Stress axis plasticity during vestibular compensation in the adult cat.

The postural, ocular motor, perceptive and neurovegetative syndromes resulting from unilateral vestibular neurectomy (UVN) symptoms could generate a stress and thereby activate the hypothalamo-pituitary-adrenal (HPA) axis. This study was aimed at determining whether UVN causes changes in the activity of the HPA axis, and if so, evaluating the time course of changes associated with UVN syndrome. At the cellular level, corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) immunoreactivity (Ir) were analyzed and quantified in the paraventricular nucleus (PVN) and the vestibular nuclei (VN) complex of cats killed early (1 and 7 days) or late (30 and 90 days) after UVN. Dopamine-beta-hydroxylase (DbetaH), the enzyme synthesizing noradrenaline was examined in the locus coeruleus (LC) in these same cats. At the behavioral level, the time course of recovery of the postural and locomotor functions was quantified at the same postoperative delays in another group of UVN cats. Results showed a significant bilateral increase in the number of both AVP-Ir and CRF-Ir neurons in the PVN and an increase of DbetaH-Ir neurons in the LC at 1, 7 and 30 days after UVN. This increased number of neurons was no longer observed at 90 days. Conversely, a significant bilateral decrease of CRF-Ir neurons was observed in the VN at these same postlesion times, with a similar return to control values at 90 days. Our behavioral observations showed strong posturo-locomotor functional deficits early after UVN (1 and 7 days), which had recovered partially at 30 days and completely by 90 days postlesion. We demonstrate a long-lasting activation of the HPA axis, which likely reflects a chronic stress, experienced by the animals, which corresponds to the time course of full vestibular compensation, and which is no longer present when the animals are completely free of posturo-locomotor symptoms at 90 days.