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At least 559 records · Page 31Linked to original sources
PubMed1992

An LH-RH antagonist inhibits the behavioral effects of the agonist D-TRP-6-LH-RH in mice.

The effects of a potent LH-RH receptor antagonist, [Ac-4-Cl-D-Phe1,2,D-Trp3,D-Arg6,D-Ala10]LH-RH (ORG 30276), on the behavioral actions of the LH-RH agonist, D-Trp-6-LH-RH, were studied in mice. The subcutaneous (SC) administration of 100 micrograms/kg D-Trp-6-LH-RH inhibited ambulation in an open-field, produced analgesia in the hot-plate and tail-flick tests. These effects of the agonist were totally antagonized by pretreatment with ORG 30276 at a dose of 100 micrograms/kg SC. In the apomorphine-induced cage-climbing test, both the agonist and the antagonist alone or together suppressed the duration of stereotyped behavior in dose-dependent manner, but, as there was no additive synergism after combined treatments, it seems that the two substances mutually diminish each other's effects. The results indicate that the behavioral effects of the LH-RH agonist can be antagonized by pretreatments with a potent LH-RH antagonist designed to block pituitary LH-RH receptors, with the exception of the suppression of apomorphine-induced cage-climbing, where special type of receptors and/or mechanisms might be involved.

Analgesia↗
PubMed1995

The dorsal raphe nucleus is a site of action mediating the behavioral effects of the benzodiazepine receptor inverse agonist DMCM.

Systemic administration of benzodiazepine receptor inverse agonists leads to behavioral changes similar to those produced by inescapable shock (IS). The dorsal raphe nucleus (DRN) is a critical structure mediating IS effects. The present experiments determined whether the DRN is a site mediating the behavioral changes produced by benzodiazepine receptor inverse agonists. Microinjection of the inverse agonist Methyl 6,7-Dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) in the region of the DRN produced enhancement of fear conditioning as assessed by the amount of freezing in the presence of shock cues as well as interference with shuttlebox escape learning assessed 24 hr later. Furthermore, lesion of the DRN blocked the effects of systemic DMCM on fear conditioning and escape learning. These data suggest that the DRN is indeed critical in mediating these behavioral consequences of DMCM and further support a role for the DRN in producing the behavioral changes induced by IS.

Animals↗
PubMed1994

Effects of an A1 adenosine receptor agonist on the neurochemical, behavioral and histological consequences of ischemia.

Untreated rats and rats given the A1 receptor adenosine agonist, R-phenylisopropyladenosine (R-PIA), were subjected to four vessel ischemia. The effect of R-PIA on hippocampal amino acid release, hippocampal neuronal damage, exploratory behavior, learning capacity and global neurological score were evaluated. R-PIA decreased by half the glutamate released during ischemia and improved the global neurological scores 3, 24, 48, 78 h and 7 days after ischemia. But R-PIA had no effect on taurine/GABA release (during ischemia), hippocampal neuronal damage (7 days post-ischemia), exploratory behavior (48 h post-ischemia) or learning capacity (7 days post-ischemia). Thus, a decrease in glutamate release by R-PIA is not systematically correlated with an improvement of histological damage or learning capacity. Reduced glutamate release is not therefore a sufficient criterion on which to evaluate the neuroprotective capacity of a drug.

Amino Acids↗
PubMed2002

PNU-96391A (OSU6162) antagonizes the development of behavioral sensitization induced by dopamine agonists in a rat model for Parkinson's disease.

PNU-96391A is a weak dopamine (DA) D(2) receptor antagonist with behavioral stabilizing properties. Previous experiments revealed that PNU-96391A antagonizes the expression of L-DOPA induced behavioral sensitization (dyskinesias) in lesioned primates without inducing akinesia or reducing the anti-Parkinsonian efficacy of L-DOPA. This study evaluated the ability of PNU-96391A to block the development of DA agonist-induced behavioral sensitization in rats with unilateral 6-OH-DA lesions of the median forebrain bundle. Repeated twice daily treatment with L-DOPA and the decarboxylase inhibitor benserazide (15 and 5 mg/kg, IP, respectively), or quinpirole (D(2)/D(3) agonist, 0.1 mg/kg, SC) increased the contralateral rotations measured on day 7 and 14 as compared to day 1. PNU-96391A (10-60 mg/kg, SC, bid.) antagonized the development of behavioral sensitization induced by both agonists. The basal activity of L-DOPA was not affected while a reduction of quinpirole-induced rotations was observed after 30-60 mg/kg, SC of PNU-96391A. Neurochemical analyses confirmed >99 % reductions of striatal DA levels, unilaterally. Concomitant treatment with PNU-96391A and L-DOPA did not affect plasma levels of PNU-96391A indicating that the effects observed are not related to pharmacokinetic interactions. These results suggest that PNU-96391A could be therapeutically useful to prevent the development of behavioral sensitization induced by DA agonists.

