Activation of astrocytes in the spinal cord contributes to the development of bilateral allodynia after peripheral nerve injury in rats.

Activation of spinal cord microglia and astrocytes after peripheral nerve injury contributes to the development of behavioral hypersensitivity. Suppression of spinal cord glial activation attenuates the development of nerve injury-induced allodynia. The contribution of spinal cord glia to existing allodynia, however, is not known.

Carbon dioxide exhalation temporarily increases during electroconvulsive therapy.

Electroconvulsive therapy induces hypermetabolism and elevates oxygen and energy demands, while more carbon dioxide is produced than usual. The purpose of the present study was to determine the elevated carbon dioxide exhalation and the adequate ventilation volume during electroconvulsive therapy. Carbon dioxide exhalation during an electrically induced seizure was continuously monitored by capnography and spirography in 15 patients with endogenous depression.

Antiallodynic effects of intrathecally administered 5-HT(2C) receptor agonists in rats with nerve injury.

Intrathecal administration of serotonin type 2 (5-HT(2)) receptor agonists, alpha-methyl-5-hydroxytryptamine maleate (alpha-m-5-HT) or (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI), produces antiallodynic effects in a rat model of neuropathic pain. In the present study, we examined the antiallodynic effects of intrathecally administered agents which are selective for 5-HT(2C) receptors. Allodynia was produced by tight ligation of the left L5 and L6 spinal nerves, and was measured by applying von Frey filaments to the left hindpaw.