Cardiovascular Deconditioning Induces Changes in the Excitatory Neurotransmission and Active Properties of Nucleus Tractus Solitarii Neurons

Abstract

Hindlimb‐unloading (HU) in rats induces cardiovascular deconditioning analogous to that observed in individuals exposed to microgravity or bed rest. Among other physiological changes, HU rats exhibit autonomic imbalance, increased baseline heart rate and altered baroreflex and chemoreflex. Considering that the nucleus tractus solitariis (nTS) is an important central region for autonomic control and integration of cardiovascular reflex function, in this study we aimed to investigate the effects of HU on glutamatergic synaptic transmission and intrinsic properties of nTS neurons. For this purpose, stainless steel wire rings were positioned in the tail of male Sprague‐Dawley rats (3 weeks) and after one week of recovery the rings was connected to a suspension apparatus. HU rats were suspended at an angle of 30–35° for two weeks with free access to food and water, while control animals were maintained under normal postural conditions. After this period, coronal brainstem slices were obtained and the whole‐cell patch clamp technique was performed to evaluate the electrophysiological properties of nTS neurons. The effectiveness of the HU protocol was confirmed by significant hindlimb muscle atrophy. Adrenal weight was comparable between HU and control rats. Resting membrane potential of nTS neurons from HU rats was comparable to neurons from controls. However, HU reduced the percentage of neurons that exhibited spontaneous firing activity (Control: 46% vs HU: 11%). In addition, HU induced a significant increase in the action potential rheobase and A‐type potassium current of nTS neurons, which may contribute to altered basal firing rate. Furthermore, the frequency, but not the amplitude of spontaneous excitatory postsynaptic currents (sEPSC) was significantly higher in the neurons of HU rats in comparison to the control. Taken together the data indicated that HU increases glutamatergic neurotransmission and reduces the excitability of NTS neurons. Therefore, the results suggest that changes in neuronal activity and synaptic transmission in the nTS may contribute to the cardiovascular reflex alterations observed in HU rats.Support or Funding InformationSupport: HL132836This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.