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PubMed1988

Behavioral effects of acute and chronic buspirone.

The effects of buspirone were studied in squirrel monkeys trained to lever-press under a fixed-interval schedule involving suppressed responding. Buspirone (0.01-0.1 mg/kg) generally did not increase rates of suppressed responding. Buspirone (0.01-0.1 mg/kg) generally did not increase rates of suppressed responding; 0.3 mg/kg of buspirone decreased rate. In comparison, diazepam (0.1-1.0 mg/kg) and CL 218872 (0.3-3.0 mg/kg) increased responding. Additionally, the effects of buspirone (0.01-0.3 mg/kg) were unchanged over a 12-day period of daily administration. The results show that buspirone has effects on schedule-controlled behavior of squirrel monkeys that differ from those of typical anxiolytic drugs.

Animals↗
PubMed1993

Comparison of the effect of buspirone and 1-(2-pyrimidinyl)-piperazine on cerebral glucose utilization in the rat.

The novel anxiolytic and antidepressant, buspirone, and its main metabolite 1-(2-pyrimidinyl)-piperazine (1-PP), which is pharmacologically active, were examined for their effect on regional cerebral glucose utilization in awake rats using quantitative 2-deoxyglucose autoradiography. At a dose of 1 mg/kg, buspirone reduced glucose utilization in the hippocampus by approximately 15%, whilst 1-PP at the same dose had no effect. In comparison, at a higher dose, 10 mg/kg of both buspirone and 1-PP decreased glucose utilization in the hippocampus by 20% and 27%, respectively. In addition, widespread reductions in local cerebral glucose utilization were noted with this higher dose of 1-PP; such generalized effects are compatible with those reported for alpha 2 adrenoceptor antagonists. Buspirone at 1 and 10 mg/kg increased glucose utilization by 40% and 65%, respectively, in the lateral habenular nucleus, whilst 1-PP at 1 and 10 mg/kg had no effect. The findings suggest that buspirone's effects on glucose utilization cannot be attributed to 1-PP, unless high doses of buspirone are administered.

Animals↗
PubMed1985

The non-benzodiazepine anxiolytic buspirone inhibits stress-induced renin secretion and lowers heart rate.

The non benzodiazepine drug, buspirone, produces a dose-dependent biphasic effect on plasma renin activity in non-stressed rats. Low doses (0.1 - 2.0 mg/kg i.p.) decrease while high doses (10.0 - 50.0 mg/kg i.p.) increase plasma renin activity. The maximal decrease in plasma renin activity produced by buspirone (1.0 mg/kg i.p.) was observed 30 minutes post-injection. In addition, buspirone (0.5 and 2.0 mg/kg i.p.) blocked the stress-induced rise in plasma renin activity. This effect of buspirone is in contrast to the previously observed failure of the benzodiazepine anxiolytics to alter the effect of stress on plasma renin activity. Administration of buspirone (0.5 mg/kg i.p.) produced a sustained reduction (15%) in heart rate but did not affect mean arterial pressure. The present data support the view that the mechanism of the anxiolytic action of buspirone is different from that of the benzodiazepines.

Animals↗
PubMed1987

Presynaptic control of dopamine metabolism in the nucleus accumbens. Lack of effect of buspirone as demonstrated using in vivo voltammetry.

Buspirone is a non-benzodiazepine drug with anxiolytic properties. It has been reported to induce a marked increase in the metabolism of dopamine in the striatum and the nucleus accumbens which is similar to that induced by neuroleptics. It has been suggested that the effect observed in the striatum reflects an action of buspirone on dopaminergic autoreceptors in both terminals and cell bodies. In the present study, presynaptic effects of buspirone on dopaminergic metabolism in the nucleus accumbens were investigated, and they were compared to the effects of the classical neuroleptic, haloperidol. Dopaminergic terminals were isolated by infusion of tetrodotoxin into the median forebrain bundle in order to evaluate the effects of buspirone and haloperidol on presynaptic receptors. Changes in dopamine metabolism were determined by in vivo voltammetry. Buspirone administered after interruption of the impulse flow did not affect dopamine metabolism. In contrast haloperidol treatment led to an increase in metabolism of dopamine. It is concluded that buspirone did not act at the presynaptic level and furthermore on dopaminergic autoreceptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Role of alpha1-adrenoceptors in the reduction of external carotid blood flow induced by buspirone and ipsapirone in the dog.

