Research Article: Control of Somatosensory Cortical Processing by Thalamic Posterior Medial Nucleus: A New Role of Thalamus in Cortical Function

Date Published: January 28, 2016

Publisher: Public Library of Science

Author(s): Carlos Castejon, Natali Barros-Zulaica, Angel Nuñez, Miguel Maravall.

http://doi.org/10.1371/journal.pone.0148169

Abstract

Current knowledge of thalamocortical interaction comes mainly from studying lemniscal thalamic systems. Less is known about paralemniscal thalamic nuclei function. In the vibrissae system, the posterior medial nucleus (POm) is the corresponding paralemniscal nucleus. POm neurons project to L1 and L5A of the primary somatosensory cortex (S1) in the rat brain. It is known that L1 modifies sensory-evoked responses through control of intracortical excitability suggesting that L1 exerts an influence on whisker responses. Therefore, thalamocortical pathways targeting L1 could modulate cortical firing. Here, using a combination of electrophysiology and pharmacology in vivo, we have sought to determine how POm influences cortical processing. In our experiments, single unit recordings performed in urethane-anesthetized rats showed that POm imposes precise control on the magnitude and duration of supra- and infragranular barrel cortex whisker responses. Our findings demonstrated that L1 inputs from POm imposed a time and intensity dependent regulation on cortical sensory processing. Moreover, we found that blocking L1 GABAergic inhibition or blocking P/Q-type Ca2+ channels in L1 prevents POm adjustment of whisker responses in the barrel cortex. Additionally, we found that POm was also controlling the sensory processing in S2 and this regulation was modulated by corticofugal activity from L5 in S1. Taken together, our data demonstrate the determinant role exerted by the POm in the adjustment of somatosensory cortical processing and in the regulation of cortical processing between S1 and S2. We propose that this adjustment could be a thalamocortical gain regulation mechanism also present in the processing of information between cortical areas.

Partial Text

Cortical functioning cannot be properly understood without taking into account the thalamic influence [1–9]. Knowledge of thalamocortical influence in sensory processing comes mainly from studying lemniscal core thalamic systems that project to granular layers of primary sensory cortices [3, 7, 10]; however, less is known about paralemniscal thalamic systems.

Our experiments were designed to study thalamic POm influence in somatosensory cortical processing. First, we studied and characterized the firing pattern of POm responses to whisker deflections. After that, to test whether POm activity modulates cortical tactile processing, we investigated whisker response changes in barrel cortex by electrically stimulating the POm immediately before whisker stimulus or by muscimol-induced inactivation of the POm. Finally, we pharmacologically blocked GABAergic inhibitory transmission in L1 to understand the contribution of this layer in POm regulation of cortical processing.

Here, using a combination of electrophysiology and pharmacology in vivo, we show that POm modulates magnitude and duration of supra- and infragranular barrel cortex whisker responses. Our findings demonstrate that L1 inputs from POm impose a time and intensity dependent regulation on cortical sensory processing. Moreover, we found that L1 GABAergic system mediates this process and that blocking P/Q-type Ca2+ channels in L1 prevents POm adjustment of whisker responses in the barrel cortex. Additionally, we found that POm is also controlling the sensory processing in S2 and this regulation is modulated by corticofugal activity from L5 in S1. Taken together, our data demonstrate the determinant role exerted by the POm in the adjustment of somatosensory cortical processing and in the regulation of cortical processing between S1 and S2. We propose that this adjustment could be a thalamocortical gain regulation mechanism also present in the processing of information between cortical areas.

 

Source:

http://doi.org/10.1371/journal.pone.0148169