A role for anterior thalamic nuclei in affective cognition: Interaction with environmental conditions

Abstract

Damage to anterior thalamic nuclei (ATN) is a well-known cause of diencephalic pathology that produces a range of cognitive deficits reminiscent of a hippocampal syndrome. Anatomical connections of the ATN also extend to cerebral areas that support affective cognition. Enriched environments promote recovery of declarative/relational memory after ATN lesions and are known to downregulate emotional behaviors. Hence, the performance of standard-housed and enriched ATN rats in a range of behavioral tasks engaging affective cognition was compared. ATN rats exhibited reduced anxiety responses in the elevated plus maze, increased activity and reduced corticosterone responses when exploring an open field, and delayed acquisition of a conditioned contextual fear response. ATN rats also exhibited reduced c-Fos and phosphorylated cAMP response element-binding protein (pCREB) immunoreactivity in the hippocampal formation and the amygdala after completion of the contextual fear test. Marked c-Fos hypoactivity and reduced pCREB levels were also evident in the granular retrosplenial cortex and, to a lesser extent, in the anterior cingulate cortex. Unlike standard-housed ATN rats, enriched ATN rats expressed virtually no fear of the conditioned context. These results show that the ATN regulate affective cognition and that damage to this region may produce markedly different behavioral effects as a function of environmental housing conditions.

Dissociable effects of anterior and mediodorsal thalamic lesions on spatial goal-directed behavior

“…Two ATN and three MD rats had only minimal damage and were discarded from further analysis. The ATN lesions were highly specific, comparable to previous work (Dupire et al 2013;Marchand et al 2013;Wolff et al 2006Wolff et al , 2008a. Damage to other non-target thalamic structures including midline nuclei was generally minimal, with the exception of the inter-anteromedial nucleus, the centromedial and the parataenial nucleus; there was minor damage to the laterodorsal nucleus and negligible damage for paraventricular and posterior paraventricular nuclei, anterior paraventricular nucleus, reuniens nucleus, and rhomboid nuclei.…”

“…Indeed, previous findings have demonstrated that ATN lesions did not impact the sensitivity to instrumental devaluation ). In addition, available data suggest that ATN rats, like Sham rats, are able to attribute a predictive value to both discrete and complex Pavlovian stimuli (Aggleton et al 1996(Aggleton et al , 2011Dupire et al 2013;Ward-Robinson et al 2002). The impact of ATN lesions on changing outcome value in a pure Pavlovian setup is, however, unknown and further studies are warranted.…”

Mediodorsal but not anterior thalamic nuclei lesions impair acquisition of a conditional discrimination task

“…Additional damage occurred at the level of the intralaminar nuclei, more especially the centrolateral and the paracentral nuclei and modest damage in the centromedian nuclei. The ATN lesions were highly specific, comparable to previous work Dupire et al, 2013;Wolff, Gibb, Cassel, & Dalrymple-Alford, 2008). Damage to other non-target thalamic structures including midline nuclei was generally minimal, with the exception of the interanteromedial nucleus, the centromedial and the parataenial nucleus.…”

“…A recent review of rodent data indicates a major functional dissociation within the limbic thalamus between the anterior (ATN) and mediodorsal (MD) thalamic nuclei, the former supporting essentially hippocampal functions and the latter contributing to prefrontal cortical functions . At the crossroad between direct and indirect hippocampal and midbrain inputs, the ATN are essential to spatial navigation (Jankowski et al, 2013), but recent experimental data (Dupire et al, 2013;Law & Smith, 2012;Marchand, Faugere, Coutureau, & Wolff, 2013;) as well as the study of clinical cases (Carlesimo, Lombardi, & Caltagirone, 2011;Gold & Squire, 2006;Harding, Halliday, Caine, & Kril, 2000;Pergola & Suchan, 2013) indicate that this region may play a broader role in cognition. The MD, on the other hand, entertains privileged links with all divisions of the prefrontal cortex, including the OFC and the mPFC (Groenewegen, 1988).…”

Caramiphen edisylate as adjunct to standard therapy attenuates soman-induced seizures and cognitive deficits in rats

“…The amygdala and hippocampus are thought to be involved in cued fear conditioning and contextual fear conditioning (Goosens and Maren, 2001;Maren, 2008). In addition, the thalamus is thought to play a critical role in auditory fear conditioning beyond its role of sensory relays (Dupire et al, 2013;Parsons et al, 2006;Weinberger, 2011). Several regions of the thalamus are particularly damaged following exposure to seizure-inducing doses of GD and are postulated to be important for the impairment of auditory and contextual fear responses following GD exposure in rats (Moffett et al, 2011).…”