The effects of the 5-HT1A receptor agonist with anxiolytic properties, buspirone and ipsapirone, in the external carotid bed of anaesthetized dogs were analyzed. Since these agonists produce several vascular effects via activation of both 5-HT receptors and alpha1-adrenoceptors, their effects were compared with those elicited by the 5-HT agonist, quipazine, and the alpha1-adrenoceptor agonist, methoxamine. 1-Min intracarotid (i.c.) infusions of buspirone (300 microgram/min), ipsapirone (40 microgram/min), quipazine (300 microgram/min) and methoxamine (15 microgram/min) produced consistent decreases in external carotid blood flow (ECBF); since these changes in blood flow were not accompanied by modifications in systemic blood pressure, the agonists produced parallel increases in external carotid resistance. After interruption of the sympathetic tone by bilateral cervical vagosympathectomy, the vasoconstrictor responses to all the agonists remained unaffected. The intravenous (i.v.) administration of the nonselective 5-HT1-like receptor antagonist, methiothepin (1-100 microgram/kg), potently and dose-dependently antagonized buspirone-, ipsapirone- and quipazine-induced vasoconstriction; methiothepin similarly antagonized the vasoconstrictor responses to methoxamine. Interestingly, the alpha1-adrenoceptor antagonist, prazosin (1-100 microgram/kg, i.v.), also antagonized the vasoconstrictor responses to buspirone, ipsapirone and methoxamine in a dose-dependent manner. Finally, buspirone (300 microgram/min, i.c.) and ipsapirone (40 microgram/min, i.c.) did not modify the responses to noradrenaline (10 microgram/min, i.c.) or tyramine (100 microgram/min, i.c.). It is concluded that canine external carotid vasoconstriction induced by buspirone and ipsapirone is mainly mediated by activation of alpha1-adrenoceptors located in vascular smooth muscle. These data further highlight the ability of the above anxiolytics to produce significant vascular effects under in vivo conditions.

Adrenergic alpha-Agonists↗
PubMed1983

Selective effects of buspirone and molindone on dopamine metabolism and function in the striatum and frontal cortex of the rat.

The hypothesis that the nerve endings of the dopamine projection of the frontal cortex lack autoreceptors for regulation of tyrosine hydroxylase was tested by using the preferential inhibitors of dopamine autoreceptors, molindole and buspirone. In contrast to haloperidol, which elevates dopamine metabolism in the striatum and frontal cortex, both molindone and buspirone elicited little change in dopamine metabolism in the frontal cortex at doses up to 3.0 mg/kg, which cause the same maximal response in the corpus striatum as does haloperidol. Thus, the lack of autoreceptors in the frontal cortex is of pharmacological importance. That preferential inhibition of striatal dopamine autoreceptors may reverse catalepsy by enhancing synthesis and release of dopamine was tested by first inducing catalepsy with different drugs and then administering molindone or buspirone. Only buspirone (1.0 mg/kg) reversed catalepsy. This effect does not require presynaptic dopamine as catalepsy was reversed by buspirone in the dopamine-depleted rat (with 2.0 mg/kg R04-1284) as well as after postsynaptic dopamine receptor blockade by haloperidol of cis-flupenthixol. Thus, the mechanism for the reversal of catalepsy appears to be located efferent from the dopamine neuron. Buspirone, a non-benzodiazepine anti-anxiety drug, may prove useful for treatment of extrapyramidal motor disorders of either iatrogenic or idiosyncratic origin.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Buspirone increases social investigation in pair-housed male mice; comparison with the effects of chlordiazepoxide.

