scholarly journals p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease

Neuron ◽  
2005 ◽  
Vol 47 (1) ◽  
pp. 29-41 ◽  
Author(s):  
Byoung-Il Bae ◽  
Hong Xu ◽  
Shuichi Igarashi ◽  
Masahiro Fujimuro ◽  
Nishant Agrawal ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Behavioral Abnormalities ◽  
Cellular Dysfunction

scholarly journals Intraparenchymal Striatal Transplants Required for Maintenance of Behavioral Recovery in an Animal Model of Huntington's Disease

1989 ◽  
Vol 1 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Paul R. Sanberg ◽  
Magda Giòrdano ◽  
Mark A. Henault ◽  
David R. Nash ◽  
Michael E. Ragozzino ◽  
...  
Keyword(s):  
Animal Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Kainic Acid ◽  
Lateral Ventricle ◽  
Functional Interaction ◽  
Behavioral Recovery ◽  
Behavioral Abnormalities ◽  
Vital Element ◽  
Host Brain

Rats which receive injections of kainic acid (KA) into the striatum show many of the anatomical, biochemical and behavioral abnormalities seen in patients with Huntington's disease. Recently, it has been reported that fetal striatal transplants into the lesioned striatum could normalize the neurological and behavioral abnormalities produced by the KA lesion. The present study examined the issue of transplant integration in producing behavioral recovery. In one experiment, lesioned animals with transplants located within the lateral ventricle were compared against parenchymally transplanted rats. It was found that unless the ventricular transplant grew into the lesioned striatum there was no recovery. The second experiment demonstrated that electrolytic destruction of a successful fetal striatal transplant could reverse the transplant-induced behavioral recovery. These results suggest that the integrity of the transplant is important in maintaining behavioral recovery. A continuing functional interaction between the host brain and transplanted tissue may be a vital element in the success of the fetal striatal transplant.

scholarly journals Behavioral abnormalities precede neuropathological markers in rats transgenic for Huntington's disease

2006 ◽  
Vol 15 (21) ◽  
pp. 3177-3194 ◽  
Author(s):  
Huu Phuc Nguyen ◽  
Philipp Kobbe ◽  
Henning Rahne ◽  
Till Wörpel ◽  
Burkard Jäger ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Behavioral Abnormalities

Plastic and behavioral abnormalities in experimental Huntington's disease: A crucial role for cholinergic interneurons

2006 ◽  
Vol 22 (1) ◽  
pp. 143-152 ◽  
Author(s):  
Barbara Picconi ◽  
Enrica Passino ◽  
Carmelo Sgobio ◽  
Paola Bonsi ◽  
Ilaria Barone ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Crucial Role ◽  
Cholinergic Interneurons ◽  
Behavioral Abnormalities

Neuroprotective potential of Cilostazol in 3-NP provoked Huntington's disease-associated symptoms

2021 ◽  
pp. 2472-2478
Author(s):  
Surbhi Gupta ◽  
Bhupesh Sharma
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neuronal Damage ◽  
Lipid Peroxides ◽  
Acetylcholinesterase Activity ◽  
Nitropropionic Acid ◽  
Behavioral Abnormalities ◽  
Plus Maze ◽  
Nissl Stain ◽  
And Behavior

Huntington's disease (HD), a neurodegenerative condition specified by mitochondrial deficits, psychiatric and cognitive impairment developed due to neuronal damage in the brain. 3-nitropropionic acid (3-NP), an inhibitor of succinate dehydrogenase develops behavioral, biochemical as well as histological alterations in the striatal region of brain, which resembles HD in humans. Phosphodiesterases (PDEs) participate in cognition, motor functions, and behavior as well as also offers neuroprotection. The present investigation was framed to analyze the neuro-defensive characteristics of cilostazol PDE3 inhibitor over the 3-NP induced behavioral, striatal and mitochondrial deficits. Administration of 3-NP (10mg kg-1; i.p.) for the duration of 14 days has shown considerable alterations in behavior such as decreased locomotion (actophotometer), reduced grip strength (rota-rod test), spatial learning memory (elevated plus maze and Morris water maze). In parallel to, 3-NP treated rats exhibit biochemical changes such as increased oxidative stress (enhanced lipid peroxides, reduced glutathione, catalase, and superoxide dismutase), disturbed cholinergic function (increased acetylcholinesterase activity), increased inflammation (more myeloperoxidase) and mitochondrial dysfunction (reduced complex I, II and IV activity). Histopathological changes (Nissl stain) like chronic neuronal gap, pyknotic nuclei as well as injured cells in the cerebral cortex and hippocampus were also observed in 3-NP treated rats. Administration of cilostazol considerably restored behavioral abnormalities, biochemical and histopathological alterations. In this investigation, cilostazol offered neurodefensive effects which were established by behavioral and biochemical paradigms, which confirmed the potent neurodefensive aspect of cilostazol in 3-NP provoked behavioral and biochemical abnormalities.

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