ABSTRACT
Background and Purpose: The insular cortex (IC) is a brain
structure involved in the modulation of autonomic, cardiovascular and
neuroendocrine adjustments during stress situations. However, the local
neurochemical mechanisms involved in the control of these responses by
the IC are poorly understood. Glutamate is a prominent excitatory
neurotransmitter in the brain. Thus, the current study aimed to
investigate the involvement of glutamatergic neurotransmission within
the IC in cardiovascular, autonomic and neuroendocrine responses to
acute restraint stress.
Experimental Approach: The selective NMDA glutamate receptor
antagonist LY235959 (1 nmol/100 nL) and the selective non-NMDA glutamate
receptor antagonist NBQX (1 nmol/100 nL) were microinjected into the IC
10 min before the onset of restraint stress.
Key Results: The antagonism of NMDA receptors within the IC
potentiated the restraint-evoked increases in both arterial pressure and
heart rate, while non-NMDA blockade had no effect on these parameters.
Spontaneous baroreflex analysis demonstrated that microinjection of
LY235959 into the IC decreased baroreflex activity during restraint
stress. The decrease in tail skin temperature during restraint stress
was shifted to an increase in animals treated with the NMDA receptor
antagonist. Moreover, the blockade of IC glutamate receptors did not
affect the increase in circulating corticosterone levels during
restraint stress.
Conclusion and Implications: Overall, our findings provide
evidence that IC glutamatergic signalling, acting via NMDA receptors,
plays a prominent role in the control of autonomic and cardiovascular
responses to restraint stress but does not affect neuroendocrine
adjustments.