Physical exercise decreases neuronal activity in the posterior hypothalamic area of spontaneously hypertensive rats

• Published in: Journal of applied physiology (1985) 2005-02, Vol.98 (2), p.572-578
• Main Authors: Beatty, Joseph A, Kramer, Jeffery M, Plowey, Edward D, Waldrop, Tony G
• Format: Article
• Language: English
• Subjects: Action Potentials; Adaptation, Physiological; Animals; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Brain; Cardiology. Vascular system; Electroencephalography - methods; Exercise; Experimental diseases; Hypertension; Hypertension - physiopathology; Hypothalamus, Posterior - physiopathology; Male; Medical sciences; Neurology; Neuronal Plasticity; Neurons; Physical Conditioning, Animal - methods; Physical Exertion; Rats; Rodents
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00184.2004

Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois Submitted 19 February 2004 ; accepted in final form 1 October 2004 Recently, physical exercise has been shown to significantly alter neurochemistry and neuronal function and to increase neurogenesis in discrete brain regions. Although we have documented that physical exercise leads to molecular changes in the posterior hypothalamic area (PHA), the impact on neuronal activity is unknown. The purpose of the present study was to determine whether neuronal activity in the PHA is altered by physical exercise. Spontaneously hypertensive rats (SHR) were allowed free access to running wheels for a period of 10 wk (exercised group) or no wheel access at all (nonexercised group). Single-unit extracellular recordings were made in anesthetized in vivo whole animal preparations or in vitro brain slice preparations. The spontaneous firing rates of PHA neurons in exercised SHR in vivo were significantly lower (8.5 ± 1.6 Hz, n = 31 neurons) compared with that of nonexercised SHR in vivo (13.7 ± 1.8 Hz, n = 38 neurons; P < 0.05). In addition, PHA neurons that possessed a cardiac-related rhythm in exercised SHR fired significantly lower (6.0 ± 1.8 Hz, n = 11 neurons) compared with nonexercised SHR (12.1 ± 2.4 Hz, n = 18 neurons; P < 0.05). Similarly, the spontaneous in vitro firing rates of PHA neurons from exercised SHR were significantly lower (3.5 ± 0.3 Hz, n = 67 neurons) compared with those of nonexercised SHR (5.6 ± 0.5 Hz, n = 58 neurons; P < 0.001). Both the in vivo and in vitro findings support the hypothesis that physical exercise can lower spontaneous activity of neurons in a cardiovascular regulatory region of the brain. Thus physical exercise may alter central neural control of cardiovascular function by inducing lasting changes in neuronal activity. hypertension; electrophysiology; plasticity Address for reprint requests and other correspondence: J. A. Beatty, Dept. of Molecular and Integrative Physiology, Univ. of Illinois at Urbana-Champaign, 524 Burrill Hall, 407 South Goodwin Ave., Urbana, IL 61801-3704 (E-mail: jbeatty{at}life.uiuc.edu )