Objective: 

The possible role of melatonin on the estrogen neuroprotection effects of following traumatic brain injury (TBI) is not known. The objective of this study was to assess the possible role of the MT1 melatonin receptor on the effects of estrogen following TBI.

Methods: 

Diffuse TBI was induced by Marmarou method in ovariectomized (OVX) female rats, which were divided into 4 groups with each including three subgroups; OVX+TBI; ovx+ E2; OVX+Veh+E2; and OVX + Luzindole + E2.Drugs injections were given 30 minutes after Luzindole injection which was immediately given after TBI. Drugs and vehicles were injected in a volume of 0.33 ml/rat by intraperitoneal (ip) route. Twenty-four hours after TBI, brain water content was measured, while brain Evans blue content was determined 5 h after TBI. intracranial pressure (ICP) was measured in spinal cord and cerebral perfusion pressure(CPP) calculated by subtracting the mean arterial pressure (AMP) from ICP in time interval one hour before trauma induction and at 0, 1, 4, 24 hours minutes after TBI.

Results: 

The results showed that after TBI, brain water content in OVX + Luzindole + E2;significantly increased compared OVX+Veh+E2 group (p >0.01). Brain Evans blue content in OVX + Luzindole + E2; group significantly increased compared to other groups (p >0.001). CPP 1 hours after in OVX + Luzindole + E2 group significantly increased compare to OVX+Veh+E2 (p<0.01).

Conclusions: 

We conclude that melatonin MT1 receptor inhibition prevented from estrogen's protective effects on brain water content and blood-brain barrier; and CPP after TBI.