Influence of repeated treatment with buspirone on central 5-hydroxytryptamine and dopamine synthesis

Tunnicliff, G.; Brokaw, James J.; Hausz, J. A.; Matheson, G.K.; White, Gary W.

doi:10.1016/0028-3908(92)90099-b

Cited by 25 publications

(11 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Using microdialysis, it was shown that acute reserpine administration increases the extracellular concentration of 5-HT (Martin and Artigas 1992), which could stimulate 5-HT autoreceptors and decrease 5-HT synthesis through a feedback mechanism (Briley and Moret 1993). This is supported by the findings that acute (Tunnicliff et al 1992) or local (Invernizzi et al 1991) administration of buspirone (a 5-HT1A agonist) reduces 5-HT synthesis. However, both investigations determined that 5-HT synthesis using 5-HTP accumulation after NSD-1015 induced inhibition of decarboxylase activity.…”

Section: C) 14mentioning

confidence: 89%

The Acute Effects of Reserpine and NSD-1015 on the Brain Serotonin Synthesis Rate Measured by an Autoradiographic Method

Mück‐Šeler

Dikšić

1995

Neuropsychopharmacology

View full text Add to dashboard Cite

The rate of serotonin (5-HT) synthesis was measured in the discrete regions of the rat brain utilizing an autoradiographic method and a[ 14 CJ methyl-L-tryptophan as a tracer after an acute treatment with reserpine (10 mg/kg IP) or NSD-1015 (m-hydroxybenzylhydrazine) (100 mg/kg IPIn the 1970s and the 1980s abundant investigations of the central serotoninergic system has led to the conclusion that serotonin (5-HT) plays a role in the regulation 1993 (abstract No. 126.18).

show abstract

Section: C) 14mentioning

confidence: 89%

The Acute Effects of Reserpine and NSD-1015 on the Brain Serotonin Synthesis Rate Measured by an Autoradiographic Method

Mück‐Šeler

Dikšić

1995

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…Specifically, since buspirone seems to block preferentially presynaptic dopamine receptors as compared to the postsynaptic ones (19), it was suggested that the ability of chronic buspirone treatment to attenuate the development of behavioral supersensitivity could be related to the development of presynaptic dopamine receptor supersensitivity (leading to a decreased availability of dopamine in the synaptic cleft). In line with this possibility, while Tunnicliff et al (20) showed that withdrawal from repeated treatment with buspirone led to marked reductions in the synthesis of dopamine in the rat striatum, we have shown that the drug potentiates yawning behavior induced by small doses of apomorphine (16), which is considered a behavioral parameter of nigrostriatal dopaminergic presynaptic function (21). In addition, we have demonstrated that withdrawal from longterm haloperidol treatment at doses that selectively block dopamine autoreceptors decreases open-field behavior, suggesting that the development of dopamine autoreceptor supersensitivity can attenuate the behavioral effects produced by postsynaptic dopamine receptor supersensitivity (22).…”

mentioning

confidence: 83%

Acute buspirone abolishes the expression of behavioral dopaminergic supersensitivity in mice

Queiroz

Alcântara

Yagüe

et al. 2002

Braz J Med Biol Res

View full text Add to dashboard Cite

Previous studies have shown that rats withdrawn from long-term treatment with dopamine receptor blockers exhibit dopaminergic supersensitivity, which can be behaviorally evaluated by enhanced general activity observed in an open-field. Recently, it has been reported that co-treatment with the non-benzodiazepine anxiolytic buspirone attenuates the development of haloperidol-induced dopaminergic supersensitivity measured by open-field behavior of rats. The aims of the present study were: 1) to determine, as previously reported for rats, if mice withdrawn from long-term neuroleptic treatment would also develop dopaminergic supersensitivity using open-field behavior as an experimental paradigm, and 2) to examine if acute buspirone administration would attenuate the expression of this behavioral dopaminergic supersensitivity. Withdrawal from longterm haloperidol treatment (2.5 mg/kg, once daily, for 20 days) induced a significant (30%) increase in ambulation frequency (i.e., number of squares crossed in 5-min observation sessions) but did not modify rearing frequency or immobility duration in 3-month-old EPM-M1 male mice observed in the open-field apparatus. Acute intraperitoneal injection of buspirone (3.0 and 10 but not 1.0 mg/kg, 12-13 animals per group) 30 min before open-field exposure abolished the increase in locomotion frequency induced by haloperidol withdrawal. These data suggest that the open-field behavior of mice can be used to detect dopaminergic supersensitivity, whose expression is abolished by acute buspirone administration.

show abstract

“…Previously, we have shown that a decrease in brain 5-HT metabolism owing to the stimulation of somatodendritic 5-HT-1A receptors is involved in the anticataleptogenic profile of buspirone (Haleem et al, 2004). Other authors have reported that repeated administration of buspirone decreases the responsiveness of somatodendritic 5-HT-1A receptors (Tunnicliff et al, 1992;Okazawa et al, 1999). It is therefore possible that on repeated administration tolerance is produced to the anticataleptogenic effects of buspirone.…”

Section: Introductionmentioning

confidence: 92%

Reversal of haloperidol-induced extrapyramidal symptoms by buspirone: a time-related study

Haleem

Samad²,

Haleem³

2007

Behavioural Pharmacology

View full text Add to dashboard Cite

Effects of coadministration of buspirone were investigated on the time course of haloperidol-induced extrapyramidal symptoms in rats. Rats treated with haloperidol at a dose of 1 mg/kg exhibited impaired motor coordination and a decrease in exploratory activity. Coadministration of buspirone at a dose of 1 mg/kg attenuated haloperidol-induced deficits of motor coordination but no effect was produced on the deficits of exploratory activity, possibly because of a 'floor effect'. Long-term administration of haloperidol (1 mg/kg) twice a day for 5 weeks did not produce tolerance to haloperidol-induced deficits of exploratory activity. The deficits of motor coordination were attenuated after 4-5 weeks of drug administration. Coadministration of buspirone for 3-5 weeks attenuated and reversed haloperidol-induced deficits of exploratory activity. Deficits of motor coordination were smaller in rats cotreated with buspirone after 1 week but not after 2-5 weeks. Administration of haloperidol for 2 weeks elicited vacuous chewing movements with twitching of facial musculature that increased in a time-dependent manner as the treatment continued to 5 weeks. Animals cotreated with buspirone exhibited a gradual reversal of the response during 2-5 weeks of treatment. The mechanism involved in the attenuation/reversal of haloperidol-induced extrapyramidal symptoms by buspirone is discussed. Prior administration of buspirone for 2 weeks may be of help in the improvement of extrapyramidal symptoms induced by antipsychotic drugs.

show abstract

Influence of repeated treatment with buspirone on central 5-hydroxytryptamine and dopamine synthesis

Cited by 25 publications

References 17 publications

The Acute Effects of Reserpine and NSD-1015 on the Brain Serotonin Synthesis Rate Measured by an Autoradiographic Method

The Acute Effects of Reserpine and NSD-1015 on the Brain Serotonin Synthesis Rate Measured by an Autoradiographic Method

Acute buspirone abolishes the expression of behavioral dopaminergic supersensitivity in mice

Reversal of haloperidol-induced extrapyramidal symptoms by buspirone: a time-related study

Contact Info

Product

Resources

About