Animals↗
PubMed2006

Effects of mu-, delta- and kappa-opioid receptor agonists on methamphetamine-induced self-injurious behavior in mice.

Opioid receptor agonists can differentially modify the behavioral effects of direct/indirect dopamine receptor agonists, such as methamphetamine, cocaine and apomorphine. However, the effects of opioid receptor agonists on high-dose methamphetamine-induced behavior have not yet been clarified. Therefore, the present study was undertaken to investigate the effects of mu (morphine)-, delta (SNC80)- and kappa (U50,488H)-opioid receptor agonists on methamphetamine-induced self-injurious behavior and locomotor activity in mice. Methamphetamine (20 mg/kg) induced severe self-injurious behavior. In a combination test, some opioid receptor agonists significantly attenuated methamphetamine-induced self-injurious behavior, with potencies in the order morphine>buprenorphine (mu-opioid and kappa-opioid receptor agonist/antagonist) >U50,488H, as maximum effects. These results suggest that the stimulation of mu- and kappa-opioid receptors plays an inhibitory role in high-dose methamphetamine-induced stereotypic self-injurious behavior in mice, without affecting locomotor activity.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1976

Spontaneous and centrally induced behaviors in normal and thalamic opossums.

Electrical stimulation of localized areas of the opossum medulla and cerebellum induced goal-oriented eating and grooming behaviors of stereotyped gagging. Following radical telencephalic lesions, these animals showed considerable behavioral capacity and in many cases continued to demonstrate centrally induced responses. Animals with lesions, however, failed to groom or show active food-seeking behavior, and they showed poor thermoregulation in the heat, presumably because of the loss of thermoregulatory grooming. These deficits following removal of the telencephalon appear to have resulted from disruption of important sources of control over behaviors rather than from loss of basic consummatory response mechanisms, since grooming and eating, while less directed, could still be elicited by central stimulation. These results support the view that the lower brain stem may contain intrinsic neural circuits for the integration of complex behaviors.

Agonistic Behavior↗
PubMedDate not supplied

[Effect of opiate agonists administered intrathecally on the behavioral and hemodynamic manifestations of pain].

An agonist of mu-opiate receptors, D-Ala2-Gly-ol5-enkephalin (DAGO, 0.5 mcg), administered intrathecally, was found to inhibit behavioral and hemodynamic reactions induced by thermal and electrical stimulation of conscious male rats. D-Ala2-D-Leu-enkephalin (DADL, 0.5 mcg), acting on delta-receptors, was shown to potentiate nociceptive shifts of arterial blood pressure. Phencyclidine and bremazocine failed to exert any significant effect on the opioidergic mechanisms of the spinal cord.

Animals↗
PubMed2006

Behavioral effects of dopaminergic agonists in transgenic mice overexpressing human wildtype alpha-synuclein.

Overexpression of alpha-synuclein causes familial Parkinson's disease and abnormal aggregates of the protein are present in sporadic cases of the disease. We have examined the behavioral effects of direct and indirect dopaminergic agonists in transgenic mice expressing human alpha-synuclein under the Thy-1 promoter (Thy1-aSyn, alpha-synuclein overexpressor), which exhibit progressive impairments in behavioral tests sensitive to nigrostriatal dopamine dysfunction. Male Thy1-aSyn and wild-type mice received vehicle, benserazide/L-DOPA (25 mg/kg, i.p.), high (2 mg/kg, s.c.) and low doses (0.125, 0.25, 0.5 mg/kg, s.c.) of apomorphine, and amphetamine (5 mg/kg, i.p.), beginning at 3 months of age, and were tested on the challenging beam, spontaneous activity, pole test, and gait. l-DOPA had a paradoxical effect and worsened the deficits in Thy1-aSyn mice compared with controls, whereas the high dose of apomorphine only produced few deficits above those already present in Thy1-aSyn. In contrast to wild-type mice, Thy1-aSyn mice did not show amphetamine-induced stereotypies. The results indicate that chronic overexpression of alpha-synuclein led to abnormal pharmacological responses in mice.

Amphetamine↗
PubMed1992

Dynorphin A(1-13) preferentially inhibits behaviors induced by the D2 dopamine agonist RU 24213 but not by the D1 dopamine agonist SK&F 38393.

