Effects of microinjection of LY235959 or NBQX in the insular cortex on cardiovascular and tail skin temperature responses to restraint stress.
aCSF - Bilateral microinjection of aCSF (vehicle, 100 nL) into the IC did not change the basal values of MAP, HR or tail skin temperature (Table 1).
LY235959 - Bilateral microinjection of the selective NMDA glutamate receptor antagonist LY235959 (1 nmol/100 nL) into the IC did not change the basal values of MAP, HR or tail skin temperature (Table 1). However, analysis of the time-course curves of cardiovascular responses to restraint stress indicated that LY235959 microinjected into the IC enhanced the restraint-evoked increase in MAP (treatment: F(1,13) = 9.194; time: F(40,520) = 8.073; interaction:, F(40,520) = 1.761) and HR (treatment:, F(1,13) = 5.171; time: F(40,520) = 22.22; interaction: F(40,520) = 1.627) when compared to animals treated with aCSF (Fig. 2 and 3).
The antagonism of the NMDA glutamate receptor within the IC shifted the decrease in tail skin temperature in increase (treatment: F(1,13) = 8.648; interaction: F(6,78) = 5.184; time: F(6,78) = 1.931) (Fig. 4).
NBQX - Bilateral microinjection of the selective non-NMDA glutamate receptor antagonist NBQX (1 nmol/100 nL) into the IC did not change the basal values of MAP, HR or tail skin temperature (Table 1). Analysis of the time-course curves of cardiovascular responses to restraint stress also did not indicate a significant effect of IC treatment with NBQX on the restraint-evoked increase in MAP (treatment: F(1,13) = 2.402; time: F(40,520) = 15.87; interaction: F(40,520) = 1.727) and HR (treatment: F(1,13) = 0.9897; time: F(40,520) = 25.02; interaction: F(40,520) = 1.125) (Fig. 2 and 3). The blockade of non-NMDA glutamate receptors within the IC did not change the tail skin temperature values compared to animals treated with aCSF (treatment: F(1,13) = 0.002649; time: F(6,78) = 13.14; interaction: F(6,78) = 0.8501) (Fig. 4).