Central Nucleus of the Amygdala Mediates Sympathoinhibitory Responses to Activation of Paraventricular Nucleus of the Thalamus

Abstract

The paraventricular nucleus of the thalamus (PVT) is known to relay sensory information from the brainstem, and information from limbic and cortical structures involved in visceral and homeostatic regulation, and affective behaviors. In turn, PVT relays this information to a number of forebrain structures, including the amygdala. However, whether PVT is involved in mediating cardiovascular information to other central sites is not clear. This study was done to investigate whether the cardiovascular responses elicited by PVT involved a pathway that included the central nucleus of the amygdala (ACe). In the first series of experiments, a systematic mapping of PVT was done to identify cardiovascular responsive sites using microinjection of glutamate (Glu; 10 nL, 0.25 M) in chloralose anesthetized Wistar rats. Glu injections into PVT elicited decreases in systemic mean arterial pressure (MAP, −20 ± 3 mmHg) and heart rate (HR; −15 ± 5 bpm). These depressor responses were mediated through sympathoinhibition as intravenous injections of the ganglionic blocker hexamethonium bromide prevented the responses. In the second series, iontophoretic injections of the anterograde tract tracer PHA‐L were made at PVT depressor sites in the Wistar rats. Dense PHA‐L fiber and presumptive terminal labeling was found within and around the region of the lateral ACe, while light to moderate labeling was observed within the medial ACe. Additionally, extensive labeling was observed throughout the extended amygdala, including the bed nucleus of the stria terminalis. In the final series, bilateral microinjection (100 nL) of either the synaptic blocker CoCl2, the non‐specific glutamate antagonist kynurenic acid or the specific NMDA receptor antagonists 2‐amino‐5‐phosphonovalerate or MK801 were made into ACe in the chloralose anesthetized Wistar rats. Injections of these compounds did not significantly alter the resting levels of arterial pressure (AP) or HR, but significantly attenuated (p<0.01) the MAP response (mean of all injected compounds; −7 ± 5 mmHg) to activation of PVT. On the other hand, these injections into ACe did not alter the HR response (mean of all injected compounds; −12 ± 3 bpm) to PVT stimulation. These data suggest that PVT may function as a relay of sensory information that affects AP responses associated with motivated and addictive behaviors, arousal and/or stress through a sympathoinhibitory neural circuit involving ACe.Support or Funding InformationSupported in part by Heart and Stroke Foundation of Ontario.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.