L-type Ca2+ channel blockers inhibit the development but not the expression of sensitization to morphine in mice

Up-regulated l-type high voltage-gated calcium channels cause increase in diazepam binding inhibitor induced by sustained morphine exposure in mouse cerebrocortical neurons

“…Recently, several studies suggest the involvement of enhanced L-type HVCC functions in the development of morphine physical dependent and withdrawal syndrome. That is, L-type HVCC inhibitors attenuate the locomotor-stimulating effects of morphine (Zhang et al, 2003), naloxone-induced opioid supersensitivity (Gullapalli and Ramarao, 2002) and noradrenaline turnover induced by morphine withdrawal (Martinez et al, 2003). We have also demonstrated the close functional relationship between upregulated properties of L-type HVCCs and DBI expression in cerebral cortices from ethanol-and nicotine-treated animals (Katsura et al, 2000;Mohri et al, 2003) and the experimental results showing the increased expression of DBI mRNA in the brains prepared from morphine physical dependent mice (Katsura et al, 1998a).…”

Antagonism of L-type Cav channels with nifedipine differentially affects performance of wildtype and NK1R−/− mice in the 5-Choice Serial Reaction-Time Task

“…These doses were chosen because they have been reported to modify relevant aspects of mouse behavior (e.g. memory retention in a mouse passive avoidance test, Zhang et al, 2003) without affecting locomotor activity (Quartermain et al, 2001). The sequence of doses was counterbalanced across subjects (Latin square).…”

Cyclic AMP-Dependent Protein Kinase A Regulates the Alternative Splicing of CaMKIIδ

“…Ca 2+ /calmodulin–dependent kinase II (CaMKII) is a critical transducer of Ca 2+ signaling in the heart. Cardiac-specific overexpression of CaMKII induces a hypertrophic phenotype that rapidly transitions to dilated cardiomyopathy with ventricular dysfunction, loss of intracellular Ca 2+ homeostasis, and premature death [1], [2], [3], [4]. Inhibition of CaMKII by either pharmacological or genetic approaches reverses heart failure–associated changes (i.e., arrhythmias, hypertrophy, and dysfunction) in animal models of structural heart disease [5], [6].…”