Anterior thalamic nuclei lesions in rats disrupt markers of neural plasticity in distal limbic brain regions

Dumont, Julie R.; Amin, Eman; Poirier, Guillaume L.; Albasser, Mathieu M.; Aggleton, John Patrick

doi:10.1016/j.neuroscience.2012.08.027

Cited by 37 publications

(44 citation statements)

References 93 publications

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“…21 Transient selective ANT inactivation impairs contextual memory processing in a manner similar to hippocampal lesions 22 ; lesions of the ANT also cause long-lasting intrinsic changes to retrosplenial cortex. 23 In contrast, high-frequency stimulation of the ANT increases adult neurogenesis in the dentate gyrus in mice.…”

Section: Effects Of Experimental Ant Lesions and Stimulationmentioning

confidence: 99%

Anterior nucleus of the thalamus

2013

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The anterior nucleus of thalamus (ANT) is a key component of the hippocampal system for episodic memory. The ANT consist of 3 subnuclei with distinct connectivity with the subicular cortex, retrosplenial cortex, and mammillary bodies. Via its connections with the anterior cingulate and orbitomedial prefrontal cortex, the ANT may also contribute to reciprocal hippocampal-prefrontal interactions involved in emotional and executive functions. As in other thalamic nuclei, neurons of the ANT have 2 different state-dependent patterns of discharge, tonic and burst-firing; some ANT neurons also contribute to propagation of the theta rhythm, which is important for mechanisms of synaptic plasticity of the hippocampal circuit. Clinical and experimental evidence indicate that damage of the ANT or its inputs from the mammillary bodies are primarily responsible for the episodic memory deficit observed in Wernicke-Korsakoff syndrome and thalamic stroke. Experimental models also indicate that the ANT may have a role in the propagation of seizure activity both in absence and in focal seizures. Because of its central connectivity and possible role in propagation of seizure activity, the ANT has become an attractive target for deep brain stimulation (DBS) for treatment of medically refractory epilepsy. The ANT is one of the nuclei preferentially affected in prion disorders, such as fatal familial insomnia, but the relationship between ANT involvement and the clinical manifestations of these disorders remains unclear. The connectivity patterns and electrophysiology of the ANT have been the subject of several reviews.(1-4.)

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Section: Effects Of Experimental Ant Lesions and Stimulationmentioning

confidence: 99%

Anterior nucleus of the thalamus

2013

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“…Conversely, the multitude of overlapping pathways and connections across the extended hippocampal system may also permit a degree of functional redundancy across ATN neurocircuitry, and perhaps the extended system as a whole. Indeed, evidence that other structures are failing as a consequence of distal injury to the ATN, MTT and even the ventral tegmental nucleus of Gudden (Dumont et al, 2012;Dupire et al, 2013;Garden et al, 2009;Jenkins et al, 2004;Mendez-Lopez et al, 2013;Poirier and Aggleton, 2009;Reed et al, 2003;Vann and Albasser, 2009), raises an interesting question that is relevant to memory impairment associated with lesions to components of the extended hippocampal system and its related neurocircuitry. Can we reverse some of the seemingly permanent memory deficits produced by ATN lesions (and other system lesions)?…”

Section: The Anterior Thalamic Nuclei (Atn)mentioning

confidence: 99%

“…One of the most interesting consequences of ATN dysfunction in rats, discovered by John Aggleton, Seralynne Vann and their colleagues, is that ATN and mammillothalamic tract lesions (and lesions to the ventral tegmental nucleus of Gudden, the brain stem nucleus that projects to the MB) produce a dramatic, enduring and exacerbating reduction in the expression of immediate-early gene products (IEG), c-Fos and Zif268, in the retrosplenial cortex (Fig. 5) (Aggleton, 2008;Albasser et al, 2007;Amin et al, 2010;Dumont et al, 2012;Jenkins et al, 2002a,b;Jenkins et al, 2004;Poirier and Aggleton, 2009;Vann and Albasser, 2009;Vann et al, 2014).…”

Section: Recovery Using Cerebrolysin a Neurotrophic Drugmentioning

confidence: 99%

“…2). Functional changes in the hippocampus after ATN lesions have been reported, such as reduced phosphorylated CREB (pCREB) as well as IEG markers (c-Fos; zif268), but these are generally weaker (and sometimes not evident in the case of IEG markers) compared with changes in the retrosplenial cortex (Jenkins et al, 2002a,b;Dumont et al, 2012;Dupire et al, 2013). In the dorsal hippocampal CA1, enrichment increases pCREB in sham-lesion rats only, while both sham-lesion and ATN-lesion rats show a small reduction in c-Fos expression (Dupire et al, 2013).…”

Section: Recovery Of Neuronal Microintegrity In Hippocampal Ca1mentioning

confidence: 99%

“…AT, neurotoxic lesions to the anterior thalamic nuclei; SH, sham; Enr, enriched environment; Std, housed in standard group conditions. as loss of electrophysiological neuroplasticity, reduced pCREB (see Dupire et al, 2013) and transcriptome disturbances such as GABA-A receptor delta subunit, serotonin receptor 2c, zif268, fra-2, kcnab2, cox6b, mmp9, cghB, or ruvbl1 (Amin et al, 2010;Dumont et al, 2012;Dupire et al, 2013;Garden et al, 2009;Poirier et al, 2008). Similarly, a host of neurobiological changes are associated with enrichment, including increases in neurogenesis and trophic factors , so it would be interesting to know whether (2014).…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

See 2 more Smart Citations

Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive thalamus

Dalrymple‐Alford

Harland

Loukavenko

et al. 2015

Neuroscience & Biobehavioral Reviews

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

et al. 2013

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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.

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Anterior thalamic nuclei lesions in rats disrupt markers of neural plasticity in distal limbic brain regions

Cited by 37 publications

References 93 publications

Anterior nucleus of the thalamus

Anterior nucleus of the thalamus

Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive thalamus

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

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