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Thalamic reticular nucleus (TRN) is a group of inhibitory neurons surrounding the thalamus. Due to its important role in sensory information processing, TRN is considered as the target nucleus for the pathophysiological investigation of schizophrenia and autism spectrum disorder (ASD). Prepulse inhibition (PPI) of acoustic startle response, a phenomenon that strong stimulus-induced startle reflex is reduced by a weaker prestimulus, is always found impaired in schizophrenia and ASD. But the role of TRN in PPI modulation remains unknown. Here, we report that parvalbumin-expressing (PV+) neurons in TRN are activated by sound stimulation of PPI paradigm. Chemogenetic inhibition of PV+ neurons in TRN impairs PPI performance. Further investigations on the mechanism suggest a model of burst-rebound burst firing in TRN-auditory thalamus (medial geniculate nucleus, MG) circuitry. The burst firing is mediated by T-type calcium channel in TRN, and rebound burst firing needs the participation of GABAB receptor in MG. Overall, these findings support the involvement of TRN in PPI modulation.

Figure 1. Sound stimuli of PPI paradigm increases calcium activity of PV+ neurons in audTRN.

In this study, the authors show that increased PV+ neuronal activity in the audTRN is tightly coupled with sound stimulus of PPI, and inhibition of PV+ neurons in the audTRN impairs PPI performance. Moreover, they introduce a burst-rebound burst firing model between audTRN and MG neurons which regulates PPI performance. These results indicate the essential role of the audTRN–MG circuit for regulating PPI of acoustic startle response.

 
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