The effects of dynorphin A(1-13) on the D1 dopamine agonist SK&F 38393- and the D2 dopamine agonist RU 24213-induced behavioral alterations in the mouse were determined by using multidimensional behavioral analyses based upon a capacitance system. Although dynorphin A(1-13) (3.0 or 12.5 micrograms) alone did not produce any significant effects on behaviors, the peptide (12.5 micrograms) caused an inhibitory effect on the RU 24213 (3.0 mg/kg)-induced increase in behavioral patterns such as linear locomotion and circling except rearing and grooming behaviors. The antagonistic effects of dynorphin A(1-313) (12.5 micrograms) were fully reversed by the opioid antagonist M(r) 2266 (10.0 mg/kg). However, dynorphin A(1-13) (3.0 or 12.5 micrograms) failed to affect behaviors elicited by SK&F 38393 (10.0 mg/kg). These results suggest that dynorphin A(1-13) plays an inhibitory role in behaviors induced by the D2 dopamine agonist but not by the D1 dopamine agonist, possibly through the mediation of kappa-opioid receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1984

Biochemical and behavioral evaluation of pergolide as a dopamine agonist in the rat brain.

The ergot derivative pergolide was evaluated as a dopamine agonist using various behavioral and biochemical analyses. Spontaneous motor activity was decreased by small doses (0.1 mg/kg) of pergolide and increased with larger doses (above 0.5 mg/kg). Hypermotility after larger doses persisted for as long as 24 hr and was succeeded by a period of hypomotility. The doses of drug, sufficient to produce hypermotility, also produced stereotypy. With repeated daily injections (2 weeks), the period of hypermotility decreased and the ensuing period of hypomotility increased. Stereotyped behavior was similarly affected. Chronic administration of pergolide did not alter the magnitude of the behavioral responses. Levels of the dopamine (DA) metabolites, dihydroxyphenylacetate (DOPAC) and homovanillic acid (HVA), in the striatum and mesolimbic regions were decreased during the periods of hypermotility but returned to control levels during subsequent hypomotility. Activation of putative inhibitory presynaptic dopamine receptors by pergolide was studied by following accumulation of DOPA in rats treated with the dopamine neuron inhibiting agent, gamma-butyrolactone (GBL) and a DOPA-decarboxylase inhibitor. Pergolide significantly inhibited both striatal and mesolimbic accumulation of DOPA. In contrast, with changes in behavioral and metabolic indices, pergolide-induced inhibition of tyrosine hydroxylase was not affected by chronic treatment with pergolide. On the basis of both behavioral and biochemical data it is proposed that pergolide acts as a dopamine agonist with particularly long-lasting effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2001

Estrogen modulates 5-HT(1A) agonist inhibition of lordosis behavior but not binding of [(3)H]-8-OH-DPAT.

Previous studies showed that repeated estrogen treatment reduces the ability of the 5-HT(1A) receptor agonist, 8-hydroxy-2(di-n-propylamino) tetralin (8-OH-DPAT), to inhibit lordosis behavior of female rats. The present study evaluated the effects of repeated estrogen treatment on lordosis behavior and 5-HT(1A) receptor binding and coupling to G protein in the hypothalamus-preoptic area using the agonist ligand [3H]-8-OH-DPAT, which binds selectively to G-protein-coupled 5-HT(1A) receptors. Rats were injected twice with 25 or 50 microg of estradiol benzoate (EB) 7 days apart followed by 500 microg of progesterone (P) 48 h after the second EB injection. Controls received a single injection of 25 or 50 microg EB followed 48 h later by 500 microg of P. Four hours after P, 0.15 mg/kg 8-OH-DPAT was injected, and lordosis behavior examined for 30 min. Rats treated twice with EB showed significantly less 8-OH-DPAT inhibition of lordosis behavior than rats receiving a single EB injection. For receptor binding, rats received EB without P treatment. None of the estrogen treatments reduced [3H]-8-OH-DPAT binding density or affinity in the hypothalamus-preoptic area or hippocampus. These studies suggest that estrogen modulates 5-HT(1A) agonist potency without a measurable change in 5-HT(1A) receptor density or coupling to G protein.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1985

Does a single priming injection of clenbuterol alter behavioral response to beta-adrenoceptor agonists and antagonists in mice through a time-dependent process?

