Traumatic brain injury results in a concomitant increase in neocortical expression of vasopressin and its V1a receptor.

Arginine vasopressin (AVP) has been shown to promote the disruption of the blood-brain barrier (BBB) and the formation of edema in various animal models of brain injury. However, the source(s) of this AVP have not been identified. Since the cerebral cortex was considerably affected in some of these brain injury models, we sought to determine if AVP was produced in the cerebral cortex, and, if so, whether or not this cortical AVP expression was up regulated after injury. In the present study, a controlled cortical impact model of traumatic brain injury (TBI) in rats was used, and the temporal changes in expression of AVP and its V(1a) receptor were analyzed by real-time reverse-transcriptase polymerase chain reaction. The expression of AVP and its V(1a) receptor in the ipsilateral cortex adjacent to the lesion area was significantly up regulated between 4 h and 1 day post-TBI. The maximum increase in mRNA for AVP (4.3-fold) and its receptor (2.6-fold) in the ipsilateral vs. contralateral cortex was observed at 6 h post-TBI. Compared to sham-injured rats, no statistically significant changes in expression of AVP or its receptor were found in the contralateral cortex. These results suggest that the cerebral cortex is an important source of AVP in the injured brain, and the parallel increase in the expression of AVP and its cognate receptor may act to augment the actions of AVP related to promoting the disruption of the BBB and the formation of post-traumatic edema.