TY - JOUR
T1 - Participation of NMDA-glutamatergic receptors in hippocampal neuronal damage caused by adult-onset hypothyroidism
AU - Alva-Sánchez, Claudia
AU - Becerril, Adriana
AU - Anguiano, Brenda
AU - Aceves, Carmen
AU - Pacheco-Rosado, Jorge
N1 - Funding Information:
We thank Dr. Ellis Glazier and Dr. M. Sánchez-Álvarez for editing English-language text. This work was supported by SIP-IPN 20070734, CONACyT 52253 and PAPIIT 201207. J.P.-R. is fellow of DEDICT-COFAA-IPN. C.A.-S. is a fellow of CONACYT.
PY - 2009/4/10
Y1 - 2009/4/10
N2 - We analyzed the participation of N-methyl-d-aspartate (NMDA) receptors in the neuronal damage caused by adult-onset hypothyroidism. Wistar rats were randomly assigned into four groups. The euthyroid group received tap water. The hypothyroid group received methimazole (60 mg/kg) in their drinking water to induce hypothyroidism. Two more groups of rats received the antithyroid treatment and were injected daily with the NMDA antagonist ketamine (15 mg/kg, sc) or MK-801 (0.5 mg/kg, ip). Treatments were administered during 4 weeks. At the end of the respective treatments rats were deeply anaesthetized and perfused intracardially with 0.9% NaCl followed by 4% paraformaldehyde. The brains were removed from the skull, and coronal brain sections (7 μm thick) were obtained. Neurons were counted in the CA1, CA2, CA3, and CA4 hippocampal regions differentiating between normal and atrophic cells by an experimenter blind to the treatment. The percentage of neuronal damage found in the MMI group was significantly greater in the hippocampal regions compared to the euthyroid group. In contrast, both NMDA antagonists were able to prevent the neuronal damage secondary to hypothyroidism in all hippocampal regions. Our results suggest that the neuronal damage caused in the hippocampus of adult-onset hypothyroid rats requires activation of NMDA channels.
AB - We analyzed the participation of N-methyl-d-aspartate (NMDA) receptors in the neuronal damage caused by adult-onset hypothyroidism. Wistar rats were randomly assigned into four groups. The euthyroid group received tap water. The hypothyroid group received methimazole (60 mg/kg) in their drinking water to induce hypothyroidism. Two more groups of rats received the antithyroid treatment and were injected daily with the NMDA antagonist ketamine (15 mg/kg, sc) or MK-801 (0.5 mg/kg, ip). Treatments were administered during 4 weeks. At the end of the respective treatments rats were deeply anaesthetized and perfused intracardially with 0.9% NaCl followed by 4% paraformaldehyde. The brains were removed from the skull, and coronal brain sections (7 μm thick) were obtained. Neurons were counted in the CA1, CA2, CA3, and CA4 hippocampal regions differentiating between normal and atrophic cells by an experimenter blind to the treatment. The percentage of neuronal damage found in the MMI group was significantly greater in the hippocampal regions compared to the euthyroid group. In contrast, both NMDA antagonists were able to prevent the neuronal damage secondary to hypothyroidism in all hippocampal regions. Our results suggest that the neuronal damage caused in the hippocampus of adult-onset hypothyroid rats requires activation of NMDA channels.
KW - Ketamine
KW - MK-801
KW - Methimazole
KW - Neuroprotection
UR - http://www.scopus.com/inward/record.url?scp=61849095283&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2009.02.017
DO - 10.1016/j.neulet.2009.02.017
M3 - Artículo
C2 - 19429030
SN - 0304-3940
VL - 453
SP - 178
EP - 181
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -