rats. During protracted ethanol withdrawal the maximum effective dose of mCPP was reduced by 75%. A shift of the mCPP dose-response curve to the left following withdrawal from chronic ethanol may indicate that 5-HT 1C receptor sites are more sensitive to the activation by an agonist. This effect may be exploited in developing specific 5-HT 1C receptor antagonists for the treatment of ethanol withdrawal symptoms.

Spinal Cord Blood Flow After Intrathecal Injection of a N-Methyl-D-Aspartate Receptor Antagonist or an Adenosine Receptor Agonist in Rats

Evaluation of spinal cord blood flow (SCBF) is important as a preclinical screening for potential neurotoxicologic side effects before introducing new therapeutic drugs for intrathecal (IT) administration. This study was undertaken to determine whether two drugs with possible antinociceptive effects, the N-methyl-D-aspartate receptor antagonist 3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP) and the adenosine agonist R-phenylisopropyladenosine (R-PIA), would affect SCBF after IT administration in the rat. SCBF was measured 30 min after IT injection of either saline, 4 nmol of CPP or 10 nmol of R-PIA in anesthetized rats by quantitative autoradiography with [14C]iodantipyrine as a tracer. No differences in SCBF were found between groups treated with saline or CPP. In the group where R-PIA was administered IT, grey matter blood flow was 10% greater than in the group that received saline, whereas no differences were found in white matter blood flow or in the grey/white matter ratio between the groups. We concluded that neither CPP nor R-PIA, when administered IT to anesthetized rats in provocative doses within the upper pharmacologic dose range, reduces SCBF in rats 30 min after IT injection. This indicates that neither neurotoxicologic nor antinociceptive effects are likely to occur due to decrease in SCBF. Our results do not indicate that these drugs should be avoided for the treatment of pain. (Anesth Analg 1993;76:1279-83)

Spinal Cord Blood Flow After Intrathecal Injection of a N-Methyl-D-Aspartate Receptor Antagonist or an Adenosine Receptor Agonist in Rats

Evaluation of spinal cord blood flow (SCBF) is important as a preclinical screening for potential neurotoxicologic side effects before introducing new therapeutic drugs for intrathecal (IT) administration. This study was undertaken to determine whether two drugs with possible antinociceptive effects, the N-methyl-D-aspartate receptor antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) and the adenosine agonist R-phenylisopropyladenosine (R-PIA), would affect SCBF after IT administration in the rat. SCBF was measured 30 min after IT injection of either saline, 4 nmol of CPP or 10 nmol or R-PIA in anesthetized rats by quantitative autoradiography with [14C]iodantipyrine as a tracer. No differences in SCBF were found between groups treated with saline or CPP. In the group where R-PIA was administered IT, grey matter blood flow was 10% greater than in the group that received saline, whereas no differences were found in white matter blood flow or in the grey/white matter ratio between the groups. We concluded that neither CPP nor R-PIA, when administered IT to anesthetized rats in provocative doses within the upper pharmacologic dose range, reduces SCBF in rats 30 min after IT injection. This indicates that neither neurotoxicologic nor antinociceptive effects are likely to occur due to decrease in SCBF. Our results do not indicate that these drugs should be avoided for the treatment of pain.

(R)- and (S)-8-acetyl-2-(dipropylamino)tetralin (LY-41): two novel 5-HT 1A receptor agonists

Interactions between central 5-HT 1A receptors and the enantiomers of LY-41, a 2-aminotetralin derivative related to 8-OH-DPAT (8-hydroxy-2-(dipropylamino)tetralin), were studied. Both enantiomers of LY-41 behaved as potent 5-HT 1A receptor agonists in rats, inducing the 5-HT behavioural syndrome, decreasing body temperature and inhibiting the cage-leaving response. The behavioural syndrome and the hypothermia were antagonized by the 5-HT 1A receptor antagonist, (S)-UH-301. The LY-41 enantiomers also reduced brain 5-HTP accumulation in rats treated with a decarboxylase inhibitor. The pharmacology of the enantiomers of LY-41 appeared similar to that of 8-OH-DPAT. However, it is noteworthy that the stereoselective interaction of 5-HT 1A receptors with LY-41 was opposite to that of 8-OH-DPAT. Thus, (R)-8-OH-DPAT was more potent than (S)-8-OH-DPAT, whereas (S)-LY-41 appeared to be more potent than (R)-LY-41.

