Dr. Soghomonian's laboratory is interested in the functional and molecular neuroanatomy of the basal ganglia and the patho-physiology of Parkinson's disease and l-DOPA-induced dyskinesia. Current work focuses on:

1. The plasticity of GABA-mediated signaling in experimental models of Parkinson's disease.
2. The effects of l-DOPA or other agonists of dopamine receptors on the functional activity of neurons in the basal ganglia.

Dopamine and the basal ganglia
Parkinson's disease is a neurodegenerative disease, which is caused by the loss of a specific population of dopamine neurons in the brain. Motor abnormalities observed in Parkinson's disease are due to abnormal cell signaling in brain regions such as the basal ganglia. This abnormal signaling is triggered by the lack of normal dopaminergic tone. The most common and efficient therapeutic intervention in Parkinson' disease consist in administering orally the precursor of dopamine, L-dopa. However, long-term treatment with l-DOPA in patients results in severe secondary effects such as dyskinesia, which seriously alter the therapeutic efficacy of l-DOPA. One objective of the lab is to understand how l-DOPA or other agonists of dopamine receptor alter cell signaling in an experimental model of Parkinson's disease.

GABA-mediated signaling
GABA is a major neurotransmitter in the mammalian brain. It is synthesized via the decarboxylation of glutamate by the enzyme glutamate decarboxylase, which is found in GABAergic neurons as two different isoforms, GAD67 and GAD65. Current evidence suggests that the two GAD isoforms play different roles in the physiology of GABAergic neurons. The lab is also investigating the significance of these two GAD isoforms in the modulation of GABA-mediated signaling by neurons of the basal ganglia.