IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
artículos
Título:
Immunocytochemical Expression of Dopamine-related Transcription Factors Pitx3 and Nur 1 in Prenatally Stressed Adult Rats
Autor/es:
KATUNAR M, SAEZ T, BRUSCO A., ANTONELLI M
Revista:
JOURNAL OF NEUROSCIENCE RESEARCH
Editorial:
WILEY-LISS, DIV JOHN WILEY & SONS INC
Referencias:
Año: 2009 vol. 87 p. 1014 - 1022
ISSN:
0360-4012
Resumen:
Rats exposed to different types of stress during the last
week of pregnancy produce offspring that show severe
anomalies in neural development and brain morphology.
We have previously reported that prenatal stress
(PS) induced by immobilization increases D2-type dopamine
(DA) receptor levels in the adult offspring, with
a concomitant reduction in DA release in prefrontal cortex
after amphetamine stimulation. Recently, two transcription
factors, Nurr1 and Pitx3, have been identified
that are expressed at critical moments of DA neuron
differentiation. Their genetic expression is activated
immediately after these neuron determinations and
maintained through adult life. Nurr1 regulates several
proteins that are required for dopamine synthesis and
regulation, and Pitx3 is specifically involved in the terminal
differentiation and maintenance of dopamine neurons.
By means of an immunocytochemistry approach,
we studied the expression of Nurr1 and found an ubiquitous
distribution in cerebral cortex, hippocampus,
thalamus, amygdala, and midbrain, whereas Pitx3
remains restricted to the mesencephalic DA neurons
such as substantia nigra and ventral tegmental area.
Our results show that the expression of both Nurr1 and
Pitx3 increased in prenatally stressed adult offspring in
the ventral tegmental area, whereas no changes were
observed in the substantia nigra area. It might be
hypothesized that the increase of the specific dopaminergic
transcription factors might be a compensatory
mechanism to counteract the reduction in dopamine
levels previously observed as a consequence of prenatal
stress.