Agonist and antagonist activity of low efficacy D2 dopamine receptor agonists in rats discriminating d-amphetamine from saline

The ability of the low efficacy D2 agonists preclamol and SDZ 208-911 to both antagonise, and substitute for, the d-amphetamine discriminative cue was investigated in rats trained to discriminate d-amphetamine (0.5mg/kg) from saline. All doses of preclamol (2.0-16.0mg/kg) and SDZ 208-911 (0.125-1.0mg/kg) only partially antagonised d-amphetamine discrimination. In contrast, the lower efficacy D2 agonist SDZ 208-912 completely blocked the cueing properties of d-amphetamine. Preclamol (4.0 and 16.0mg/kg) and SDZ 208-911 (1.0mg/kg) also partially substituted for d-amphetamine. In an additional study, the former drug enhanced the discriminative effects of a low dose of d-amphetamine (0.125mg/kg), whilst antagonising the effects of the training dose. Preclamol also partially antagonised the ability of the selective D2 agonist quinpirole (0.125mg/kg) to substitute for d-amphetamine. In contrast to the drug discrimination findings, preclamol completely antagonised the locomotor hyperactivity induced by acute d-amphetamine, in animals which had received the same long-term d-amphetamine treatment as the drug discrimination rats. The present findings reveal that preclamol and SDZ 208-911 can exert both agonist and antagonist activity in animals trained to discriminate d-amphetamine from saline. This partial agonist profile is probably due to the low efficacy D2 agonists interacting with a postsynaptic D2 receptor population possessing a higher response capability than those D2 receptors mediating d-amphetamine-induced locomotor hyperactivity.

Synergistic behavioural effects of dopamine D 1 and D 2 receptor agonists are determined by circadian rhythms

The effects of continuous subcutaneous infusions of rats for 336 h with vehicle, SKF 38393 (a dopamine D 1 receptor agonist), (+)-4-propyl-9-hydroxynaphthoxazine (PHNO, a dopamine D 2 receptor agonist) or both D 1 and D 2 receptor agonists, on locomotor activity were investigated. Rats were maintained under constant lighting conditions, either continuous dark (dark:dark) or continuous light (light:light), before and during drug treatments in order to determine the influence of free-running circadian rhythms on drug responses. The D 2 receptor agonist initially increased locomotion in rats kept under dark:dark during both subjective night (period of maximum locomotion) and day (period of minimum locomotion), but had no effect in rats maintained in light:light throughout the 336 h of treatment. The motor stimulant effects of the D 2 receptor agonist on rats kept in dark:dark increased during the course of treatment during subjective night (sensitization), but decreased during the rats' subjective day (tolerance). The D 1 receptor agonist, SKF 38393, had no effect on its own regardless of the lighting conditions and the duration of treatment. However, the D 1 receptor agonist interacted synergistically with the D 2 receptor agonist in rats maintained under light:light, depending on the duration of treatment. Synergistic effects were also observed on initiation of treatment in rats dark:dark but only during subjective day. Tolerance to the synergistic effects of the receptor agonists occured as a function of treatment duration, but only during subjective day. The D 1 receptor agonist blocked the effects of the D 2 receptor agonist during the rats' subjective night after 100h of traatment, but not after 25 or 325 h. It is concluded that the motor stimulant effects of a D 2 receptor agonist, behavioural D 1/D 2 dopamine receptor interactions, and the development of sensitization and tolerance to the locomotor effects of a D 2 receptor agonist are determined by endogenous free-running circadian rhythms, lighting conditions and duration of treatment.

Rotation in response to selective dopamine receptor agonists in rats with electrolytic substantia nigra lesions

Rats with unilateral, electrolytic substantia nigra (ESN) lesions were tested for rotation following systemic injections of the D1 dopamine receptor agonist SKF38393 or the D2 agonist quinpirole. Only quinpirole produced significant levels of rotation, which was ipsilateral in direction. This rotation was potentiated by coadministration of the D1 agonist, and was significantly reduced by injections of either a D1 or D2 receptor antagonist. Other groups of lesioned animals were treated with reserpine for 5 days and were then tested for rotation in response to the agonists. In this case, SKF38393 produced significant levels of contralateral rotation, while quinpirole-induced rotation remained ipsilateral; coadministration of the D1 and D2 agonists resulted in pronounced ipsilateral rotation. These results stress a role for D1 receptor mechanisms in producing rotation, and suggest that different striatal efferent pathways mediate rotation in response to selective agonists following ESN lesions.

