Alternation and exploration in rats with hippocampal lesions.

Roberts, Warren W.; Dember, William N.; Brodwick, Malcolm S.

doi:10.1037/h0045168

Cited by 348 publications

(112 citation statements)

References 8 publications

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“…When placed in a situation involving inhibition of movement, rats with hippocampal lesion were unable to inhibit movement to avoid shock, suggesting impairment of passive avoidance behavior [92,93] . In another report, electrical lesions of the hippocampus resulted in increased open-field activity in rats [94] , similar to the hyperactivity observed in the above paper [92] and other previous related experiments [95,96] . Moreover, significant decreases in shock-induced aggression was observed following electrical hippocampal lesions [94] , consistent with previous findings from Blanchard and Blanchard [97] .…”

Section: Electrical Lesionsupporting

confidence: 70%

Roles of the hippocampal formation in pain information processing

2009

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Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

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Section: Electrical Lesionsupporting

confidence: 70%

Roles of the hippocampal formation in pain information processing

2009

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“…Although the principal mechanisms are unclear, one may hypothesize that by cross-linking strands of DNA/RNA and inhibiting protein synthesis, CY treatment impairs molecular mechanisms (e.g., phosphorylation) required for short-term memory formation and consolidation (Ng et al, 1991). Over the past 40 years, lesion studies demonstrating reduced SAB rate in rodents have implicated the role of the hippocampus in attention control and memory formation (Roberts et al, 1962). If so, increased degeneration in the CA3 region of MRL-lpr brains may account for deficits in formation of a spatial map.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Ballok¹,

Woulfe

Sur

et al. 2004

Hippocampus

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Systemic lupus erythematosus (SLE) is frequently accompanied by neuropsychiatric (NP) and cognitive deficits of unknown etiology. By using autoimmune MRL-lpr mice as an animal model of NP-SLE, we examine the relationship between autoimmunity, hippocampal damage, and behavioral dysfunction. Fluoro Jade B (FJB) staining and anti-ubiquitin (anti-Ub) immunocytochemistry were used to assess neuronal damage in young (asymptomatic) and aged (diseased) mice, while spontaneous alternation behavior (SAB) was used to estimate the severity of hippocampal dysfunction. The causal relationship between autoimmunity and neuropathology was tested by prolonged administration of the immunosuppressive drug cyclophosphamide (CY). In comparison to congenic MRL +/+ controls, SAB acquisition rates and performance in the "reversal" trial were impaired in diseased MRL-lpr mice, suggesting limited use of the spatial learning strategy. FJBpositive neurons and anti-Ub particles were frequent in the CA3 region. Conversely, CY treatment attenuated the SAB deficit and overall FJB staining. Similarly to mouse brain, the hippocampus from a patient who died from NP-SLE showed reduced neuronal density in the CA3 region and dentate gyrus, as well as increased FJB positivity in these regions. Gliosis and neuronal loss were observed in the gray matter, and T lymphocytes and stromal calcifications were common in the choroid plexus. Taken together, these results suggest that systemic autoimmunity induces significant hippocampal damage, which may underlie affective and cognitive deficits in NP-SLE.

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“…8b) and, in this regard, we sought to use a hippocampallinked spontaneous alternation behavioural task in the T-maze (Fig. 8d) 29,30 .…”

Section: Improved Cognitive Function In Claudin-5 Sirna-injected Micementioning

confidence: 99%

Targeted suppression of claudin-5 decreases cerebral oedema and improves cognitive outcome following traumatic brain injury

et al. 2012

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Traumatic brain injury is the leading cause of death in children and young adults globally. malignant cerebral oedema has a major role in the pathophysiology that evolves after severe traumatic brain injury. Added to this is the significant morbidity and mortality from cerebral oedema associated with acute stroke, hypoxic ischemic coma, neurological cancers and brain infection. Therapeutic strategies to prevent cerebral oedema are limited and, if brain swelling persists, the risks of permanent brain damage or mortality are greatly exacerbated. Here we show that a temporary and size-selective modulation of the blood-brain barrier allows enhanced movement of water from the brain to the blood and significantly impacts on brain swelling. We also show cognitive improvement in mice with focal cerebral oedema following administration in these animals of short interfering RnA directed against claudin-5. These observations may have profound consequences for early intervention in cases of traumatic brain injury, or indeed any neurological condition where cerebral oedema is the hallmark pathology.

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Alternation and exploration in rats with hippocampal lesions.

Cited by 348 publications

References 8 publications

Roles of the hippocampal formation in pain information processing

Roles of the hippocampal formation in pain information processing

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Targeted suppression of claudin-5 decreases cerebral oedema and improves cognitive outcome following traumatic brain injury

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