The inactivation effect of Kolliker Fuse nucleus on long cardiovascular response of L- glutamate in cuneiform nucleus in rats

Cuneiform nucleus (CnF) is in midbrain area that has several functions including cardiovascular regulation. It is reported that the cardiovascular effect of CnF nucleus is mediated by rostral ventrolateral medulla (RVLM). However, direct projection from CnF to RVLM is sparse; therefore cardiovascular response of CnF nucleus may be relayed by other nuclei such as Kolliker—Fuse nucleus (KF). To test this hypothesis, KF was inactivated by cobalt chloride (CoCl2) and its effect on long cardiovascular response of glutamate in CnF was evaluated. Rats were anesthetized and arterially canuulated. Blood pressure (BP) and heart rate (HR) were recorded throughout the experiment. The drugs were microinjected into the nuclei and maximum change was compared with that prior to injection and with the control group using descriptive statistics and unpaired t-test for data analysis. Results were given as the mean±SEM. Microinjection of glutamate into the CnF nucleus caused a long term response (high blood pressure and tachycardia). Inactivation of KF nucleus significantly attenuated the blood pressure effect of long term response reaching 10.39±2.25 mmHg which is a significant decrease compared to glutamate (19.62±2.09 mmHg) (P<0.01). Maximum change in heart rate (16.33±4.8 bpm) showed no significant difference compared to glutamate (21.6±11.9 bpm). Our results showed that long term high blood pressure effect of CnF nucleus was mediated by KF nucleus. However, since inactivation of KF cannot completely block this response, another area may also be involved in relaying this effect. Tachycardia response was not affected by inactivation of KF nucleus. This finding indicates that the pathway of tachycardia response of CnF is probably independent of KF nucleus Cuneiform nucleus, Kolliker—Fuse nucleus, Glutamate, CoCl2, Blood pressure, Rat