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.
Highlights
Cortical functioning cannot be properly understood without taking into account the thalamic influence [1,2,3,4,5,6,7,8,9]
To determine the possible role exerted by the posterior medial nucleus (POm) in the adjustment of somatosensory cortical processing between S1 and S2, we performed a complementary set of experiments investigating whisker response changes in S2 by electrically stimulating S1 and by muscimol-induced inactivation of the POm
These findings indicate that POm activity is controlling the sensory processing in S2 and this regulation is modulated by corticofugal activity from L5 in S1
Summary
Cortical functioning cannot be properly understood without taking into account the thalamic influence [1,2,3,4,5,6,7,8,9]. 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]; less is known about paralemniscal thalamic systems. The ventral posterior medial nucleus of the thalamus (VPM) projects to L4, L5B and L6A in the primary somatosensory cortex (S1). The ventral tier of VPM projects mainly to L4 and L6 [67] in the secondary somatosensory cortex (S2). In the paralemniscal pathway, the posterior medial nucleus (POm) projects to L1 and L5A in S1 and to S2 [18,19,20,21,22,23,24]. It has been proposed that, whereas these ascending pathways appear to be parallel anatomically, they may not be functionally equivalent [39]
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