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The purpose of the present study was to examine the effect of blockade of N-methyl-D-aspartate (NMDA) receptors on the depolarization associated with severe hypoglycemia, which is commonly preceded by one or a few transient depolarizations reminiscent of cortical spreading depression (CSD). In the cerebral cortices of rats [K+]e and [Ca2+]e were measured(More)
The nonopioid actions of spinal dynorphin may promote aspects of abnormal pain after nerve injury. Mechanistic similarities have been suggested between opioid tolerance and neuropathic pain. Here, the hypothesis that spinal dynorphin might mediate effects of sustained spinal opioids was explored. Possible abnormal pain and spinal antinociceptive tolerance(More)
Nerve injury can produce hypersensitivity to noxious and normally innocuous stimulation. Injury-induced central (i.e. spinal) sensitization is thought to arise from enhanced afferent input to the spinal cord and to be critical for expression of behavioral hypersensitivity. Descending facilitatory influences from the rostral ventromedial medulla have been(More)
Peptide histidine-isoleucine (PHI) is a regulatory peptide, synthesized as part of the same propeptide that includes also vasoactive intestinal peptide (VIP). The present study describes the distribution of PHI-immunoreactive nerve fibers in the sheep pineal organ and compares their location with the distribution of VIP-immunoreactive fibers in both normal(More)
This study describes the distribution of peptide sequences derived from the prepro-vasoactive intestinal polypeptide (preproVIP) molecule in perivascular nerves of rat brain arteries and arterioles. The peptides were identified by immunohistochemistry using highly specific antibodies. Five peptide sequences (preproVIP 60-76, peptide histidine isoleucine(More)
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