Participação das neurotransmissões glutamatérgica e nitrérgica no córtex insular sob as respostas autonômicas e neuroendócrinas desencadeadas pelo estresse agudo

Abstract

Insular cortex (IC) is a brain structure involved in modulating autonomic activity, such as cardiovascular system adjustments in stress situations. Glutamate and nitric oxide (NO) neurotransmitters are associated with several functions performed by the central nervous system (CNS). Thus, the present study aims to investigate the involvement of these two neurotransmissions at IC (i.e., glutamatergic and nitrergic), on restraint stress-triggered autonomic and neuroendocrine responses. We used two antagonists of glutamate receptor (NMDA: LY235959; and non-NMDA: NBQX) to evaluate glutamatergic neurotransmission effect. We used three different approaches to study nitrergic neurotransmission: selective nNOS inhibitor (NPLA), NO sequester (Carboxi-PTIO), and specific guanylate cyclase inhibitor (ODQ). All drugs were applied by microinjection in the IC. Pressure and the tachycardic response of animals submitted to restriction stress were potentiated beyond the blockade of glutamatergic neurotransmission by LY235959, as well as the blockade of nitrergic neurotransmission by NPLA, Carboxi-PTIO, and ODQ. Additionally, glutamatergic neurotransmission by non-NMDA receptors (NBQX) did not alter blood pressure and heart rate. The modulation of the deacrease in caudal temperature, a characteristic autonomic response for restraint stress, was not changed by the blockade of nitrergic and glutamatergic neurotransmission on any used drugs. NPLA and Carboxi-PTIO decrease the Glucocorticoid release. Blockade of glutamatergic neurotransmission and the use of specific guanylate cyclase inhibitor (GC) did not affect corticosterone release. This non-effect suggests that the glutamatergic and nitrergic neurotransmissions participation on IC occurs in different ways over the cardiovascular and neuroendocrine responses triggered by stress. Glutamatergic neurotransmission, through NMDA receptors, and nitrergic neurotransmission participatein the modulation of cardiovascular changes, inhibiting the stress-triggered tachycardic and blood pressure increase. However, the modulation of corticosterone release by nitrergic neurotransmission occurred from independent mechanisms independent of the activation of NMDA receptors and GC, but dependent on nNOS and NO formation, but dependent on nNOS and NO formation.