Efferent projections from the anterior thalamic nuclei to the cingulate cortex in the rat

Shibata, Hideshi

doi:10.1002/cne.903300409

Cited by 214 publications

(197 citation statements)

References 15 publications

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“…However, we identified with the PHAL and FG methods a REr input to the RSPagl, as well as massive bidirectional connections of the RSPagl with the AMv and the rostromedial LP. A projection from the AM as a whole, specifically to the RSPagl (layers 1, 5, and 6), was reported earlier (16). Finally, double injections in the RSPagl suggest relatively light bidirectional connections with the LD.…”

Section: Discussionsupporting

confidence: 69%

Evidence for a hypothalamothalamocortical circuit mediating pheromonal influences on eye and head movements.

Risold

Swanson

1995

Proc. Natl. Acad. Sci. U.S.A.

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A method for simultaneous iontophoretic injections of the anterograde tracer Phaseolus vulgaris leukoagglutinin and the retrograde tracer fluorogold was used to characterize in the rat a hypothalamothalamocortical pathway ending in a region thought to regulate attentional mechanisms by way of eye and head movements. The relevant medial hypothalamic nuclei receive pheromonal information from the amygdala and project to specific parts of the thalamic nucleus reuniens and anteromedial nucleus, which then project to a specific lateral part of the retrosplenial area (or medial visual cortex). This cortical area receives a convergent input from the lateral posterior thalamic nucleus and projects to the superior colliculus. Bidirectional connections with the hippocampal formation suggest that activity in this circuit is modified by previous experience. Striking parallels with basal ganglia circuitry are noted.The organization of circuits that mediate orienting responses to somatosensory, visual, and auditory stimuli is known at least in outline, with important components including the thalamus, motor cortical areas, and superior colliculus (1, 2). In contrast, almost nothing is understood about how pheromonal and other olfactory stimuli, which in rodents are particularly important for reproductive, aggressive, and ingestive behaviors, influence eye and head movements. Pheromonal information is relayed by sexually dimorphic pathways involving the vomeronasal organ, accessory olfactory bulb, and corticomedial amygdala to the medial zone of the hypothalamus, but there is little evidence for projections from this circuitry to thalamic, cortical, and midbrain regions concerned directly with regulating eye and head movements and, thus, visuomotor and directed attentional mechanisms (3, 4).We have recently identified dense projections from three adjacent, highly interconnected medial hypothalamic nuclei (anterior, ventromedial, and dorsal premammillary) to two adjacent nuclei of the rostral thalamus, the rostral nucleus reuniens (REr) and ventral anteromedial nucleus (AMv) (5-7). In the work presented here, a method for simultaneous injection into the same site of the anterograde axonal tracer Phaseolus vulgaris leukoagglutinin (PHAL) and the retrograde axonal tracer fluorogold (FG) was used to characterize the hypothalamic and cortical interconnections of the REr. At the cortical level, the method was used to define the connections of a very restricted area that receives a convergent input from the REr and lateral posterior thalamic nucleus (LP) and that projects back to the LP and superior colliculus. On cytoarchitectonic grounds, this cortical area has previously been regarded as either the lateralmost part of the retrosplenial area (RSP) or the medialmost part of the visual cortex in the rat or mouse (for example, see refs. 8 and 9).The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 sole...

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Section: Discussionsupporting

confidence: 69%

Evidence for a hypothalamothalamocortical circuit mediating pheromonal influences on eye and head movements.

Risold

Swanson

1995

Proc. Natl. Acad. Sci. U.S.A.

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“…On the other hand, it is well established that anterior thalamic and posterior cingulate cortical neuronal groups that are specifically vulnerable to TBI in our model, are reciprocally connected and their projections pass through the cingulum/external capsule. (Shibata, 1993;Price, 1995). Maintenance of proper synaptic connections and activity dependent trophic support between neurons and their targets is crucial for their survival in the developing brain (Burek and Oppenheim, 1998).…”

Section: Discussionmentioning

confidence: 99%

Mild traumatic brain injury to the infant mouse causes robust white matter axonal degeneration which precedes apoptotic death of cortical and thalamic neurons

