So, withdrawal (Li et al. 2009). Despite NAcc is

So, Arc involved in the formation of
plastic changes in opioid administration (Zio´?kowska et al. 2005). Arc
expression was elevated in prefrontal cortex in withdrawal rats, suggesting
that prefrontal cortex activated by morphine withdrawal (Li et al. 2009).
Despite NAcc is important in the reward learning and drug addiction, no
alteration reported in Arc expression in NAc of the morphine-treated rat (Li et al.

The coupling of the Arc transcription
places plastic cell activity in the hippocampus. The firing can prevent subsequent Arc
transcriptional activation (Guzowski et al. 2006). This electro-transcriptional
coupling leads to retaining
optimum Arc levels for subsequent synaptic homeostasis. It is reported
posttranscriptional Arc protein expression mediates via neuromodulation in
amygdala. So, Arc gene expression integrates several neural signals to enhance
information storage in other neural sites in the brain (Zio´?kowska et al. 2005). In our study, also, revealed Arc levels
elevated in hippocampus of withdrawal rats. Findings suggest this region might
be involved in the negative reinforcing effect of abuse drugs. The new findings
of the current study can use distinct from the c-fos gene to map the neural
substrates that are recruited by withdrawal from chronic morphine-withdrawal
rats (Li et al. 2009). Despite direct intracellular mechanism(s) of action of
the morphine on Arc gene expression is not fully elicited, but it seems
morphine via the µ-opioid receptor leads to stimulation of phospholipase C
(PLC), with
concomitant rises in intracellular Ca2+ levels and activation of
PKC, activation of mitogen-activated protein (MAP) kinases,
then transcription factor cAMP response element binding protein by a
PKC-dependent mechanism (Zio´?kowska et al. 2005). So, inhibition of MAP was
consistent decreases Arc by BDNF in the hippocampal neurons (Zio´?kowska et al.

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These results suggested morphine
increased Arc mRNA levels than other genes. As discussed, Arc has been
identified as a critical effector gene for BDNF in the BDNF-induced LTP in the
hippocampus. So, its gene expression can use as a prominent indicator for
memory and learning investigations.