title: Decrease of calbindin-d28k, calretinin, and parvalbumin by taurine treatment does not induce a major susceptibility to kainic acid.
abstract: Taurine, 2-aminoethanesulfonic acid, is present at high concentrations in many invertebrate and vertebrate systems, and it has several biological functions. In addition, it has been related to a neuroprotective role against several diseases, such as epilepsy. It has been reported that taurine induces a decrease of calbindin-D28k, calretinin, and parvalbumin protein levels in the hippocampus 3 days after administration. In the present work we hypothesized that the decrease of these proteins could alter the action of kainic acid (KA) and make mice more susceptible to excitotoxicity. Therefore, we treated mice with taurine and after 3 days treated them with KA. The results showed that taurine pretreatment did not induce a major susceptibility to KA. Moreover, neurodegeneration was reduced in pretreated mice. However, astrogliosis was similar to that observed in mice treated only with KA. The immunohistochemistries for calbindin-D28k, calretinin, and parvalbumin showed that these proteins were reduced as a consequence of KA treatment and of taurine treatment. However, mice pretreated with taurine prior to KA administration presented the same reduction in these proteins as mice treated with only taurine or only KA.
authors.affiliation: Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Institut de Biomedicina (IBUB), Centros de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat de Barcelona, Barcelona, Spain.
authors.forename: F
authors.initials: F
authors.lastname: Junyent
authors.forename: D
authors.initials: D
authors.lastname: Porquet
authors.forename: L
authors.initials: L
authors.lastname: de Lemos
authors.forename: R
authors.initials: R
authors.lastname: Romero
authors.forename: J
authors.initials: J
authors.lastname: Utrera
authors.forename: A
authors.initials: A
authors.lastname: Camins
authors.forename: M
authors.initials: M
authors.lastname: Pallàs
authors.forename: C
authors.initials: C
authors.lastname: Auladell
mesh_terms: D000818:Animals; D064092:Calbindin 1; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D004351:Drug Resistance / Q000187:drug effects* / Q000502:physiology; D004827:Epilepsy / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism; D007608:Kainic Acid / Q000819:agonists*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins / Q000819:agonists*; D010320:Parvalbumins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000037:antagonists & inhibitors* / Q000378:metabolism; D013654:Taurine / Q000378:metabolism / Q000633:toxicity*
chemical_list: C576499:Calb1 protein, mouse; C576511:Calb2 protein, mouse; D064092:Calbindin 1; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins; D009498:Neurotoxins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; D013654:Taurine; D007608:Kainic Acid