Dikranian

Cohen

Donald

et al. 2008

Experimental Neurology

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The immature brain in the first several years of childhood is very vulnerable to trauma. Traumatic brain injury (TBI) during this critical period often leads to neuropathological and cognitive impairment. Previous experimental studies in rodent models of infant TBI were mostly concentrated on neuronal degeneration, while axonal injury and its relationship to cell death have attracted much less attention. To address this, we developed a closed controlled head injury model in infant (P7) mice and characterized the temporospatial pattern of axonal degeneration and neuronal cell death in the brain following mild injury. Using amyloid precursor protein (APP) as marker of axonal injury we found that mild head trauma causes robust axonal degeneration in the cingulum/external capsule as early as 30 min post-impact. These levels of axonal injury persisted throughout a 24 hr period, but significantly declined by 48 hrs. During the first 24 hrs injured axons underwent significant and rapid pathomorphological changes. Initial small axonal swellings evolved into larger spheroids and clublike swellings indicating the early disconnection of axons. Ultrastructural analysis revealed compaction of organelles, axolemmal and cytoskeletal defects. Axonal degeneration was followed by profound apoptotic cell death in the posterior cingulate and retrosplenial cortex and anterior thalamus which peaked between 16 and 24 hrs post-injury. At early stages post-injury no evidence of excitotoxic neuronal death at the impact site was found. At 48 hrs apoptotic cell death was reduced and paralleled with the reduction in the number of APP-labeled axonal profiles. Our data suggest that early degenerative response to injury in axons of the cingulum and external capsule may cause disconnection between cortical and thalamic neurons, and lead to their delayed apoptotic death.

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“…Examples include the postrhinal cortex, which is innervated by the hippocampus, and the retrosplenial cortex, which is innervated by both the hippocampus and the anterior thalamic nuclei (Wyss and van Groen, 1992;Shibata, 1993). The significant reduction in postrhinal cortex contrasted with the perirhinal cortex, which also receives hippocampal inputs yet was unaffected by the fornix lesion.…”

Section: Discussionmentioning

confidence: 99%

Using Fos Imaging in the Rat to Reveal the Anatomical Extent of the Disruptive Effects of Fornix Lesions

et al. 2000

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Activity of the immediate early gene c-fos was compared across hemispheres in rats with unilateral fornix lesions. To engage Fos production, rats first performed a radial arm maze task that is severely disrupted by bilateral fornix lesions. Using immunohistochemical techniques, Fos-positive cells were visualized and counted in 39 sites in both hemispheres. Fornix lesions led to a significant reduction in Fos in all ipsilateral hippocampal subfields, as well as the entorhinal cortex and most of the subicular complex. Other sites that showed reduced activity included the ipsilateral retrosplenial, anterior cingulate, and postrhinal cortices. Subcortical regions showing significant Fos decreases included the anterior thalamic nuclei, supramammillary nucleus, diagonal band of Broca, and lateral septum. Thus, the effects of fornix lesions extended beyond the hippocampal formation and included sites not directly innervated by the tract. These changes were nevertheless selective, as shown by the lack of hemispheric difference in any of the preselected control sites, the perirhinal cortex, or nucleus accumbens. Furthermore, there were no hemispheric differences in an additional group of animals with unilateral fornix lesions that were killed directly from the home cage. The location of Fos changes closely corresponded to those brain regions that when lesioned disrupt spatial working memory. Moreover, there was a correspondence between those brain regions that show increased Fos production in normal animals performing the radial arm maze task and those affected by fornix lesions. These results show that fornix transection has widespread, but selective, effects on a network of structures normally activated by spatial memory processes, with these effects extending beyond the hippocampal formation.

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Efferent projections from the anterior thalamic nuclei to the cingulate cortex in the rat

Cited by 214 publications

References 15 publications

Evidence for a hypothalamothalamocortical circuit mediating pheromonal influences on eye and head movements.

Evidence for a hypothalamothalamocortical circuit mediating pheromonal influences on eye and head movements.

Mild traumatic brain injury to the infant mouse causes robust white matter axonal degeneration which precedes apoptotic death of cortical and thalamic neurons

Using Fos Imaging in the Rat to Reveal the Anatomical Extent of the Disruptive Effects of Fornix Lesions

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