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Striatal modulation of cAMP-response-element-binding protein (CREB) after excitotoxic lesions: implications with neuronal vulnerability in Huntington's disease.
Eur J Neurosci. 2006 Jan; 23(1):11-20.EJ

Abstract

Recent evidence has shown that the activity of cAMP responsive element-binding protein (CREB) and of CREB-binding protein (CBP) is decreased in Huntington's disease (HD) [Steffan et al. (2000)Proc. Natl Acad. Sci. USA, 97, 6763-6768; Gines et al. (2003)Hum. Mol. Genet., 12, 497-508; Rouaux et al. (2004) Biochem. Pharmacol., 68, 1157-1164; Sugars et al. (2004)J. Biol. Chem., 279, 4988-4999]. Such decrease is thought to reflect the impaired energy metabolism observed in a HD mouse model, where a decline in striatum cAMP levels has been observed [Gines et al. (2003)Hum. Mol. Genet., 12, 497-508]. Increased levels of CREB have also been demonstrated to exert neuroprotective functions [Lonze & Ginty (2002)Neuron, 35, 605-623; Lonze et al. (2002)Neuron, 34, 371-385]. Our study aimed to investigate the distribution of CREB in the neuronal subpopulations of the striatum in normal rats compared to the HD model of quinolinic acid lesion. Twenty-five Wistar rats were administered quinolinic acid 100 mm into the right striatum, and killed after 24 h, 48 h, 1 week, 2 weeks, and six weeks, respectively. The contralateral striata were used as controls. Dual-label immunofluorescence was employed using antibodies against phosphorylated CREB and each of the different neuronal subpopulations markers. Our results show that activated CREB levels decrease progressively in projection neurons and parvalbumin (PARV) and calretinin (CALR) interneurons, whereas such levels remain stable in cholinergic and somatostatin interneurons. Thus, we speculate that the ability of cholinergic interneurons to maintain their levels of CREB after excitotoxic lesions is one of the factors determining their protection in Huntington's disease.

Authors+Show Affiliations

Laboratory of Neuroanatomy, Santa Lucia Foundation IRCCS at the European Center for Brain Research, via del Fosso Fiorano 64, 00143 Rome, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16420411

Citation

Giampà, Carmela, et al. "Striatal Modulation of cAMP-response-element-binding Protein (CREB) After Excitotoxic Lesions: Implications With Neuronal Vulnerability in Huntington's Disease." The European Journal of Neuroscience, vol. 23, no. 1, 2006, pp. 11-20.
Giampà C, DeMarch Z, D'Angelo V, et al. Striatal modulation of cAMP-response-element-binding protein (CREB) after excitotoxic lesions: implications with neuronal vulnerability in Huntington's disease. Eur J Neurosci. 2006;23(1):11-20.
Giampà, C., DeMarch, Z., D'Angelo, V., Morello, M., Martorana, A., Sancesario, G., Bernardi, G., & Fusco, F. R. (2006). Striatal modulation of cAMP-response-element-binding protein (CREB) after excitotoxic lesions: implications with neuronal vulnerability in Huntington's disease. The European Journal of Neuroscience, 23(1), 11-20.
Giampà C, et al. Striatal Modulation of cAMP-response-element-binding Protein (CREB) After Excitotoxic Lesions: Implications With Neuronal Vulnerability in Huntington's Disease. Eur J Neurosci. 2006;23(1):11-20. PubMed PMID: 16420411.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Striatal modulation of cAMP-response-element-binding protein (CREB) after excitotoxic lesions: implications with neuronal vulnerability in Huntington's disease. AU - Giampà,Carmela, AU - DeMarch,Zena, AU - D'Angelo,Vincenza, AU - Morello,Maria, AU - Martorana,Alessandro, AU - Sancesario,Giuseppe, AU - Bernardi,Giorgio, AU - Fusco,Francesca R, PY - 2006/1/20/pubmed PY - 2006/4/7/medline PY - 2006/1/20/entrez SP - 11 EP - 20 JF - The European journal of neuroscience JO - Eur J Neurosci VL - 23 IS - 1 N2 - Recent evidence has shown that the activity of cAMP responsive element-binding protein (CREB) and of CREB-binding protein (CBP) is decreased in Huntington's disease (HD) [Steffan et al. (2000)Proc. Natl Acad. Sci. USA, 97, 6763-6768; Gines et al. (2003)Hum. Mol. Genet., 12, 497-508; Rouaux et al. (2004) Biochem. Pharmacol., 68, 1157-1164; Sugars et al. (2004)J. Biol. Chem., 279, 4988-4999]. Such decrease is thought to reflect the impaired energy metabolism observed in a HD mouse model, where a decline in striatum cAMP levels has been observed [Gines et al. (2003)Hum. Mol. Genet., 12, 497-508]. Increased levels of CREB have also been demonstrated to exert neuroprotective functions [Lonze & Ginty (2002)Neuron, 35, 605-623; Lonze et al. (2002)Neuron, 34, 371-385]. Our study aimed to investigate the distribution of CREB in the neuronal subpopulations of the striatum in normal rats compared to the HD model of quinolinic acid lesion. Twenty-five Wistar rats were administered quinolinic acid 100 mm into the right striatum, and killed after 24 h, 48 h, 1 week, 2 weeks, and six weeks, respectively. The contralateral striata were used as controls. Dual-label immunofluorescence was employed using antibodies against phosphorylated CREB and each of the different neuronal subpopulations markers. Our results show that activated CREB levels decrease progressively in projection neurons and parvalbumin (PARV) and calretinin (CALR) interneurons, whereas such levels remain stable in cholinergic and somatostatin interneurons. Thus, we speculate that the ability of cholinergic interneurons to maintain their levels of CREB after excitotoxic lesions is one of the factors determining their protection in Huntington's disease. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/16420411/Striatal_modulation_of_cAMP_response_element_binding_protein__CREB__after_excitotoxic_lesions:_implications_with_neuronal_vulnerability_in_Huntington's_disease_ L2 - https://doi.org/10.1111/j.1460-9568.2005.04545.x DB - PRIME DP - Unbound Medicine ER -