The level of
mRNA encoding
calcyon (measured by in situ hybridization), one of the
dopamine receptor interacting
proteins, has been examined in the rat brain in the established animal model used to study the mechanisms of
cocaine addiction (
cocaine self-administration involving a yoked procedure). Two weeks of
cocaine self-administration (maintenance) did not affect the level of
calcyon mRNA, regardless of the way
cocaine was delivered, except for tuberculum olfactorium, where
calcyon mRNA was increased after
cocaine treatment. In the reinstatement phase of the experiment
cocaine alone induced an increase in the
calcyon mRNA expression in most of the brain region studied (caudate putamen; tuberculum olfactorium; paraventricular thalamic nucleus; ventromedial hypothalamic nucleus and paraventricular hypothalamic nucleus) but only in the yoked saline control group. In other words, these results show that the single dose of
cocaine (10 mg/kg) was able to induce an alteration in the level of
calcyon mRNA in these rats which never before experienced any
cocaine administration. The most significant effects were observed in the ventromedial hypothalamic nucleus and paraventricular hypothalamic nucleus. Interestingly, a similar effect was observed when the reinstatement of
cocaine-seeking behaviour was evoked by cue (conditioned stimuli) that indicates that no
cocaine was necessary to induce the changes in the level of
calcyon mRNA expression. This effect was significant in tuberculum olfactorium, ventromedial hypothalamic nucleus and paraventricular hypothalamic nucleus. Such a result together with the brain areas involved in these effects might suggest the role of
calcyon similar to the CART
peptides and special vulnerability of
calcyon expression rather to acute than chronic stimuli.