Brain research
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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)
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The effect of dopamine (DA) receptor agonists and antagonists on hypoxia/hypoglycemia (ischemia)-induced decrease in CA1 presynaptic fiber spikes elicited by the stimulation of Schaffer collateral were investigated using hippocampal slices. Treatment with D1 dopamine receptor antagonist, SCH23390 produced a concentration-dependent attenuation of the ischemia-induced decrease of presynaptic potentials. The magnitude of recovery of the CA1 presynaptic potential in SCH233390-treated slices at 10 and 100 microM was 28 and 54%, respectively. ⋯ The decrease of CA1 presynaptic potential by ischemia was affected by neither D2 dopamine receptor agonist, bromocriptin and quinpirole nor D2 dopamine receptor antagonist, sulpiride. The neuroprotective effect of SCH23390 was completely blocked by cotreatment with SKF38393. The present results demonstrated that the blockade of D1 dopamine receptor function played a neuroprotective role in ischemic damage, suggesting a facilitatory role of D1 dopamine receptor-operated function in ischemia-induced neuronal deficits.
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Bradykinin is a nonapeptide that plays a central role in the production of pain and inflammation. A horizontal spinal cord slice preparation with attached dorsal root and dorsal root ganglion was used to study the effect of bradykinin on afferent fibers. Intracellular recordings were made from dorsal root ganglion and dorsal horn neurons. ⋯ However, the stimulatory effects, both depolarization and firing of action potentials, of bradykinin were resistant to TTX. Replacement of sodium ions with TRIS completely abolished the stimulatory effect of bradykinin on the sensory neurons. Bradykinin potentiated the postsynaptic potentials induced by electrical stimulation of TTX-resistant afferent fibers.(ABSTRACT TRUNCATED AT 250 WORDS)
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Cholecystokinin (CCK) has been shown to reduce the spinal antinociceptive effects of opioid agonists such as morphine. The present study examined the effect of CCK and CCKB antagonists on the spinal antinociception mediated by the selective alpha 2-adrenergic agonist dexmedetomidine. Extracellular recordings of noxious-evoked C fibre responses of dorsal horn convergent neurones were made in the halothane-anaesthetized rat. ⋯ Both CCKB antagonists did increase the inhibition of C fibre-evoked responses by the mu opioid agonists DAGOL and morphine. The results suggest CCK is able to inhibit spinal antinociception mediated via the activation of alpha 2-adrenergic receptors in addition to its well-documented interaction with spinal opioid analgesia. However the antagonist studies indicate an endogenous CCK control of spinal mu opioid mediated antinociception which does not extend to alpha 2-adrenergic antinociception.
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Experiments were conducted to study the effect of the opioid, codeine, on different components of the cough motor pattern. Midcollicular decerebrate cats were paralyzed and artificially ventilated by a pump triggered by the phrenic neurogram. Inspiratory (phrenic) and expiratory (cranial iliohypogastric) neurograms were recorded. ⋯ There was a positive linear relationship between phrenic and cranial iliohypogastric burst amplitudes during fictive cough (r = 0.82, P < 0.001). Codeine destabilized the motor pattern during fictive cough by disrupting this relationship between inspiratory and expiratory burst amplitudes. We conclude: (a) the central pattern generator for cough is functionally organized into a cough frequency generator, an expiratory burst amplitude generator and an inspiratory burst amplitude generator, each of which have different sensitivities to codeine (b) there exists a specific codeine-sensitive neural mechanism matching the relative magnitude of central drive to inspiratory and expiratory motoneurons during cough.