Brain research
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Comparative Study
Postischemic mild hypothermia reduces neurotransmitter release and astroglial cell proliferation during reperfusion after asphyxial cardiac arrest in rats.
The present study investigated whether postischemic mild hypothermia attenuates the ischemia-induced striatal glutamate (GLU) and dopamine (DA) release, as well as astroglial cell proliferation in the brain. Anesthetized rats were exposed to 8 min of asphyxiation, including 5 min of cardiac arrest. The cardiac arrest was reversed to restoration of spontaneous circulation (ROSC), by brief external heart massage and ventilation within a period of 2 min. ⋯ Histological analysis of the brain showed that postischemic mild hypothermia reduced brain damage, ischemic neurons, as well as astroglial cell proliferation. Thus, postischemic mild hypothermia reduces the excitotoxic process, brain damage, as well as astroglial cell proliferation during reperfusion. Moreover, these results emphasize the trigger effect of dopamine on the excitotoxic pathway.
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Comparative Study
Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain.
Recently, our laboratory has proposed the avulsion of rat brachial plexus as a new and reliable model for the study of neuropathic pain. In this model, the neuropathy can be detected even at distant sites from the injury, both in ipsilateral and contralateral hindpaws. The purpose of this study was to pharmacologically characterise this behavioural model of persistent peripheral neuropathic pain by assessing the effects of several analgesic drugs currently used in clinical practice. ⋯ The non-steroidal anti-inflammatory drug diclofenac (100 mg/kg, i.p.), the steroidal anti-inflammatory dexamethasone (1.5 mg/kg, i.p.) and the antidepressant imipramine (10 mg/kg, i.p.) all failed to significantly attenuate both mechanical and cold allodynia in the rats following avulsion of brachial plexus. These findings suggest that avulsion-associated mechanical and cold allodynia, two classic signs of persistent neuropathic pain, were consistently prevented by several analgesics currently available in clinical practice, namely morphine, clonidine, ketamine and gabapentin, and to a lesser extent by celecoxib and lidocaine. Therefore, this new proposed model of persistent nociception seems to be suitable for the study of the underlying mechanisms involved in neuropathic pain and for the identification of potential clinically relevant drugs to treat this aspect of peripheral neuropathy.
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Differences exist in vascular function and disease susceptibility in males and females, and estrogen is apparently a primary factor. One mechanism by which estrogen may influence vascular function is by affecting vasomotor innervation. We have shown previously that estrogen increases calcitonin gene-related peptide (CGRP)-immunoreactive sensory innervation of the rat mammary gland, but it is not known if this occurs in other tissues. ⋯ However, estrogen did not affect CGRP-immunoreactive nerve density of superficial epigastric, femoral, or uterine arteries, or foot skin. Therefore, estrogen increases sensory innervation of arterioles, but not of large arteries or skin. We conclude that sensory nociceptor vasodilatory innervation of arterioles is selectively enriched by estrogen, which may influence cardiovascular function in health and disease.
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Reward is an important factor motivating food intake in satiated animals. Two sites involved in the reward response are the ventral tegmental area (VTA) and the nucleus accumbens shell region (sNAcc), between which communication is partially regulated by opioids and dopamine (DA). Previous studies have shown that the mu-opioid agonist Tyr-D-Ala-Gly-MePhe-Gly(ol)-enkephalin (DAMGO) dose-dependently enhances food intake in satiated animals when injected into either the VTA or the sNAcc. ⋯ Food intake elicited by DAMGO (2 or 5 nmol) injected unilaterally into the VTA was dose-dependently diminished by bilateral injection of NTX (2.5, 5, and 25 g/side) or the D1 antagonist SCH 23390 (3, 1, 0.3, 0.15, 0.05, and 0.015 nmol/side) into the sNAcc. When DAMGO (5 nmol) was injected into the sNAcc, the resulting food intake was decreased by doses of SCH 23390 ranging from 0.05 to 100 nmol/side injected bilaterally into the VTA, but not by equimolar doses of Raclopride, a D2 antagonist. These results, combined with previous findings, suggest a signaling pathway between the VTA and the sNAcc in which opioids and DA facilitate feeding in an interdependent manner.
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Comparative Study
Nitric oxide pathway in the nucleus raphe magnus modulates hypoxic ventilatory response but not anapyrexia in rats.
Nucleus raphe magnus (NRM) is one of the cellular groups of the brainstem that is involved in the physiologic responses to hypoxia and contains nitric oxide (NO) synthase. In the present study, we assessed the role of NO pathway in the NRM on the hypoxic ventilatory response (HVR) and anapyrexia (a regulated decrease in body temperature). To this end, pulmonary ventilation (VE) and body temperature (Tb) of male Wistar rats were measured before and after microinjection of N-monomethyl-L-arginine (L-NMMA, a nonselective nitric oxide synthase inhibitor, 12.5 microg/0.1 microl) into the NRM, followed by hypoxia. ⋯ Typical hypoxia-induced hyperventilation and anapyrexia were observed after saline treatment. L-NMMA into the NRM reduced the HVR but did not affect hypoxia-induced anapyrexia. In conclusion, the present study indicates that NO in the NRM is involved in HVR, exerts an inhibitory modulation on the NRM neurons but does not mediate hypoxia-induced anapyrexia.