Potentiation by serotonergic inhibition of yawning induced by dopamine receptor agonists in rats

Low doses of the dopamine D 2-receptor agonist, B-HT 920 (25 μg/kg, SC), and the dopamine D 1/D 2-receptor agonists, apomorphine (50 μg/kg, SC) and piribedil (1 mg/kg, SC), evoked yawning. However, the dopamine D 1-receptor agonist, SK&F 38393 (2 mg/kg, SC), failed to induce yawning. The yawning responses induced by B-HT 920, apomorphine or piribedil were markedly increased without eliciting stereotypy by pretreatment with reserpine (5 mg/kg, IP, 24 hr). These yawning responses were also enhanced by p-chlorophenylalanine (PCPA) (300 mg/kg, IP, 72 hr), but not by α-methyl-p-tyrosine (300 mg/kg, IP, 6 hr). The yawning induced by B-HT 920 given alone and in combination with reserpine or PCPA was inhibited by spiperone (0.5 mg/kg, IP) or scopolamine (0.5 mg/kg, IP), but not by SCH 23390 (0.5 mg/kg, IP). The present results suggest that yawning is evoked by stimulation of dopamine D 2-receptors having a high affinity and consequent muscarinic activation, and that the yawning induced by dopamine receptor agonists is potentiated by decreases in serotonergic neuron activity.

Rotation following intranigral injections of a selective D 1 or a selective D 2 dopamine receptor agonist in rats

Injections of various nonselective dopamine agonists into the substantia nigra, pars reticulata (SNpr), have been reported to produce contralateral rotation in rats. Since a number of recent dopamine receptor distribution studies have indicated a preponderance of D 1 compared to D 2 dopamine receptor subtypes within the SNpr, we examined the relative behavioral functions of these two subtypes within the nigra by studying rotation following unilateral, local injections of a D 1 (SKF38393) and D 2 (quinpirole) agonist, Significant, dose-dependent contralateral rotation was observed following injections of R,S-SKF38393. This effect was found to be stereoselective to the R-enantiomer, suggesting that the effect is receptor mediated. In contrast, quinpirole (LY171555) produced significant, dose-dependent ipsilateral rotation following nigral injection. These results suggest that the rotation seen following intranigral injections of nonselective dopamine agonists is due to the stimulation of the D 1 dopamine receptor, and that nigral D 1 and D 2 dopamine receptors may play opposite roles in the control of behavior.

Similar regulation of central and peripheral benzodiazepine binding sites by GABA receptor agonists in rats

Central and peripheral benzodiazepine binding sites were studied in vitro after the administration of GABAA and GABAB agonists. Cerebral cortex and kidney homogenates were used in this study. Muscimol (1.5 mg/kg, intraperitoneally) pretreatment significantly increased the affinity of benzodiazepine binding sites not only in the cerebral cortex but also in the kidneys. Similar changes were obtained with (-) and (+) baclofen (5 mg/kg, intraperitoneally), with the only exception that (-) baclofen in addition to changes in the affinity caused a marked decrease in the number of binding sites in both structures studied. The mechanism of action of GABA agonists on peripheral benzodiazepine binding sites is discussed.

Effects of selective dopamine receptor agonists in rats trained to discriminate apomorphine from saline

Rats (N=12) were trained to discriminate apomorphine (0.25 mg/kg, IP) from saline in a two-lever, food-reinforced (FR 30) drug discrimination paradigm. When the discrimination was acquired, various doses of apomorphine as well as several other dopamine receptor agonists were injected before test sessions. Apomorphine (0.03–0.25 mg/kg, IP) produced a dose-related increase in the percent of responses that occurred on the drug lever during test sessions. The selective DA 2 receptor agonist piribedil (0.25–8.0 mg/kg, IP) produced a dose-related increase in drug lever responding that was similar to that seen with apomorphine. On the other hand, administration of the selective DA 1 receptor agonist SKF 38393 (1.0–32 mg/kg, IP) resulted in principally saline lever responding, even at doses that substantially reduced the rate of responding. Administration of dopamine (1.0–8.0 mg/kg, IP), which does not readily cross the blood-brain barrier, also resulted in principally saline lever responding. These results suggest that the discriminative stimulus properties of apomorphine are based on its action at a receptor that is similar to the DA 2 receptor that has been characterized in the periphery and that this receptor is centrally located.

Hypotensive activity of serotonin receptor agonists in rats is related to their affinity for 5-HT 1 receptors

Hypotensive activity of serotonin receptor agonists in rats is related to their affinity for 5-HT 1 receptors

Modification of vascular response to serotonin by drugs.

ArticleModification of Vascular Response to Serotonin by DrugsIrvine H. Page, and J. W. McCubbinIrvine H. PageFrom the Research Division of the Cleveland Clinic Foundation and The Frank E. Bunts Educational Institute, Cleveland, Ohio, and J. W. McCubbinFrom the Research Division of the Cleveland Clinic Foundation and The Frank E. Bunts Educational Institute, Cleveland, OhioPublished Online:01 Sep 1953https://doi.org/10.1152/ajplegacy.1953.174.3.436MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe role of serotonin receptors in the control of cardiovascular functionOh, the places you'll go! My many colored serotonin (apologies to Dr. Seuss)Stephanie W. 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