J Appl Physiol. 2011 Dec;111(6):1877-87. doi: 10.1152/japplphysiol.00313.2011. Epub 2011 Aug 11.
Electroacupuncture increased cerebral blood flow and reduced ischemic brain injury: dependence on stimulation intensity and frequency.
Zhou F, Guo J, Cheng J, Wu G, Xia Y.
Source
Shanghai Research Center for Acupuncture and Meridians, Shanghai, China.
Abstract
Stroke causes ischemic brain injury and is a leading cause of neurological disability and death. There is, however, no promising therapy to protect the brain from ischemic stress to date. Here we show an exciting finding that optimal electroacupuncture (EA) effectively protects the brain from ischemic injury. The experiments were performed on rats subjected to middle cerebral artery occlusion (MCAO) with continuous monitoring of cerebral blood flow. EA was delivered to acupoints of "Shuigou" (Du 26) and "Baihui" (Du 20) with different intensities and frequencies to optimize the stimulation parameters. The results showed that 1) EA at 1.0-1.2 mA and 5-20 Hz remarkably reduced ischemic infarction, neurological deficit, and death rate; 2) the EA treatment increased the blood flow by >100%, which appeared immediately after the initiation of EA and disappeared after the cessation of EA; 3) the EA treatment promoted the recovery of the blood flow after MCAO; 4) "nonoptimal" parameters of EA (e.g., <0.6 mA or >40 Hz) could not improve the blood flow or reduce ischemic injury; and 5) the same EA treatment with optimal parameters could not increase the blood flow in naive brains. These novel observations suggest that appropriate EA treatment protects the brain from cerebral ischemia by increasing blood flow to the ischemic brain region via a rapid regulation. Our findings have far-reaching impacts on the prevention and treatment of ischemic encephalopathy, and the optimized EA parameters may potentially be a useful clue for the clinical application of EA.
PMID: 21836043 [PubMed - indexed for MEDLINE] PMCID: PMC3233896 Free PMC Article







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Med Hypotheses. 2008 Nov;71(5):668-81. doi: 10.1016/j.mehy.2008.06.030. Epub 2008 Aug 30.
Electrical stimulation therapies for CNS disorders and pain are mediated by competition between different neuronal networks in the brain.
Faingold CL.
Source
Department of Pharmacology, Southern Illinois University School of Medicine, P.O. Box 19629, Springfield, IL 62794-9629, USA. cfaingold@siumed.edu
Abstract
CNS neuronal networks are known to control normal physiological functions, including locomotion and respiration. Neuronal networks also mediate the pathophysiology of many CNS disorders. Stimulation therapies, including localized brain and vagus nerve stimulation, electroshock, and acupuncture, are proposed to activate "therapeutic" neuronal networks. These therapeutic networks are dormant prior to stimulatory treatments, but when the dormant networks are activated they compete with pathophysiological neuronal networks, disrupting their function. This competition diminishes the disease symptoms, providing effective therapy for otherwise intractable CNS disorders, including epilepsy, Parkinson's disease, chronic pain, and depression. Competition between stimulation-activated therapeutic networks and pathophysiological networks is a major mechanism mediating the therapeutic effects of stimulation. This network interaction is hypothesized to involve competition for "control" of brain regions that contain high proportions of conditional multireceptive (CMR) neurons. CMR regions, including brainstem reticular formation, amygdala, and cerebral cortex, have extensive connections to numerous brain areas, allowing these regions to participate potentially in many networks. The participation of CMR regions in any network is often variable, depending on the conditions affecting the organism, including vigilance states, drug treatment, and learning. This response variability of CMR neurons is due to the high incidence of excitatory postsynaptic potentials that are below threshold for triggering action potentials. These subthreshold responses can be brought to threshold by blocking inhibition or enhancing excitation via the paradigms used in stimulation therapies. Participation of CMR regions in a network is also strongly affected by pharmacological treatments (convulsant or anesthetic drugs) and stimulus parameters (strength and repetition rate). Many studies indicate that treatment of unanesthetized animals with antagonists (bicuculline or strychnine) of inhibitory neurotransmitter (GABA or glycine) receptors can cause CMR neurons to become consistently responsive to external inputs (e.g., peripheral nerve, sensory, or electrical stimuli in the brain) to which these neurons did not previously respond. Conversely, agents that enhance GABA-mediated inhibition (e.g., barbiturates and benzodiazepines) or antagonize glutamate-mediated excitation (e.g., ketamine) can cause CMR neurons to become unresponsive to inputs to which they responded previously. The responses of CMR neurons exhibit extensive short-term and long-term plasticity, which permits them to participate to a variable degree in many networks. Short-term plasticity subserves termination of disease symptoms, while long-term plasticity in CMR regions subserves symptom prevention. This network interaction hypothesis has value for future research in CNS disease mechanisms and also for identifying therapeutic targets in specific brain networks for more selective stimulation and pharmacological therapies.




J Appl Physiol. 2011 December; 111(6): 1877–1887.
Published online 2011 August 11. doi: 
10.1152/japplphysiol.00313.2011

PMCID: PMC3233896

Mechanisms of Beneficial Effects of Physical Activity on Atherosclerosis and Coronary Heart Disease
Electroacupuncture increased cerebral blood flow and reduced ischemic brain injury: dependence on stimulation intensity and frequency
Fei Zhou,1 Jingchun Guo,2 Jieshi Cheng,2 Gencheng Wu,2 and Ying Xiacorrauth3,4
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Abstract
Stroke causes ischemic brain injury and is a leading cause of neurological disability and death. There is, however, no promising therapy to protect the brain from ischemic stress to date. Here we show an exciting finding that optimal electroacupuncture (EA) effectively protects the brain from ischemic injury. The experiments were performed on rats subjected to middle cerebral artery occlusion (MCAO) with continuous monitoring of cerebral blood flow. EA was delivered to acupoints of “Shuigou” (Du 26) and “Baihui” (Du 20) with different intensities and frequencies to optimize the stimulation parameters. The results showed that 1) EA at 1.0–1.2 mA and 5–20 Hz remarkably reduced ischemic infarction, neurological deficit, and death rate; 2) the EA treatment increased the blood flow by >100%, which appeared immediately after the initiation of EA and disappeared after the cessation of EA; 3) the EA treatment promoted the recovery of the blood flow after MCAO; 4) “nonoptimal” parameters of EA (e.g., <0.6 mA or >40 Hz) could not improve the blood flow or reduce ischemic injury; and 5) the same EA treatment with optimal parameters could not increase the blood flow in naive brains. These novel observations suggest that appropriate EA treatment protects the brain from cerebral ischemia by increasing blood flow to the ischemic brain region via a rapid regulation. Our findings have far-reaching impacts on the prevention and treatment of ischemic encephalopathy, and the optimized EA parameters may potentially be a useful clue for the clinical application of EA.
Keywords: acupuncture, brain protection, infarction, neurological deficits