Neuroscience letters
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Neuroscience letters · Aug 2002
Involvement of adenosine in the anti-allodynic effect of amitriptyline in streptozotocin-induced diabetic rats.
Recent observations suggest the involvement of adenosine in the peripheral antinociceptive effect of amitriptyline in nerve-injury-induced neuropathic pain. The aim of the present investigation was to evaluate, firstly, the peripheral and systemic effects of amitriptyline on tactile allodynia in the streptozotocin (STZ)-induced diabetic rat model of neuropathic pain and, secondly, whether caffeine coadministration affects the actions of amitriptyline. Diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (50 mg/kg), and tactile allodynia was detected by application of von Frey filaments to the ventral surface of the hindpaw. ⋯ Coadministration of caffeine (5 mg/kg, i.p.; 1500 nmol, s.c.), at doses which produced no effect on its own, partially reversed systemic and local anti-allodynic effects of amitriptyline. These results indicate an anti-allodynic effect of both peripheral and systemic amitriptyline, and suggest the involvement of endogenous adenosine in the action of amitriptyline in this rat model of painful diabetic neuropathy. These data also suggest that topical application of tricyclic antidepressants may be useful in treating neuropathic pain in diabetics.
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Neuroscience letters · Aug 2002
Attentional modulation of human pain processing in the secondary somatosensory cortex: a magnetoencephalographic study.
The influence of attention on the processing of pain in the secondary somatosensory cortex (SII) was analyzed using magnetoencephalography in response to painful infra-red heat stimuli applied to the left hand in six male healthy subjects, aged 22-28 years. Three experimental paradigms were chosen to deliver attention dependent results under comparable levels of vigilance. ⋯ In contrast, further increase of attention from mid-level to high was not accompanied by an additional enhancement of SII activity. It therefore is concluded that activation patterns of SII follow a saturation function which cannot be enlarged by maximizing the relevance of the painful stimuli.