POST-TREATMENT WITH PROLACTIN PROTECTS HIPPOCAMPAL CA1 NEURONS OF THE OVARIECTOMIZED FEMALE RAT AGAINST KAINIC ACID-INDUCED NEURODEGENERATION
Por:
Reyes-Mendoza, Julio, Morales, Teresa
Publicada:
22 jul 2016
Categoría:
Neuroscience (miscellaneous)
Resumen:
Kainic acid (KA) is a glutamate agonist widely used in studies of
neurodegeneration due to its ability to induce excitotoxic damage in the
rodent brain. Previously, we reported that pre-treatment with prolactin
(PRL) prevents the neuron loss induced by KA administration in CA1, CA3
and CA4 of the hippocampus of the female rat. Here, we investigated if
PRL has a neuroprotective effect in the dorsal hippocampus when it is
administered after KA. For this, 100 ng of KA or 0.9% saline was
administered intracere-broventricularly (ICV) to ovariectomized female
rats. One hour later, they received subcutaneous PRL (103 mu g/day for 7
days) or saline through an osmotic minipump. Also, to determine the
hippocampal neurogenesis rate, the rats were administered
bromodeoxyuridine along with the PRL treatment. Immunostaining for NeuN
revealed that neuronal loss is lower in the CA1 of PRL-treated rats
compared with the untreated group, but PRL did not confer any protection
in the CA3 and CA4 subfields. Furthermore, PRL prevented the KA-induced
cognitive deficit measured as a better performance in the novel object
recognition test. The PRL treatment did not modify the neurogenesis
rate. These data indicate that post-treatment with PRL confers
differential neuroprotection against KA-induced neuronal loss in
hippocampal subfield CA1, which correlates with a more mild cognitive
deficit compared with the untreated control group. (C) 2016 IBRO.
Published by Elsevier Ltd. All rights reserved.
Filiaciones:
Reyes-Mendoza, Julio:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Celular & Mol, Queretaro 76230, Qro, Mexico
Morales, Teresa:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Celular & Mol, Queretaro 76230, Qro, Mexico
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