L-Type Ca²⁺Channels Mediate Adaptation of Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in the Ventral Tegmental Area after Chronic Amphetamine Treatment

Abstract

L-type

Role of calcineurin in the VTA in rats behaviorally sensitized to methamphetamine

“…Recently, growing evidence suggests an important role for calcineurin in the regulation of neurotransmitter release and synaptic plasticity in the brain (Pulipparacharuvil et al 2008 specific calcineurin knockout mice exhibited impaired working memory and multiple abnormal behaviors, similar to those described in schizophrenia (Miyakawa et al 2003;Zeng et al 2001), indicating the essential role of calcineurin in the regulation of both physiological and pathological processes. The present study showed that the calcineurin A subunit (catalytic subunit) increased in chronic METH-treated rats in the VTA, which is consistent with a previous study in which calcineurin increased in rats chronically treated with another psychostimulant, amphetamine (Rajadhyaksha et al 2004). Nevertheless, another recent study found that calcineurin decreased in the striatum in rats behaviorally sensitized to METH (Carlezon and Nestler 2002), suggesting differential METH-induced effects on calcineurin in different brain areas.…”

NMDA receptors in the rat VTA: a critical site for social stress to intensify cocaine taking

“…Immunoblot analysis-Immunoblots were processed as previously described in Rajadhyaksha et al 2004. Briefly, brains were sectioned in a cryostat to the rostral end of the NAc (shell and core; spanning 1.2 to 1.7 mm relative to the bregma; Paxinos and Watson 1997) and a 1-mm bilateral punch was obtained with an 18-gauge stainless steel stylet.…”

Drug-induced Alterations in the Extracellular Signal-regulated Kinase (ERK) Signalling Pathway: Implications for Reinforcement and Reinstatement

“…The ERK phosphorylation increase has only been reported in animals receiving acute amphetamine administration. The chronic administration of the amphetamine has no effect on ERK phosphorylation, unless inhibition of the L-type Ca 2+ channels (Rajadhyaksha et al 2004). The increase in ERK phosphorylation after acute amphetamine-treated, but not after chronic amphetamine-treated, is different from findings that have been reported for cocaine .…”

“…The increase in ERK phosphorylation after acute amphetamine-treated, but not after chronic amphetamine-treated, is different from findings that have been reported for cocaine . The reason for the different results may be attributable to the different drugs used and paradigm of drug administration Rajadhyaksha et al 2004). ERK activation is also involved in amphetamine-induced preproenkephalin and preprodynorphin mRNA transcription in the striatum as revealed by inhibition by site-injection of U0126 and systemic administration of SL327 (Shi and McGinty 2006).…”