INVESTIGADORES
CABRERA KREIKER Ricardo Jorge
artículos
Título:
Neuromodulatory effect of progesterone on the dopaminergic, glutamatergic, and GABAergic activities in a male rat model of Parkinsons disease
Autor/es:
CASAS S.; GIULIANI F.; CREMASCHI F.; YUNES R; CABRERA, R
Revista:
NEUROLOGICAL RESEARCH.
Editorial:
MANEY PUBLISHING
Referencias:
Lugar: London; Año: 2013
ISSN:
0161-6412
Resumen:
Objectives: Progesterone has been reported to have a neuroprotective role in depression-like rats in a
hemiparkinsonian model of the disease. In this work, we investigate if this hormone affects the three
principal neurochemicals striatal systems (dopaminergic, glutamatergic, and GABAergic) that are involved
in the physiopathology of the disease in a hemiparkinsonim male rat model at 8 weeks post-chemical injury.
Methods: For this purpose, we design three experimental groups: (1) sham group; (2) hemiparkinsonian
group; and (3) hemiparkinsonian group subcutaneously injected with progesterone at 7 days postchemical
injury. Animals were tested in an automated rotational device at 8 weeks post-chemical injury.
After behavioral test, Kz-evoked [3H]-dopamine, [3H]-glutamate, and [3H]-gamma aminobutyric acid
release from striatum slices were analyzed by superfusion experiments.
Results: The hemiparkinsonian group showed distinctive alterations that are produced by neurodegeneration
of left nigrostriatal dopaminergic pathway by 6-hydroxydopamine hydrobromide (6-OHDA). On the
other hand, the administration of progesterone 7 days after the injection of the neurotoxin was able to (1)
improve the Kz-evoked [3H]-dopamine release from the damaged striata (left); (2) avoid significant
increase in the Kz-evoked [3H]-glutamate release from the left striata; and (3) progesterone does not
modify the Kz-evoked [3H]-gamma aminobutyric acid release from the left striata.
Discussion: These results suggest that progesterone does have neuroprotective and neuromodulatory
effects on striatal neurotransmission systems in the hemiparkinsonian male rats. The possible mechanisms
would involve genomic and non-genomic actions of this neuroactive steroid which would modulate the
activity of dopaminergic, glutamatergic, and GABAergic pathways.