Buspirone is approved in the United States by the FDA for the treatment of anxiety disorders and the short-term relief of the symptoms of anxiety. Likewise in Australia, buspirone is licensed for the treatment of anxiety disorders. In the United Kingdom, buspirone is indicated only for the short-term treatment of anxiety.
Buspirone has been shown in vitro to be metabolized by CYP3A4. This finding is consistent with the in vivo interactions observed between buspirone and these inhibitors inducers of cytochrome P450 3A4 (CYP3A4), among others:
Commercial grapefruit juice: contains rind, the source of the competing compound: Significantly increases the plasma levels of buspirone
The likely mechanism of the interaction caused by grapefruit juice is delayed gastric emptying or inhibition by a substance in grapefruit rind of cytochrome P450 3A4-mediated first-pass metabolism of buspirone.
The occurrence of elevated blood pressure has been reported when buspirone hydrochloride has been added to a regimen including a monoamine oxidase inhibitor (MAOI).
Activated charcoal is believed to be an effective treatment for overdose, provided the patient is treated promptly. Expected symptoms (based on symptoms in male healthy volunteers treated with 375 mg/day — compared to the maximum daily licensed dosage in Australia, the UK, and the US): 
Buspirone appears to be relatively benign in cases of single-drug overdose, although no definitive data on this subject appear to be available. 
Pharmacology and mechanism
Buspirone functions as a serotonin5-HT1A receptorpartial agonist (IA = 0.465). It is this action that is thought to mediate its anxiolytic and antidepressant effects. Additionally, it functions as a presynaptic dopamine antagonist at the D2, D3 and D4 receptors. Buspirone is also a partial α1 receptor agonist. Buspirone also appears to produce some oxytocin stimulation via 5-HT1A receptor-induced action. 
Binding Profile of Buspirone (towards cloned human receptors)
In a 1996 study, buspirone was shown to be effective as an augmentative agent for the treatment of alcohol dependence.
Several studies have shown the administration of buspirone can improve spatial learning and memory function following a traumatic brain injury.
New research is being conducted to test the antagonist properties of buspirone at both D3 and D4 receptors as a pharmacological treatment for cocaine dependence.
In a 2007 study conducted on rats, buspirone showed a complete remission of haloperidol-induced tardive vacuous chewing symptoms when coadministered for five weeks.
Positive results for the treatment of depression when buspirone was combined with melatonin has been shown. It is suspected that the method of action differs from SSRI medications. Preliminary research suggests that the combination of buspirone and melatonin stimulates the growth of new neurons in the brain, also known as neurogenesis.
Comparison to benzodiazepines
Buspirone's efficacy is comparable to that of members of the benzodiazepine family in treating GAD, although it tends to have a delayed onset of action.
Abrupt discontinuation of diazepam after six weeks of continuous administration resulted in withdrawal symptoms. This was not the case when administration of buspirone was ceased after six weeks. It may take several weeks before buspirone's anxiolytic effects become noticeable, and many patients may also need a higher dosage to adequately respond to treatment.
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