Pharmacology, biochemistry, and behavior
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Pharmacol. Biochem. Behav. · Nov 2014
Controlled Clinical Trial7 mg nicotine patch fails to enhance P300 neural indices of cognitive control among nonsmokers.
Nicotine administration facilitates and nicotine deprivation reduces cognitive control in smokers. Importantly, nicotine effects on cognition may reinforce smoking behavior, especially among individuals who have cognitive deficits. The target P300 (P3b) and distracter P300 (P3a) are well-validated electrocortical markers of attention- and memory-related cognitive control processes. ⋯ Nicotine did not enhance P3b or P3a amplitudes, nor did trait cognitive control moderate the influence of nicotine on these indices. Nicotine-induced changes in P3 amplitudes may be limited to nicotine deprivation and/or nonsmokers may be fundamentally different with respect to the influence of nicotine on P3b/P3a indices of cognitive control. Directions for future research that may further examine the effects of nicotine on P3b/P3a independent of withdrawal reversal are discussed.
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Pharmacol. Biochem. Behav. · Nov 2014
Establishment and characterization of an optimized mouse model of multiple sclerosis-induced neuropathic pain using behavioral, pharmacologic, histologic and immunohistochemical methods.
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) that causes debilitating central neuropathic pain in many patients. Although mouse models of experimental autoimmune encephalomyelitis (EAE) have provided insight on the pathobiology of MS-induced neuropathic pain, concurrent severe motor impairments confound quantitative assessment of pain behaviors over the disease course. To address this issue, we have established and characterized an optimized EAE-mouse model of MS-induced neuropathic pain. ⋯ Single bolus doses of amitriptyline (1-7mg/kg), gabapentin (10-50mg/kg) and morphine (0.1-2mg/kg) evoked dose-dependent analgesia in the bilateral hindpaws of EAE-mice; the corresponding ED50s were 1.5, 20 and 1mg/kg respectively. At day 39 p.i. in EAE-mice exhibiting mechanical allodynia in the hindpaws, there was marked demyelination and gliosis in the brain and lumbar spinal cord, mirroring these pathobiologic hallmark features of MS in humans. Our optimized EAE-mouse model of MS-associated neuropathic pain will be invaluable for future investigation of the pathobiology of MS-induced neuropathic pain and for efficacy profiling of novel molecules as potential new analgesics for improved relief of this condition.
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Pharmacol. Biochem. Behav. · Oct 2014
Possible involvement of CA1 5-HT1B/1D and 5-HT2A/2B/2C receptors in harmaline-induced amnesia.
In the present study, effects of the serotonergic system of the dorsal hippocampus (CA1) on harmaline-induced amnesia were examined. A single-trial step-down passive avoidance task was used for the assessment of memory retention in adult male NMRI mice. Pre-training intra-peritoneal (i.p.) administration of harmaline (1mg/kg) induced impairment of memory retention. ⋯ Furthermore, pre-training intra-CA1 injection of subthreshold dose of CP94253 (0.05 ng/mouse) or GR127935 (0.005 ng/mouse) reversed impairment of memory acquisition induced by harmaline (1 mg/kg, i.p.). However, pre-training intra-CA1 infusion of subthreshold dose of α-methyl 5-HT (0.005 ng/mouse) or cinancerine (0.005 ng/mouse) with the administration of harmaline (0.5 and 1 mg/kg, i.p.) heighten impairment of memory acquisition. These findings implicate the involvement of CA1 serotonergic mechanism in harmaline-induced impairment of memory acquisition.
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Pharmacol. Biochem. Behav. · Oct 2014
Effects of intrathecal and intracerebroventricular administration of luteolin in a rat neuropathic pain model.
Luteolin, a major component of flavones, is known to have various physiological properties. Although luteolin reportedly has an antinociceptive effect on acute and inflammatory pain, little is known about its effect on neuropathic pain. The aim of the present study was to determine whether luteolin could ameliorate hyperalgesia in the central nervous system using a neuropathic pain model. ⋯ Supraspinal application of luteolin had no antihyperalgesic effects in any test. These findings suggest that luteolin ameliorates mechanical and cold hyperalgesia at least in part by activating GABAA receptors in a flumazenil-insensitive manner and μ-opioid receptors in the spinal cord, but that the supraspinal regions are unlikely to contribute to the antihyperalgesic action of luteolin. Luteolin could be a candidate therapeutic agent for neuropathic pain.
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Pharmacol. Biochem. Behav. · Oct 2014
Ibuprofen suppresses depressive like behavior induced by BCG inoculation in mice: role of nitric oxide and prostaglandin.
Prostaglandins (PGs) and nitric oxide (NO) may be involved in the pathophysiology of depression. Since NSAIDs decrease PGs and NO production, they may have an antidepressant effect. The aim of the present work was to explore a possible antidepressant action of ibuprofen in the new model of Bacillus Calmette-Guerin (BCG) induced depression. ⋯ On the other hand, l-arginine administered at a dose of 6 g/l in drinking water together with ibuprofen or fluoxetine reversed their effect on FST, TST and cerebral PGE2 and NO levels. Immunohistochemistry showed a decrease in COX-1 and i-NOS immunoreactivity in the CA1 and CA3 areas of the hippocampus following ibuprofen treatment. These results suggest that ibuprofen may have an antidepressant effect through inhibition of PGE2 and NO production, especially in depression secondary to chronic inflammation.