CONICET | Buscador de Institutos y Recursos Humanos

Objectives: Progesterone has been reported to have a neuroprotective role in depressed-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 seven days post chemical injury. Animals were tested in an automated rotational device at eight weeks post chemical injury. After behavioral test, K+ evoked [3H]-Dopamine, [3H]-Glutamate and [3H]-Gamma aminobutyric acid release from striatum slices were analysed by superfusion experiments. Results: The hemiparkinsonian group showed distinctive alterations that are produced by neurodegeneration of left nigrostriatal dopaminergic pathway by 6-OHDA. On the other hand the administration of progesterone 7 days after the injection of the neurotoxin was able to 1) improve the K+-evoked [3H]-Dopamine release from the damaged striata (left), 2) avoid significant increase in the K+-evoked [3H]-Glutamate release from the left striata and 3) progesterone does not modify the K+-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.