Brain research
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Met-Enkephalin, which can be induced by estrogen in the ventromedial nucleus of hypothalamus (VMH), has been proposed to help mediate estrogenic action on lordosis behavior by acting on midbrain periaqueductal gray (PAG) neurons. Also, in the PAG, GABA may locally regulate the levels of lordosis behavior through GABAA receptors. Therefore, we examined the effects of both Met-enkephalin and GABA-related agents on neuronal activity of PAG neurons in slices. ⋯ Moreover, 76% of neurons inhibited by enkephalin were found to be tonically inhibited by endogenous GABA through GABAA receptors. It is argued, therefore, that increased enkephalinergic influences from the VMH to the PAG in estrogen-treated females could participate in the PAG neuronal control of lordosis by acting on the same neurons as are innervated by intrinsic GABAergic neurons. Since GABAA agonists actually facilitate lordosis in the PAG, these PAG neurons inhibited by both GABA and enkephalin may themselves facilitate behaviors which are antagonistic to lordosis, such as defensive behaviors.
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We tested the ability of Mg2+ therapy to block the heat-hyperalgesia, mechano-allodynia and mechano-hyperalgesia that are seen in rats with an experimental painful peripheral neuropathy (the CCI model of Bennett and Xie). Systemic Mg2+ (magnesium sulfate, 600 mg/kg, s.c.) significantly reduced heat-hyperalgesia and mechano-allodynia for 2-24 h post-injection, but had no effect on mechano-hyperalgesia. Intrathecal (i.t.) injections of Mg2+ (185-750 micrograms) at the level of the lumbar spinal cord significantly reduced heat-hyperalgesia, but perineural application (750 and 7,000 micrograms) to the site of nerve injury had no effect. ⋯ Mg2+ had any effect on the responses from the control, sham-operated side. We conclude that Mg2+ has a spinal site of action. Mg2+ therapy may be of limited use in the treatment of human painful peripheral neuropathy.
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The purpose of this investigation was to determine the effect of experimental conditions on the concentrations of atenolol and acetaminophen in brain microdialysate, and to investigate the feasibility of performing repeated experiments within individual rats. Following intravenous bolus administration, reproducible concentration-time profiles were obtained in plasma and in brain dialysate. Based on corrections for in vitro recoveries of the intracerebral probe, the estimated ratio of the AUC in brain extracellular fluid (AUCbrain ECF) over the AUC in plasma (AUCplasma) +/- S. ⋯ Using a hypotonic perfusion solution the ratio of AUCbrain ECF values was 100: 154: 114% for acetaminophen and 100: 378: 427% for atenolol. A clear effect of the temperature of the hypotonic perfusate (24 vs 38 degrees C) on acetaminophen AUCbrain ECF values was revealed. The ratio of AUCbrain ECF values obtained at 24: 38 degrees C was 192: 100%.(ABSTRACT TRUNCATED AT 250 WORDS)