A model of dynamic exercise: the decerebrate rat locomotor preparation

Bedford, T. G.; Loi, Poh Kheng; Crandall, CG

doi:10.1152/jappl.1992.72.1.121

Cited by 46 publications

(56 citation statements)

References 15 publications

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“…This stimulation also evoked both left and right tibial nerve discharges supplying triceps surae muscles after muscle paralysis. These data were consistent with previous studies by others (5,9,28,43,50).…”

Section: Methodssupporting

confidence: 94%

“…Stimulating the MLR in paralyzed animals has been extensively used to study the physiological roles played by central command (5,7,14,21,28,43). However, in this experimental preparation, it is difficult to equate the MLR stimulation with the way that this site is activated as central command during actual exercise.…”

Section: Discussionmentioning

confidence: 99%

“…After the recovery period, the junction of the superior and inferior colliculus was searched to find the site of the MLR with electrical stimulation at 30-to 40-A current intensity (60 Hz, 1-ms duration) with a needle-type bipolar microelectrode (CBBPE75, FHC) connected to an electronic stimulator (S88, Grass Instruments). The detailed procedure is described in the previous studies (5,21). The determination of the site of the MLR was affirmed from the physiological criteria as follows: 1) threshold of locomotion with reciprocal limb movement Ͻ40 A, 2) stimulus-bound locomotion, and 3) graded activity of locomotion and gait changes with increased stimulation current (5, 21).…”

Section: Methodsmentioning

confidence: 99%

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Sympathetic responses to exercise in myocardial infarction rats: a role of central command

Koba¹,

Gao²,

Xing³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Koba, Satoshi, Zhaohui Gao, Jihong Xing, Lawrence I Sinoway, and Jianhua Li. Sympathetic responses to exercise in myocardial infarction rats: a role of central command. Am J Physiol Heart Circ Physiol 291: H2735-H2742, 2006. First published July 14, 2006 doi:10.1152/ajpheart.00522.2006.-In congestive heart failure (CHF), exaggerated sympathetic activation is observed during exercise, which elicits excess peripheral vasoconstriction. The mechanisms causing this abnormality are not fully understood. Central command is a central neural process that induces parallel activation of motor and cardiovascular systems. This study was undertaken to determine whether central command serves as a mechanism that contributes to the exaggerated sympathetic response to exercise in CHF. In decerebrated rats, renal and lumbar sympathetic nerve responses (RSNA and LSNA, respectively) to 30 s of fictive locomotion were examined. The fictive locomotion was induced by electrical stimulation of the mesencephalic locomotor region (MLR). The study was performed in control animals (fractional shortening Ͼ 40%) and animals with myocardial infarctions (MI; fractional shortening Ͻ 30%). With low stimulation of the MLR (current intensity ϭ 20 A), the sympathetic responses were not significantly different in the control (RSNA: ϩ18 Ϯ 4%; LSNA: ϩ3 Ϯ 2%) and MI rats (RSNA: ϩ16 Ϯ 5%; LSNA: ϩ8 Ϯ 3%). With intense stimulation of the MLR (50 A), the responses were significantly greater in MI rats (RSNA: ϩ127 Ϯ 15%; LSNA: ϩ57 Ϯ 10%) than in the control rats (RSNA: ϩ62 Ϯ 5%; LSNA: ϩ21 Ϯ 6%). In this study, the data demonstrate that RSNA and LSNA responses to intense stimulation of the MLR are exaggerated in MI rats. We suggest that intense activation of central command may play a role in evoking exaggerated sympathetic activation and inducing excessive peripheral vasoconstriction during exercise in CHF.congestive heart failure; mesencephalic locomotor region; renal sympathetic nerve activity; lumbar sympathetic nerve activity EXERCISE ACTIVATES THE SYMPATHETIC nervous system, increases blood pressure, and leads to an increase in blood flow to exercising skeletal muscle. This increase in muscle blood flow is associated with reduced renal blood flow (23). Two principal neural mechanisms are proposed to increase sympathetic nerve activity (SNA) and regulate the cardiovascular system during exercise. These are termed the exercise pressor reflex and central command. The exercise pressor reflex is a neural reflex that arises from receptors sensitive to mechanical and metabolic stimuli in exercising skeletal muscles and stimulates the medulla through the muscle thin afferent fibers (18). Central command is a feed-forward neural mechanism that induces parallel activation of motor and cardiovascular systems (9, 50). The brain sites that generate motor signals also send descending projections to sympathetic neurons (19,20,22).Congestive heart failure (CHF) includes abnormal cardiovascular regulation in exercise. Specifically, sympathetic tone to muscle is elevat...

