Pharmacology, biochemistry, and behavior
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Pharmacol. Biochem. Behav. · Sep 2014
Antidepressant-like effects of salidroside on olfactory bulbectomy-induced pro-inflammatory cytokine production and hyperactivity of HPA axis in rats.
Salidroside (SA) is the primary bioactive marker compound in the standardized extracts from Rhodiola rosea. Although it has potential antidepressant activity in a rat behavioral despair model, the mechanisms of antidepressant effect for SA remain unclear. The objective of this study was to evaluate the antidepressant effects of SA and to discuss the potential mechanisms in olfactory bulbectomized (OBX) rats. ⋯ The antidepressant mechanisms of SA might be associated with its anti-inflammatory effects and the regulation of HPA axis activity. Reversal of abnormalities of GR may be partly responsible for those effects. These findings suggested that SA might become a beneficial agent to prevent and treat the depression.
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Pharmacol. Biochem. Behav. · Sep 2014
Chronic activation of sigma-1 receptor evokes nociceptive activation of trigeminal nucleus caudalis in rats.
Primary headache disorders, including migraine, are thought to be mediated by prolonged nociceptive activation of the trigeminal nucleus caudalis (TNC), but the precise mechanisms are poorly understood. Our past studies demonstrated that sigma-1 receptors (Sig-1R) facilitate spinal nociceptive transmission in several pain models. Based on these findings, this study asked if chronic activation of Sig-1R by intracisternal administration of the selective Sig-1R agonist, PRE084, produced TNC neuronal activation as a migraine trigger in rats. ⋯ Following 14 days of PRE084 infusion, the number of Fos-IR increased until day 7 after final infusion. Moreover, by day 14, Fos-IR associated with PRE084 infusion was significantly reversed by NMDA receptor antagonist MK801, rather than BD1047. These findings indicated that chronic activation of Sig-1R could evoke prolonged neuronal activation in the trigeminovascular system.
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Pharmacogenetic research has the potential to explain the variation in treatment efficacy within patient populations. Understanding the interaction between genetic variation and medications may provide a method for matching patients to the most effective therapeutic options and improving overall patient outcomes. ⋯ Genetic variants in OPRM1, particularly the non-synonymous polymorphism A118G, have been repeatedly associated with the efficacy of treatments for pain and various types of dependence. This review focuses on the current understanding of the pharmacogenetic impact of OPRM1, primarily with regard to the treatment of pain and addiction.
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Pharmacol. Biochem. Behav. · Jul 2014
Randomized Controlled TrialBaseline-dependent modulating effects of nicotine on voluntary and involuntary attention measured with brain event-related P3 potentials.
Cholinergic stimulation produces cognitive effects that vary across individuals, and stimulus/task conditions. As of yet, the role of individual differences in moderating the effects of the nicotinic acetylcholine receptor agonist nicotine on specific attentional functions and their neural and behavioral correlates is not fully understood. ⋯ Exhibiting an inverted-U nicotine response profile, target P3b and standard N1 amplitudes were increased and decreased in participants with low and high baseline amplitudes, respectively. In all, the findings corroborate the involvement of nicotinic mechanisms in attention, generally acting to increase attentional capacity in relatively low attentional functioning (reduced baseline ERPs) individuals, while having negative or detrimental effects in those with medium/high attentional levels (increased baseline ERPs), and in a manner that is differentially expressed during bottom-up (involuntary) attentional capture and top-down (voluntary) attentional allocation.
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Pharmacol. Biochem. Behav. · Jul 2014
Intrathecal injection of selected peptide Myr-RC-13 attenuates bone cancer pain by inhibiting KIF17 and NR2B expression.
Although bone cancer pain is a common intractable clinical symptom, its underlying mechanisms are still elusive. Accumulating evidence reveals that the N-methyl-D-aspartate (NMDA) receptor containing a 2B subunit (NR2B) in the spinal cord contributes to bone cancer pain. Our preliminary study demonstrated that intrathecal injection of fusion peptide Myr-RC-13 could disrupt spinal KIF17/mLin10 interaction, which is an essential component of KIF17-mediated NR2B transport. ⋯ In addition, repetitive spinal delivery of Myr-RC-13 relieved bone cancer-related mechanical allodynia and spontaneous pain behaviors, and down-regulated expression of spinal KIF17 and NR2B. Finally, our results demonstrated that selected peptide Myr-RC-13 was able to attenuate bone cancer pain via decreasing spinal KIF17 and NR2B expressions. Therefore, selected peptide Myr-RC-13 might be a potential analgesic strategy for bone cancer pain.