IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
artículos
Título:
nicotine-conditioned place preference induced CREB phosphorylation and Fos expression in the adult rat brain
Autor/es:
PASCUAL M, PASTOR V AND BERNABEU R
Revista:
PSYCHOPHARMACOLOGY
Editorial:
springer
Referencias:
Año: 2009 p. 57 - 71
ISSN:
0033-3158
Resumen:
Rationale Experimental evidence indicates that nicotine
causes long-lasting changes in the brain associated with
behavior. Although much has been learned about factors
participating in this process, less is known concerning the
mechanisms and brain areas involved in nicotine preference.Experimental evidence indicates that nicotine
causes long-lasting changes in the brain associated with
behavior. Although much has been learned about factors
participating in this process, less is known concerning the
mechanisms and brain areas involved in nicotine preference.
Objectives The objective of this study is to examine the
participation of brain structures during the development of
nicotine-conditioned place preference (CPP).The objective of this study is to examine the
participation of brain structures during the development of
nicotine-conditioned place preference (CPP).
Methods To identify brain regions activated in CPP, we have
measured the levels of phosphorylated cyclic AMP response
element binding protein (pCREB) and Fos protein using a
behavioral CPP and conditioned place aversion (CPA)
paradigms.To identify brain regions activated in CPP, we have
measured the levels of phosphorylated cyclic AMP response
element binding protein (pCREB) and Fos protein using a
behavioral CPP and conditioned place aversion (CPA)
paradigms.
Results Rats developed reliable and robust CPP and also
CPA. During nicotine preference and reinstatement behaviors,
a significant increase of both pCREB and Fos protein
expression occurs in the nucleus accumbens (NAc) and
ventral tegmental area (VTA) and also in the prefrontal cortex
(PFC), dorsal striatum (DStr), amygdala, and hippocampus.
These increases were abolished by the administration of
mecamylamine or by a CPA protocol, showing a specific
activation of pCREB in drug preference animals, mediated by
nicotinic receptors. Specifically in the VTA, nicotine-induced
preference and reinstatement of the preference caused the
activation of dopaminergic and GABAergic cells in different
proportions.Rats developed reliable and robust CPP and also
CPA. During nicotine preference and reinstatement behaviors,
a significant increase of both pCREB and Fos protein
expression occurs in the nucleus accumbens (NAc) and
ventral tegmental area (VTA) and also in the prefrontal cortex
(PFC), dorsal striatum (DStr), amygdala, and hippocampus.
These increases were abolished by the administration of
mecamylamine or by a CPA protocol, showing a specific
activation of pCREB in drug preference animals, mediated by
nicotinic receptors. Specifically in the VTA, nicotine-induced
preference and reinstatement of the preference caused the
activation of dopaminergic and GABAergic cells in different
proportions.
Conclusion The results indicate that the phosphorylation of
CREB and expression of Fos protein, as indicators of neural
activity, accompany the acquisition and maintenance of
nicotine-induced CPP but not CPA in mesolimbic areas
(NAc, VTA, PFC, and DStr) as well as in memory
consolidation structures (hippocampus and amygdala) and
nicotinic receptor are involved in this process. Taken together,
these studies identify the brain regions where pCREB activity
is essential for nicotine preference.The results indicate that the phosphorylation of
CREB and expression of Fos protein, as indicators of neural
activity, accompany the acquisition and maintenance of
nicotine-induced CPP but not CPA in mesolimbic areas
(NAc, VTA, PFC, and DStr) as well as in memory
consolidation structures (hippocampus and amygdala) and
nicotinic receptor are involved in this process. Taken together,
these studies identify the brain regions where pCREB activity
is essential for nicotine preference.