This article is titled “Inhibition of the substantia nigra pars reticulata produces divergent effects on sensorimotor gating in rats and monkeys.” It piqued my interest because I am a part of Karine Fenelon’s lab here on campus, in which we investigate the neural circuits that modulate sensorimotor gating. In the study, the GABAA receptor agonist muscimol was used to test the role of the SNpr in auditory pre-pulse inhibition (PPI), a key component of sensorimotor gating. From class, we know that GABA is the major inhibitory amino acid neurotransmitter, so muscimol must mimic its inhibitory effects on target neurons. In the study, it was found that the inhibition of the SNpr using muscimol disrupted PPI in rats, while facilitated PPI in rhesus macaques. This study discovered these divergent effects. I wonder what differences in neuron connections contribute to this divergence, because there must be a difference either upstream or downstream of the point of innervation of the SNpr. I also wonder what the effect of muscimol on the SNpr in mice is, since this is the model organism we use in lab.
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