Effects of buspirone (1, 5 and 10 mg/kg, i.p.) on the behaviour of adult male CD1 mice have been compared with those of chlordiazepoxide (1, 4 and 8 mg/kg, i.p.). Commencing at 30 min after injection, the behaviour of each mouse was examined by ethological procedures during 5 min social encounters with an untreated partner in the animal's home cage and in the more aversive situation of an unfamiliar neutral cage. In both test environments, buspirone at 1 and 5 mg/kg and chlordiazepoxide (CDP) at 1 and 4 mg/kg increased social investigation and some of its constituent elements, while decreasing non-social activity and the element, "explore" (and for CDP, of "scanning" also). In both test environments, the increase of social investigation by buspirone and CDP was less marked at 10 and 8 mg/kg, respectively. For CDP, although not for buspirone, this effect was related to dose-dependent increases of immobility coupled with reductions of exploratory non-social activity and scanning below those occurring at the intermediate dose level. Buspirone at 5 mg/kg increased social investigation to a greater extent in the home cage (P < 0.01) than in the unfamiliar neutral cage (P < 0.05), whereas CDP was approximately equipotent in the two test situations. In the neutral cage, buspirone at all dose levels showed an additional effect of increasing the time spent by the mice in digging, whereas chlordiazepoxide dose-dependently increased aggression. These results indicate anxiolytic activity by both compounds after acute administration, and identify certain differences in the profile of their other effects on social behaviour.

Analysis of Variance↗
PubMed1988

5-Hydroxytryptamine1A receptor-mediated effects of buspirone, gepirone and ipsapirone.

The effects of the nonbenzodiazepine anxiolytic agents, buspirone, gepirone and ipsapirone on body temperature and corticosterone secretion were studied in the rat. The administration of buspirone, gepirone and ipsapirone resulted in dose-related decreases in body temperature and increases in the plasma concentration of corticosterone. Spiperone produced a dose-related inhibition of the hypothermic and corticosterone responses to gepirone. Spiperone also inhibited ipsapirone-induced changes in body temperature and hormone secretion. Although spiperone also blocked the buspirone-induced stimulation of corticosterone, it did not attenuate the hypothermic response to buspirone at the dose tested. (-)-Pindolol, a potent 5-HT1A antagonist, prevented gepirone- and ipsapirone-induced hypothermia and corticosterone secretion. (-)-Pindolol also blocked the hypothermic but not the corticosterone response to buspirone. Ketanserin, a 5-HT2 antagonist, did not inhibit the hypothermic or corticosterone responses produced by these novel anxiolytic agents. It is concluded that buspirone, gepirone and ipsapirone produce hypothermia and increase plasma concentrations of corticosterone by activating 5-HT1A receptor mechanisms.

Animals↗
PubMed1990

Effects of intrathecal and systemic administration of buspirone on genital reflexes and mating behavior in male rats.

Buspirone was studied to determine whether the detailed profile of male sexual behavior observed following treatment with the prototypical 5-HT1A ligand, 8-OH-DPAT, can be generalized to other 5-HT1A agonist drugs. Systemic and intrathecal (IT) routes of administration were compared. Like DPAT, significant reduction in intromission frequency followed IT infusion of buspirone (80-160 micrograms) as did intraperitoneal (IP) injection (1-4 mg/kg). IT doses of 80-160 micrograms and all IP doses significantly reduced ejaculation latency. Intercopulatory interval significantly decreased following IP buspirone but not after IT infusion although there were trends in that direction. All IP doses and 80 micrograms IT significantly shortened the postejaculatory interval. Buspirone inhibited erection and/or ejaculation in the ex copula reflex test. A decrease in percentage of rats displaying erections and ejaculation occurred following either route of administration. Ejaculation was significantly inhibited at the low IT dose of 40 micrograms. We conclude that buspirone affects sexual behavior very much like DPAT or other 5-HT1A drugs, to the extent known. Sexual effects of buspirone were generally similar regardless of route of administration, but the effective doses were clearly lower with IT treatment.

Animals↗
PubMed1991

Comparison of routes of administration and time course effects of zacopride and buspirone in mice using an automated light/dark test.

The behavioral effects of zacopride and buspirone were assessed in mice in a fully automated 2-compartment light/dark test. A significant increase in time mice spent in the lit area was used as an indication of anxiolytic-like action. Doses of zacopride from 0.0001 to 17.8 mg/kg, IP, and buspirone from 3.16 to 17.8 mg/kg, IP, produced significant increases in time mice spent in the lit area of the chamber. In addition, zacopride and buspirone were compared for oral potency and for duration of action after IP and PO administration. Zacopride and buspirone produced anxiolytic-like activity between doses of 0.001 to 100.0 mg/kg, PO, and 10.0 to 56.2 mg/kg, PO, respectively. The duration of effect of buspirone was 2 to 4 h after IP or PO administration, while that for zacopride was greater than or equal to 16 h by either route of administration. Thus, when compared for anxiolytic-like effects in this test, zacopride is a more potent and longer acting agent than buspirone.

