Hypothalamic neurochemical changes in long-term recovered bilateral subdiaphragmatic vagotomized rats
Abstract BackgroundVagus nerve is one of the crucial routes in communication between immune and central nervous systems. Impaired vagal nerve function may intensify peripheral inflammatory processes. This effect subsides along with prolonged recovery after permanent nerve injury. One of the results of such compensation is a normalized plasma concentration of stress hormone corticosterone – a marker of hypothalamic-pituitary-adrenal (HPA) axis activity. In the present work we strive to explain this corticosterone normalization by studying the mechanisms responsible for compensation-related neurochemical alterations in the hypothalamus. Methods Using microarrays and HPLC we measured genome-wide gene expression and major amino acid neurotransmitters content in hypothalamus of bilaterally vagotomized rats, one month after surgery.ResultsOur results show that, in the long-term, vagotomy affects hypothalamic amino acids concentration but not mRNA expression of tested genes.ConclusionsWe propose an alternative pathway of immune to CNS communication after vagotomy, leading to activation of HPA axis, by influencing central amino acids and subsequent monoaminergic neurotransmission.