Fig. 6.
Phosphodiesterase 2A in the spinal cord modulates hypersensitivity induced by cyclic adenosine monophosphate (cAMP). Time course of mechanical hypersensitivity induced by intrathecal administration of cAMP (40 nmol; n = 8; A), the cAMP analog Sp-8-Br-cAMPS (20 nmol; n = 8; B), cyclic guanosine monophosphate (cGMP; 40 nmol; n = 6; C), or the nitric oxide donor NOC-5 (10 μg; n = 8; D). One hour before intrathecal drug delivery, mice were intraperitoneally pretreated with 3 mg/kg BAY 60–7550 or vehicle. Data indicate that the BAY 60–7550 pretreatment increased the extent of hypersensitivity induced by cAMP or Sp-8-Br-cAMPS (*P < 0.05, representing group main effects) but not the hypersensitivity evoked by cGMP or NOC-5. n.s. = not significant.

Phosphodiesterase 2A in the spinal cord modulates hypersensitivity induced by cyclic adenosine monophosphate (cAMP). Time course of mechanical hypersensitivity induced by intrathecal administration of cAMP (40 nmol; n = 8; A), the cAMP analog Sp-8-Br-cAMPS (20 nmol; n = 8; B), cyclic guanosine monophosphate (cGMP; 40 nmol; n = 6; C), or the nitric oxide donor NOC-5 (10 μg; n = 8; D). One hour before intrathecal drug delivery, mice were intraperitoneally pretreated with 3 mg/kg BAY 60–7550 or vehicle. Data indicate that the BAY 60–7550 pretreatment increased the extent of hypersensitivity induced by cAMP or Sp-8-Br-cAMPS (*P < 0.05, representing group main effects) but not the hypersensitivity evoked by cGMP or NOC-5. n.s. = not significant.

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