Control of somatosensory cortical processing by thalamic posterior medial nucleus: A new role of thalamus in cortical function

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.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.This work was supported by a grant from Ministerio de Economia y Competitividad (BFU2012- 36107

Gambling disorder and substance-related disorders: Similarities and differences

Gambling disorder (GD) has important similarities with substance use disorders (SUDs) in terms of both diagnostic criteria and underlying mechanisms of action. With regard to diagnostic criteria, only craving is not present as a formal criterion in DSM-5 GD, and chasing losses is not present in SUDs. All other major diagnostic criteria such as loss of control over gambling, tolerance, withdrawal, and negative consequences due to gambling overlap with those of SUD. With regard to underlying mechanisms and vulnerability factors, higher impulsivity, abnormalities in decision-making, deficient executive functions, and related fronto-striatal brain circuitry abnormalities are related to the development and course of both SUD and GD. However, there are also differences between GD and SUD. In gambling, cognitive factors such as risk-taking and decision-making are intrinsically related to the addictive behavior itself, whereas in SUD these effects can also be associated with the pharmacological effect or the neurotoxicity related to (chronic) substance use. Moreover misperceptions with regard to gambling, the experience and interpretation of near misses, and the processing of (potential) rewards and losses influence the experience of gambling, which is not true for SUD. Importantly, these aspects also differ between disordered gamblers and non-problematic gamblers and are thus unique for GD and consitute a risk for relapse. Both shared and unique mechanisms are relevant as targets for the treatment of GD. This chapter concludes with a discussion on novel treatment methods that target some of the working mechanisms shared by GD and SUDs