Administration, Oral↗
PubMed1993

Atypical anxiolytic profile of buspirone and a related drug, SM-3997, in a modified forced swim test employing straw suspension.

Previous reports have shown that immobility time increases in the presence of suspended straws in association with an inhibition of straw-climbing behavior after acute administration of a prototypical anxiolytic benzodiazepine (BZD) such as diazepam. In this modified forced swim (MFS) test employing straw suspension, the effects of two new non-BZD compounds were tested and compared with those of diazepam (0.5, 1, and 5 mg/kg, IP) used in a previous MFS test. After a 5-min test of forced swimming, four straws were suspended just above the surface of the water and subsequently the straw-climbing trials were counted for 5 min as an index of escape behaviors induced by negative emotionality (stress and/or anxiety). Rats were injected IP with either saline, buspirone HCl (0.5, 1, and 5 mg/kg), or a related compound, SM-3997 (5, 10, and 20 mg/kg), 30 min before testing. At lower doses, both buspirone (0.5, 1 mg/kg) and SM-3997 (5, 10 mg/kg) reduced the duration of immobility, as opposed to that of diazepam. Conversely, buspirone at the highest dose of 5 mg/kg significantly prolonged the duration of immobility, and SM-3997 at 20 mg/kg also prolonged its duration, indicating a biphasic effects. All doses of buspirone and SM-3997 inhibited straw-climbing counts, in the same manner as diazepam. These results suggest that buspirone may possess relatively weak and/or atypical anxiolytic effects at lower doses, whereas at 5 mg/kg this compound may have an anxiolytic effect. In addition, SM-3997 may be a less potent anxiolytic drug than buspirone in the MFS test following a single-injection protocol.

Animals↗
PubMed1994

Perceptual masking of the chlordiazepoxide discriminative cue by both caffeine and buspirone.

Twelve male Sprague-Dawley rats were trained to discriminate between the interoceptive stimulus attributes of 5 mg/kg chlordiazepoxide (CDP) and saline in a two-lever operant task under a fixed-ratio 10 (FR-10) schedule of food reinforcement. Caffeine, buspirone, and Ro 15-1788 failed to engender complete generalization when tested in combination with saline. In drug interaction test sessions caffeine (56 mg/kg) blocked the discriminative stimulus properties of the training dose of CDP and shifted the CDP discriminative dose-response function to the right. This rightward shift in CDP discriminative function was paralleled by a concomitant downward shift in the rate-of-responding dose-response function. Drug interaction test sessions conducted with 3.2 mg/kg of buspirone in combination with various doses of CDP engendered a downward shift in both the discriminative and rate-of-responding dose-response functions. Because 3.2 mg/kg buspirone in combination with the training dose of CDP resulted in complete response rate suppression, additional combination tests were conducted with 3 mg/kg CDP, a dose which reliably engendered > 90% CDP-appropriate responding, and various doses of buspirone. Similar to the CDP-caffeine interactions, buspirone blocked the cueing properties of 3 mg/kg CDP with a parallel reduction in response rates. Interaction test sessions conducted with Ro 15-1788 and CDP resulted in rightward shifts in both the discriminative and rate functions of CDP. We suggest that the interactions between CDP and both caffeine and buspirone resulted from the perceptual masking of the interoceptive (subjective) effects of CDP, whereas the interaction between Ro 15-1788 and CDP reflect pharmacological antagonism.

Animals↗
PubMed1996

Protective effects of maternal buspirone treatment on serotonin reuptake sites in ethanol-exposed offspring.

