Prolactin prevents the kainic acid-induced neuronal loss in the rat hippocampus by inducing prolactin receptor and putatively increasing the VGLUT1 overexpression.

Neuroprotective effects of short prolactin (PRL) pre-treatment against kainic acid (KA)-induced damage include neuron loss avoidance in all hippocampal regions and attenuation of seizures. Recent evidence points PRL receptor (PRL-R) as mediator of such neuroprotective effects and seizures as regulators of neuronal marker transcript expression in the hippocampus. Here, we investigated if a daily PRL dose of 100 µg or vehicle for 14 days in ovariectomized rats (OVX) prevents neuron loss induced by KA administered on the third day of PRL treatment in a systemic single dose of 7.5 mg/kg or vehicle, and promotes PRL-R, vesicular glutamate transporter 1 (VGLUT1) and glutamic acid decarboxylase 65 (GAD65) expression changes in the hippocampus of sacrificed rats 27 days after the KA administration. Immunostaining for Neu-N and PRL-R revealed significant neuron number and PRL-R expression reduction induced by KA that was prevented and turned into overexpression respectively in all hippocampal regions when PRL was added; while VGLUT1,and GAD65 immunostaining displayed expression decrease in the CA1 of injured rats, prevented in the last case and turned into VGLUT1, overexpression when administered PRL. These data indicate that chronic PRL administration before damage induces hippocampal neuroprotection associated with PRL-R and VGLUT1 overexpression, the latter in a regiondependent way.