The present study investigated the extent to which a single priming injection of clenbuterol, a beta-adrenoceptor agonist, could alter the behavioral response (locomotor activity recorded for 30 min with photocell counters) of mice to the subsequent administration of beta-adrenoceptor agonists or antagonists. In mice pretreated with clenbuterol (0.25 mg/kg), the dose-response curve of clenbuterol (0.06 to 2 mg/kg) for reducing locomotor activity was shifted to the right with minimal alteration of the maximal response. The magnitude of the shift was dependent on both the priming dose of clenbuterol and the time interval between the priming and the test injections (maximum between 15 to 24 h, disappearance for intervals exceeding 72 h). The coadministration of propranolol (0.5; 2; 8 mg/kg) dose dependently antagonized the effects of the priming injection of clenbuterol. A previous injection of clenbuterol was also found to reduce the ability of another beta-adrenoceptor stimulant, salbutamol (8 mg/kg), but not apomorphine, to reduce locomotor activity. Finally, previous beta-adrenoceptor stimulation resulted in an enhanced ability of two beta-adrenoceptor antagonists, propranolol (0.125 to 8 mg/kg) and penbutolol (0.5 to 32 mg/kg), to reduce locomotor activity in mice. All these data add to the evidence concerning the remarkable plasticity of central beta-adrenoceptors and indicate that initial stimulation of a class of beta-adrenoceptors may trigger a relatively important, time-dependent alteration in the behavioral reactivity to beta-adrenoceptor agonists and antagonists.

Adrenergic beta-Agonists↗
PubMed1985

Estrogen action in anterior and ventromedial hypothalamus and the modulation of heterosexual behavior in female golden hamsters.

Changes in heterosexual patterns of agonistic, marking, and sexual behavior were examined in female hamsters over a three day period following implantation of either estrogen or cholesterol in the hypothalamus. Animals were habituated to large arenas that permit the display of a wide range of behavior. Estrogen implants located in the ventromedial (VMH) but not the anterior (AH) portion of the hypothalamus were effective in facilitating the occurrence of vaginal marking, over a two day estrogen priming period. During this two day period, the exhibition of agonistic behavioral patterns declined significantly. Systemic administration of progesterone elicited sexual receptivity in 75% of the females in the VMH group, in contrast to only 25% in the AH group. Females with hypothalamic implants of cholesterol remained unreceptive following progesterone injections. The results provide important information on the estrogen sites of action at the hypothalamus in mediating heterosexual interactions.

Agonistic Behavior↗
PubMed2006

The partial dopamine D2-like receptor agonist terguride functions as an agonist in preweanling rats after a 5-day reserpine regimen.

RATIONALE: Treating children and adolescents with partial D2-like agonists is becoming increasingly common, although few developmental animal studies have assessed the psychopharmacology of this class of drug. Contrary to results from adult rat studies, it has been reported that partial D2-like agonists may not induce agonist-like behavioral effects in preweanling rats during states of low dopaminergic tone. OBJECTIVE: The purpose of the present study was to determine whether a partial D2-like agonist would act as an agonist in preweanling rats after a 5-day regimen of the dopamine-depleting agent reserpine or the tyrosine hydroxylase inhibitor alpha-methyl-DL-p-tyrosine (AMPT). METHODS: Sprague-Dawley rats were pretreated with reserpine (1 mg kg(-1) per day) or AMPT (3 x 200 mg kg(-1) per day) on postnatal day (PD) 16-PD 20. Either 2 h (AMPT) or 5 h (reserpine) after the last pretreatment injection, rats were treated with saline, the partial D2-like agonist terguride, or the full D2-like agonist R(-)-propylnorapomorphine (NPA). Distance traveled and repetitive motor movements were measured for 60 min. RESULTS: After repeated reserpine treatment, both terguride and NPA increased the distance-traveled scores of preweanling rats; however, only NPA, but not terguride, increased distance-traveled scores after a 5-day regimen of AMPT or an acute injection of reserpine. CONCLUSIONS: It is now apparent that partial D2-like agonists are capable of inducing agonist-like behavioral effects in preweanling rats during a state of low dopaminergic tone. For agonistic actions to be observed, the pretreatment regimen must result in substantial and prolonged dopamine depletion.

Animals↗
PubMed1991

Chronic nicotine-induced changes in dopaminergic system: effect on behavioral response to dopamine agonist.

The effect of chronic nicotine on dopamine-agonist-mediated locomotor activity response was measured in BALB/cBy and C57BL/6 mice. Mice were injected twice daily for 10 days with 1.2 mg/kg SC (-)-nicotine di-(+)tartrate. Subsequent locomotor activity response to apomorphine (1 mg/kg SC) was measured. Apomorphine induced hypomotility in both strains of mice, with the BALB/cBy mice showing a greater hypomotility compared to the C57BL/6 mice. The response to apomorphine was attenuated in both strains of mice that were treated previously with repeated injections of nicotine. The results suggest that chronic nicotine may induce changes in the dopaminergic system, which is reflected in altered behavioral response to a dopamine agonist.

Animals↗