Previous work in this laboratory demonstrated that in utero ethanol exposure is associated with abnormal development of the serotonergic system. Specific abnormalities included deficiencies of serotonin (5-HT) and its metabolites, and cortical 5-HT reuptake sites. The concentration of 5-HT1A receptors was also altered. The serotonin deficit was detected in the fetal ethanol-exposed brain, at an age when 5-HT would normally function as an essential trophic factor. Thus, it was hypothesized that the early 5-HT ethanol-associated deficit of an essential trophic factor (e.g. 5-HT) could contribute to subsequent developmental abnormalities in serotonergic neurons. In the present investigation we used quantitative autoradiography (QAR) to more fully characterize the developmental abnormalities in 5-HT reuptake sites in developing offspring of ethanol-fed rats. In addition, we attempted to overcome the potential negative impact of the ethanol-associated deficit of fetal 5-HT, by administering a 5-HT1A agonist, buspirone, to pregnant rats. These investigations demonstrated that postnatal (PN) 19 and/or 35 day ethanol-exposed offspring had a significant decrease in [3H]citalopram binding to 5-HT reuptake sites in the frontal cortex, parietal cortex, lateral hypothalamus, substantia nigra, medial septum, and striatum. In contrast, [3H]citalopram binding was increased in the dorsal raphe on PN5 and in the median raphe on PN19. No significant ethanol-associated changes were detected in the hippocampus CA3 region or in the amygdala. When [3H]citalopram binding was compared in the offspring of saline- and buspirone-treated dams, it appeared that maternal treatment with buspirone prevented or reversed most of the ethanol-associated developmental abnormalities in 5-HT reuptake sites. Buspirone prevented the decline in binding of [3H]citalopram in the frontal cortex, lateral hypothalamus, substantia nigra and medial septum. Similarly, buspirone treatment prevented the ethanol-associated increase in binding in the dorsal and median raphe. Additional experiments are needed to elucidate the impact of maternal buspirone treatment on the development of other neurotransmitter systems in offspring.

Animals↗
PubMed1987

Comparison of withdrawal of buspirone and diazepam: a placebo controlled study.

In a 8-week double-blind placebo controlled study, 48 outpatients with generalized anxiety disorder were randomized to diazepam, buspirone, a non-benzodiazepine anxiolytic, or placebo. During the treatment phase of 4 weeks duration diazepam was found to be significantly better than placebo and buspirone. Following abrupt withdrawal by placebo substitution the diazepam group showed a gradual relapse maximal after two weeks while the buspirone and the placebo groups did not differ. There were more cases of rebound anxiety with diazepam as compared to buspirone or placebo. In addition, there were three early terminations related to rebound anxiety in the diazepam group while there were none in the placebo and buspirone groups. There were significantly more new symptoms in the diazepam group than in the placebo or buspirone group.

Adult↗
PubMed1996

Acute administration of buspirone increases the escape of hypothalamic-pituitary-adrenal-axis hormones from suppression by dexamethasone in depression.

Recently, our laboratory found a significant enhancing effect of L-5-hydroxy-tryptophan (L-5-HTP) on post-dexamethasone (DST) plasma adrenocorticotropic hormone (ACTH) and cortisol levels in major-but not in minor-depression. To further elucidate the effects of central serotonin (5-HT) activity on the negative feedback of glucocorticoids on hypothalamic-pituitary-adrenal (HPA)-axis function in depression, this study investigates the effects of buspirone, a 5-HT1A receptor agonist, on post-DST ACTH and cortisol levels in 75 depressed subjects. Plasma post-DST ACTH and cortisol concentrations were significantly increased by the acute administration of buspirone (30 mg PO) compared to placebo. There were no differences in buspirone-induced post-DST ACTH or cortisol responses between minor and major depression. There were significant correlations between post-DST ACTH and cortisol, and between post-DST-buspirone ACTH and cortisol. The buspirone-induced post-DST cortisol responses were significantly higher in depressed women than men. It is concluded that buspirone may augment ACTH and, consequently, cortisol escape from suppression by dexamethasone in major as well as in minor depression.

Adrenocorticotropic Hormone↗
PubMed1996

Simultaneous quantitation of buspirone and its major metabolite 1-(2-pyrimidinyl)piperazine in human plasma by high-performance liquid chromatography with coulometric detection.

