Abstract
The substantia nigra pars reticulata (SNr) is one of the output nuclei of the basal ganglia (BG) and plays a vital role in movement execution. Death of dopaminergic neurons in the neighboring nucleus, the substantia nigra pars compacta (SNc), leads to Parkinson's disease. The ensuing dopamine depletion affects all BG nuclei. However, the long-term effects of dopamine depletion on BG output are less characterized. In this in vitro study, we applied electrophysiological and immunohistochemical techniques to investigate the long-term effects of dopamine depletion on GABAergic transmission to the SNr. The findings showed a reduction in firing rate and regularity in SNr neurons after unilateral dopamine depletion with 6-OHDA, which we associate with homeostatic mechanisms. The strength of the GABAergic synapses between the globus pallidus (GP) and the SNr increased but not their short-term dynamics. Consistent with this observation, there was an increase in the frequency and amplitude of spontaneous inhibitory synaptic events to SNr neurons. Immunohistochemistry revealed an increase in the density of vGAT-labeled puncta in dopamine depleted animals. Overall, these results may suggest that synaptic proliferation can explain how dopamine depletion augments GABAergic transmission in the SNr.
Highlights
The substantia nigra is one of the basal ganglia (BG) nuclei located in the ventral midbrain and is divided into the substantia nigra pars compacta (SNc) and the substantia nigra pars reticulata (SNr)
We found that dopamine depletion leads to a decrease in the intrinsic excitability of the GABAergic neurons after blocking synaptic transmission
We observed an increase in IPSP amplitude and a decrease in its latency in dopamine depleted rats
Summary
The substantia nigra is one of the basal ganglia (BG) nuclei located in the ventral midbrain and is divided into the substantia nigra pars compacta (SNc) and the substantia nigra pars reticulata (SNr). The SNc contains neurons projecting to the striatum and modulate striatal activity by releasing dopamine (Freund et al, 1984), while the SNr projects primarily to the thalamus, and serving as one of the primary output nuclei of the BG (Albin et al, 1989). This output nucleus plays a critical role in motor activity, of the eyes and head (Sakamoto and Hikosaka, 1989; Mink, 2003; Dybdal et al, 2013). SNr GABAergic neurons receive excitatory input from the subthalamic nucleus (STN) (Kita and Kitai, 1987) and inhibitory input from the striatum (STR) and the globus pallidus (GP) (Grofova, 1975)
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