IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
PRENATAL RESTRAINT STRESS AND VULNERABILITY OF DOPAMINERGIC NEURONS
Autor/es:
BAIER CJ1, KATUNAR MR1, ADROVER E1, PALLARÉS ME1, RAISMAN-VOZARI2 R AND ANTONELLI MC1
Reunión:
Congreso; V Congreso de la Sociedad de Neurotoxicidad (NTS); 2011
Resumen:
It has been demonstrated in
animal models that maternal disturbance can influence the offsprings brain
chemistry, endocrine function, emotionality, and learning ability. Exposure to
adverse events in early life can alter adult behaviors and neurochemical
indicators of midbrain dopamine (DA) activity, suggesting that the development
of the DA system is sensitive to disruption by brief exposure to early
stressors. In humans, dysfunction of dopaminergic system is associated with
development of several neurological disorders such as Parkinsons disease (PD),
schizophrenia, attention-deficit hyperactivity disorder and depression. The
pathological hallmark of PD is the relatively selective loss of DA neurons in
the substantia nigra compacta (SNc) in the ventral midbrain with posterior loss
of DA in the nigroestriatal system, and presence of cell bodies enriched in a-synuclein
aggregates. Oxidative stress and neuroinflammation participate in the pathogenesis
of PD. The neurotoxin 6-hydroxydopamine (6-OHDA) is a classical and valuable model
of PD in the rat. The aim of the present study was to investigate whether
prenatal restrain stress increases the vulnerability of DA neurons to
degenerate after striatal 6-OHDA injection in the adulthood. Dopaminergic neuron
degeneration was determined by tirosine hydroxylase (TH) immunohistochemistry in
striatum and SNc. We found no significant differences in TH levels between
control and prenatally stressed animals treated with 6-OHDA in both areas. Additionally
we investigated the expression and localization of neuronal nitric oxide
synthase and glial markers in prenatally stressed rats.