2009
DOI: 10.1016/j.neuroscience.2009.02.021
|View full text |Cite
|
Sign up to set email alerts
|

Post-surgical interval and lesion location within the limbic thalamus determine extent of retrosplenial cortex immediate-early gene hypoactivity

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

8
38
0

Year Published

2011
2011
2018
2018

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 36 publications
(46 citation statements)
references
References 68 publications
8
38
0
Order By: Relevance
“…The progression of these disruptions within the RSC is consistent with the idea that the granular RSC is more closely connected with limbic regions, while the dysgranular RSC is more closely connected with neocortical regions. For example, ATN lesions lead to dysregulation of IEG expression in the granular RSC in as little as 1 week, but did not affect the dysgranular RSC until around 1 year (Jenkins et al, 2004; Poirier and Aggleton, 2009). In contrast, lesions of the postrhinal cortex lead to IEG dysregulation in the dysgranular RSC without affecting the granular RSC (Jenkins et al, 2004).…”
Section: Functional Anatomymentioning
confidence: 99%
“…The progression of these disruptions within the RSC is consistent with the idea that the granular RSC is more closely connected with limbic regions, while the dysgranular RSC is more closely connected with neocortical regions. For example, ATN lesions lead to dysregulation of IEG expression in the granular RSC in as little as 1 week, but did not affect the dysgranular RSC until around 1 year (Jenkins et al, 2004; Poirier and Aggleton, 2009). In contrast, lesions of the postrhinal cortex lead to IEG dysregulation in the dysgranular RSC without affecting the granular RSC (Jenkins et al, 2004).…”
Section: Functional Anatomymentioning
confidence: 99%
“…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%
“…The diencephalon and recognition www.learnmem.org activity in diencephalic amnesia (Fazio et al 1992;Joyce et al 1994;Paller et al 1997;Reed et al 2003), (2) evidence that anterior thalamic strokes causing amnesia are sufficient to cause posterior cingulate hypoactivity (Clarke et al 1994), and (3) studies with rats showing how selective anterior thalamic lesions and mammillothalamic tract lesions can markedly reduce immediate-early gene expression in the posterior cingulate (retrosplenial) cortex and hippocampus yet leave both structures seemingly intact (Jenkins et al 2002(Jenkins et al , 2004Poirier and Aggleton 2009;Vann and Albasser 2009). These distal activity changes do not merely reflect the loss of afferent stimulation; there are also subtle intrinsic changes to the cortex itself (Poirier et al 2008).…”
Section: Toward a Model Of Diencephalic Contributions To Recognition mentioning
confidence: 99%