Buspirone is a member of the azapirone group of anxiolytic drugs and has one major metabolite, 1-(2-pyrimidinyl)piperazine (1-PP). The analyte, its metabolite and the internal standard were extracted from plasma utilizing solid-phase extraction columns. Chromatography was performed using isocratic reversed-phase high-performance liquid chromatography with coulometric end-point detection. The calibration graph was linear over the range 0-50 ng ml-1 of plasma. The lower limits of quantitation for buspirone and 1-PP were 0.5 and 2 ng ml-1, respectively, when 1 ml of plasma was extracted. The intra-assay relative standard deviations (RSD) over the range of the calibration graph varied from 4 to 12.5% for buspirone and 1-PP. The inter-assay RSD was 6.9% for 1-PP and 9.6% for buspirone. The recovery averaged 96% for buspirone and 66% for 1-PP. Plasma profiles of buspirone and 1-PP following oral dosing are presented.

Adult↗
PubMedDate not supplied

Buspirone attenuates volitional alcohol intake in the chronically drinking monkey.

Four macaque monkeys which showed excessive preference for ethyl alcohol solutions in a self-selection paradigm were used as subjects. Earlier these animals had been given intracerebroventricular (ICV) injections of human cerebrospinal fluid, which produced pharmacologically significant effects on the animals' alcohol consumption. The purpose of the present investigation was to determine whether the parenteral administration of a new anxiolytic compound, buspirone, would alter the pattern of alcohol drinking already established in the monkey. Initially the maximally selected concentration of alcohol of 12% was determined on the basis of a standard ad lib alcohol-water preference screen. Each monkey was offered 12% alcohol and water for a basal pre-injection period of 4 days. Then, on each of the next three days, either the saline control vehicle or buspirone, 1.25, 5.0 or 20.0 mg/kg, was injected intramuscularly at 930 and 1630 hours. On these days, behavioral observations were recorded before and after buspirone's administration in order to evaluate the latency as well as recovery from the drug's effect. Subsequently, a four-day post-injection, 12% alcohol-water test was conducted. Although the saline control and 1.25 mg/kg dose of buspirone were without effect on alcohol intake, both the 5.0 and 20.0 mg/kg doses of buspirone attenuated significantly the consumption of alcohol by the monkeys. This reduction in terms of absolute g/kg as well as the proportion of alcohol to water ingested was approximately 30-60% of baseline intakes. Following buspirone treatment, the amount of alcohol consumed returned essentially to previously high levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggression↗
PubMedDate not supplied

Buspirone alters alcohol drinking induced in rats by tetrahydropapaveroline injected into brain monoaminergic pathways.

The effect of the novel anxiolytic, buspirone, administered systemically was determined in Sprague-Dawley rats induced to drink ethyl alcohol chronically by repeated microinjections of 25 ng/microliter tetrahydropapaveroline HBr (THP) into brain-stem monoaminergic pathways. Self-selection of alcohol in concentrations from 3% to 30% was determined for each rat in a free-choice drinking situation with water available as the alternative fluid. After stereotaxic implantation of guide tubes, THP was microinjected repeatedly into striatal lemniscal and preoptic sites which were found to mediate significant increases in alcohol preference. After the baseline level of intake of a single, maximally preferred alcohol concentration was established, each rat was treated with either saline vehicle or buspirone given intramuscularly b.i.d. in doses of 5.0 mg/kg or 20 mg/kg. Overall, the repeated administration of either dose of buspirone produced a significant decrease in the voluntary alcohol intake of the rats as measured by the proportion measure and absolute g of alcohol ingested. However, the alteration in drinking varied from animal to animal with respect to both magnitude and duration of the anxiolytic's effect. The response to buspirone seemed to be dependent in part on the individual site in each animal at which THP had been infused to evoke alcohol intake. Post-mortem histological analysis revealed that buspirone-treated rats reduced alcohol consumption by 83% if THP had been microinjected into substantia nigra; by 60% if given in the nucleus accumbens-preoptic area; and by 34% when injected into the medial lemniscus-zona incerta. These results suggest, therefore, that buspirone can exert a specific effect in attenuating the consumption of alcohol of the rat in a free-choice situation. In relation to the differential actions of the anxiolytic, it is envisaged that on an anatomical basis the antagonism of alcohol drinking may be mediated by a pharmacological alteration of circumscribed pathways associated with dopaminergic or serotonergic neurons.

Alcohol Drinking↗