Neonatal shaking brain injury changes psychological stress-induced neuronal activity in adult male rats

Abstract

Neonatal shaking brain injury (SBI) leads to increases in anxiety-like behavior and altered hormonal responses to psychological stressors as adults. These abnormalities are hypothesized to be due to a change in sensitization in neuronal circuits as a consequence of neonatal SBI. We examined the effects of neonatal SBI on neuronal activity in the anxiety- and/or stress-related areas of adult rats using Fos immunohistochemistry. Exposure to a novel elevated plus maze (EPM) resulted in a marked increase in Fos expression in the parvocellular (PVNp) and magnocellular parts of the paraventricular nucleus and the ventral part of the bed nucleus of the stria terminalis (vBNST) of shaken rats (S group) compared to non-shaken control rats (C group). On the contrary, Fos expression was significantly lower in the medial nucleus of the amygdala and the ventral subiculum (vS) of S group rats than C group rats exposed to EPM. Although we found no significant correlation in the number of Fos-expressing cells in the vBNST and PVNp in the C group rats, these numbers were significantly correlated in the S group rats. Furthermore, in the S group rats, but not in the C group rats, the number of Fos-expressing cells in the vBNST was inversely correlated with that in the vS. Interestingly, previous neuronal tracing studies have demonstrated direct projections from the vS to the vBNST and from the vBNST to the PVNp. The present data suggest that neonatal SBI can alter neuronal activity in anxiety- and/or stress-related neuronal circuits.