All these findings support the neuroprotective role of (MeOPhSe)(2) in a mice model of SDAT induced by i.c.v. STZ. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated

by drugs of abuse, GSK126 solubility dmso using nonspecific beta-adrenergic receptor (beta-AR) antagonists. Remarkably little is known about the role of the specific beta-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of beta(1) and beta(2), as well as alpha(1)-adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the beta(2) antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the alpha(1) antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated preference during a subsequent test, while

the beta(1) antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Pexidartinib nmr Furthermore, post-test microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for alpha(1)- and beta(2)-specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.”
“The transient receptor potential vanilloid type 1 (TRPV1) is a non-selective Selleck JIB04 ligand-gated cationic channel. The distribution

of TRPV1 mRNA in various regions of the brain has been successfully established. Methamphetamine (MAP) is a psychostimulant and a major drug of abuse in many parts of the world. The powerful rewarding properties of MAP are attributed to multiple pharmacological actions, but the mechanistic association between TRPV1 expression and MAP-induced drug addiction has not established. In the present study, we conducted a time-course analysis of TRPV1 mRNA levels in the frontal cortex, striatum, and hippocampus of mouse brain following repeated MAP (2 mg/kg, i.p.) treatment. Our results demonstrate that expression of TRPV1 mRNA is significantly increased 1, 2, 6, 24, 48 h, and 1 week after the last MAP treatment in the frontal cortex but not in the striatum or hippocampus. These data support a potential role for TRPV1 in the treatment of MAP-induced drug addiction. (C) 2010 Elsevier Ireland Ltd. All rights reserved.