Neurogastroenterology and motility · 2018
The central effects of buspirone on abdominal pain in rats.
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Panteleev S S, Sivachenko I B, Lyubashina O A
Аннотация
BACKGROUND: Buspirone, a partial agonist of the 5-HT1a receptor (5-HT1a R), owing to potential antinociceptive properties may be useful in treatment of abdominal pain in IBS patients. The pain-related effects of buspirone are mediated via the 5-HT1a Rs, specifically located within the ventrolateral medulla (VLM). The most animal studies of the 5-HT1a R involvement in pain control have been carried out with somatic behavioral tests. The 5-HT1a R contribution in visceral pain transmission within the VLM is unclear. The objective of our study was to evaluate the 5-HT1a R contribution in abdominal pain transmission within the VLM.
METHODS: Using animal model of abdominal pain (urethane-anaesthetized rats), based on the noxious colorectal distension (CRD) as pain stimulus we studied effects of buspirone (1.0-4.0 mg kg-1 , iv) on the CRD-induced VLM neuron and blood pressure responses as markers of abdominal pain before and after the 5-HT1a R blockade by antagonist, WAY 100,635.
RESULTS: The CRD induced a significant increase in VLM neuron activity up to 201.5 ± 18.0% and depressor reactions up to 68 ± 1.8% of baseline. Buspirone (1.0-4.0 mg kg-1 , iv) resulted in an inhibition of the CRD-induced neuron responses which were changed inversely with dose increase and decreased depressor reactions directly with dose increase. These effects were antagonized by intracerebroventricular WAY 100,635.
CONCLUSION: Buspirone exerts complex biphasic action on the pain-related VLM neuron activity inversely depending on dose. The final effect of buspirone depends on the functional balance between of activation the pre- and postsynaptic 5-HT1a Rs in mediating pain control networks.
METHODS: Using animal model of abdominal pain (urethane-anaesthetized rats), based on the noxious colorectal distension (CRD) as pain stimulus we studied effects of buspirone (1.0-4.0 mg kg-1 , iv) on the CRD-induced VLM neuron and blood pressure responses as markers of abdominal pain before and after the 5-HT1a R blockade by antagonist, WAY 100,635.
RESULTS: The CRD induced a significant increase in VLM neuron activity up to 201.5 ± 18.0% and depressor reactions up to 68 ± 1.8% of baseline. Buspirone (1.0-4.0 mg kg-1 , iv) resulted in an inhibition of the CRD-induced neuron responses which were changed inversely with dose increase and decreased depressor reactions directly with dose increase. These effects were antagonized by intracerebroventricular WAY 100,635.
CONCLUSION: Buspirone exerts complex biphasic action on the pain-related VLM neuron activity inversely depending on dose. The final effect of buspirone depends on the functional balance between of activation the pre- and postsynaptic 5-HT1a Rs in mediating pain control networks.