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Section: Methodssupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Sympathetic responses to exercise in myocardial infarction rats: a role of central command

Koba¹,

Gao²,

Xing³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…4,24,25 Our findings indicate that tonic and reflex cardiovascular adjustments are also evoked from the PPT via direct cholinergic projections to the RVLM. These data support our hypothesis that cholinergic input to the RVLM is involved in central command.…”

Section: Padley Et Al Cholinergic Inputs To Rvlm In Central Commandmentioning

confidence: 63%

“…Previous studies have shown that the PPT is involved in initiation of movement and modulation of muscle tone during locomotion, exercise, and arousal. 4,24,25 Additionally, the PPT connects albeit indirectly with both motor and sympathetic outflows. 5 We aimed, firstly, to determine the role of the RVLM in the autonomic responses and effects on reflex control of the circulation evoked by central mAChR activation.…”

mentioning

confidence: 99%

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

Padley

Kumar

et al. 2007

Circulation Research

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Abstract-Central command is a feedforward neural mechanism that evokes parallel modifications of motor and cardiovascular function during arousal and exercise. The neural circuitry involved has not been elucidated. We have identified a cholinergic neural circuit that, when activated, mimics effects on tonic and reflex control of circulation similar to those evoked at the onset of and during exercise. Central muscarinic cholinergic receptor (mAChR) activation increased splanchnic sympathetic nerve activity (SNA) as well as the range and gain of the sympathetic baroreflex via activation of mAChR in the rostral ventrolateral medulla (RVLM) in anesthetized artificially ventilated SpragueDawley rats. RVLM mAChR activation also attenuated and inhibited the peripheral chemoreflex and somatosympathetic reflex, respectively. Cholinergic terminals made close appositions with a subpopulation of sympathoexcitatory RVLM neurons containing either preproenkephalin mRNA or tyrosine hydroxylase immunoreactivity. M2 and M3 receptor mRNA was present postsynaptically in only non-tyrosine hydroxylase neurons. Cholinergic inputs to the RVLM arise only from the pedunculopontine tegmental nucleus. Chemical activation of this region produced increases in muscle activity, SNA, and blood pressure and enhanced the SNA baroreflex; the latter effect was attenuated by mAChR blockade. These findings indicate a novel role for cholinergic input from the pedunculopontine tegmental nucleus to the RVLM in central cardiovascular command. This pathway is likely to be important during exercise where a centrally evoked facilitation of baroreflex control of the circulation is required to maintain blood flow to active muscle. (Circ Res. 2007;100:284-291.)Key Words: baroreflex Ⅲ exercise Ⅲ chemoreflex Ⅲ somatosympathetic A distinct pattern of tonic and reflex cardiovascular adjustments is mediated by central command to ensure appropriate muscle and organ perfusion during different arousal or behavioral states, such as sleep and exercise. [1][2][3] Limited evidence implicates some regions within the pons and hypothalamus that could provide descending input to cardiovascular control sites 4 -6 ; however, the neural circuitry and neurotransmitters involved are yet to be elucidated.Activation of the central cholinergic system has a profound effect on cardiovascular and other autonomic functions. [7][8][9][10][11][12][13][14][15][16][17][18] Systemic or central administration of acetylcholinesterase inhibitors or muscarinic agonists increases blood pressure, 7-11 lowers body temperature, 12 and alters respiration. 13,14 Pressor responses can be evoked via activation of muscarinic receptors (mAChR) within several cardiovascular nuclei, including the posterior hypothalamus, 7 nucleus of the solitary tract, 15 and rostral ventrolateral medulla (RVLM). 10,11 Effects of central mAChR activation on cardiovascular reflexes are less well understood. 8,16,17 Sympathoexcitatory and hypertensive effects of intravenously administered physostigmine are largely mediated by ...

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The pedunculopontine region and breathing in Parkinson's disease

Hyam

Wang

Roy

et al. 2019

Ann Clin Transl Neurol

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Objective Respiratory abnormalities such as upper airway obstruction are common in Parkinson's disease ( PD ) and are an important cause of mortality and morbidity. We tested the effect of pedunculopontine region ( PPN r) stimulation on respiratory maneuvers in human participants with PD , and separately recorded PPN r neural activity reflected in the local field potential ( LFP ) during these maneuvers. Methods Nine patients with deep brain stimulation electrodes in PPN r, and seven in globus pallidus interna ( GP i) were studied during trials of maximal inspiration followed by forced expiration with stimulation OFF and ON . Local field potentials ( LFP s) were recorded in the unstimulated condition. Results PEFR increased from 6.41 ± 0.63 L/sec in the OFF stimulation state to 7.5 L ± 0.65 L/sec in the ON stimulation state ( z = −2.666, df = 8, P = 0.024). Percentage improvement in PEFR was strongly correlated with proximity of the stimulated electrode contact to the mesencephalic locomotor region in the rostral PPN ( r = 0.814, n = 9, P = 0.008). Mean PPN r LFP power increased within the alpha band (7–11 Hz) during forced respiratory maneuvers (1.63 ± 0.16 μ V 2 /Hz) compared to resting breathing (0.77 ± 0.16 μ V 2 /Hz; z = −2.197, df = 6, P = 0.028). No changes in alpha activity or spirometric indices were seen with GP i recording or stimulation. Percentage improvement in PEFR was strongly positively correlated with increase in alpha power ( r = 0.653, n = 14 (7 PPN r patients recorded bilaterally), P = 0.0096). Interpretation PPN r stimulation in PD improves indices of upper airway function. Increased alpha‐band activity is seen within the PPN r during forced respiratory maneuvers. Our findings suggest a link between the PPN r and respiratory performance in PD .

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A model of dynamic exercise: the decerebrate rat locomotor preparation

Cited by 46 publications

References 15 publications

Sympathetic responses to exercise in myocardial infarction rats: a role of central command

Sympathetic responses to exercise in myocardial infarction rats: a role of central command

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

The pedunculopontine region and breathing in Parkinson's disease

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