Heart rate, blood pressure, and running speed responses to mesencephalic locomotor region stimulation in anesthetized rats

Abstract

The decerebrate rat locomotor preparation described in a previous study requires extensive brain surgery with the possibility of significant blood loss. The purpose of this study was to improve on the previous model by using lightly anesthetized instead of decerebrated rats. After initial surgery consisting of boring a small hole through the parietal bone, the animals were maintained on low levels of halothane anesthetic. The mesencephalic locomotor region was then located by physiological criteria using stereotaxic coordinates from the previous study. Locomotor speed, blood pressure and heart rate responses were then measured over a wide range of stimulation currents that elicited a maximal running speed. Stimulation currents ranged from 36 microA for walking to 82 microA for fast galloping. Locomotor speeds ranged from 20 m/min for walking to 64 m/min for fast galloping. Some animals easily achieved galloping speeds beyond 100 m/min. Blood pressure and heart rate increased with increasing stimulation currents. Blood pressure also increased during stimulation after muscular paralysis. This was not due to current spread, suggesting that the mesencephalic locomotor region might be involved in central command mechanisms. Heart rate did not increase after paralysis. This supports other multi-joint dynamic studies suggesting that movement per se may be necessary to induce heart rate changes, presumably via joint mechanoreceptors. The range of locomotor patterns and cardiovascular responses were obtained under self-supported conditions. By defining the mesencephalic locomotor region via physiological criteria, and by grouping blood pressure and heart rate measurements by gait rather than by stimulation currents, the potential use of the intact model for cardiovascular control studies was demonstrated. The animals were able to run and gallop at high speeds considering they were anesthetized. The simplified preparation will be useful for more complex cardiovascular experiments requiring intact and self-supported conditions.

Central Command Regulation of Circulatory Function Mediated by Descending Pontine Cholinergic Inputs to Sympathoexcitatory Rostral Ventrolateral Medulla Neurons

“…Electrical stimulation of the PPT increases AP, HR, and renal SNA (with a lesser increase in lumbar SNA) in decerebrate animals. 48,49 Sympathoexcitatory responses are also evoked from surrounding brain areas including the cuneiform nucleus. 50 At present, we cannot explain the lack of effect of stimulating the PPT on other reflex responses that are modified by activation of RVLM mAChR.…”

“…24,48,49 Single cholinergic neurons in the PPT have dual connections with the motor cortex and stellate ganglion, as revealed by polysynaptic viral …”

Sinoaortic denervation abolishes pressure resetting for daily physical activity in rabbits

“…This reflective pressure increase is referred to as an exercise pressor reflex or response (17) and is well known to be mediated by two mechanisms. One mechanism is a centrally generated motor command signal called "central command" (13,16) that promotes sympathoexcitation and an increase in MAP and is speculated to be generated at locomotor centers probably located in the midbrain and a superior central region (2,30). The other mechanism, called the "muscle chemoreflex" and "muscle mechanoreflex," is the afferent signals that originate from working muscles, enhancing sympathetic outflow to increase MAP (14,24,26).…”

A new conceptual framework for the integrated neural control of locomotor and sympathetic function: implications for exercise after spinal cord injury

“…Thus, electrical stimulation of the single brainstem site (MLR) induced an integrated response that included the increased frequency of flexion and extension and the concomitant increase in activation of the sympathetic nervous system to increase blood pressure and HR. After applying curare, stimulation of the MLR still increased blood pressure and activated hindlimb nerves (fictive locomotion), but without an increase in HR, and this was attributed to the absence of active input from leg afferents (Chong and Bedford 1997).…”

“…These include amplifying excitatory inputs, or setting the level of excitability in sympathetic preganglionic neurons in order to modify responses to other inputs (Schreihofer and Sved 2011). D r a f t Chong and Bedford (1997) demonstrated the parallel activation and inter-relationships between blood pressure, HR and locomotion speed with increasing intensity of tonic MLR stimulation.…”