Study on intervention mechanism of acupuncture for neuron abnormal neural coding in visual cortex area 17 of monocular deprivation rats

Study on intervention mechanism of acupuncture for neuron abnormal neural coding in visual cortex... Objective: To investigate the electrophysiological mechanism of acupuncture for the visual cortex plasticity during the sensitive period. Methods: Fifty 2-week-old Wistar rats were randomly divided into a blank control group, a model group, an early-stage acupuncture group, a middle-stage acupuncture group and a late-stage acupuncture group, 10 rats in each group. Monocular deprivation amblyopia models were prepared in rats except those in the blank control group by unilateral eyelid suture. After successful modeling, no treatment was applied to the rats in the model group. Rats in each acupuncture group were treated with acupuncture at bilateral Jingming (BL 1), Cuanzhu (BL 2), Fengchi (GB 20) and Guangming (GB 37), started from the 3rd day, 12th day or 21st day after modeling separately, once a day, for a total of 9 d treatment. The neuronal discharge frequency and action potential inter-spike interval (ISI) in the rat visual cortex area 17 of each group were measured by multi-channel microelectrode array nerve signal technique. Results: The discharge number of neurons in the visual cortex of the model group was significantly lower than that in the blank control group (P<0.05). After treatment, the discharge numbers in the early-stage acupuncture group and the middle-stage acupuncture http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Acupuncture and Tuina Science Springer Journals

Study on intervention mechanism of acupuncture for neuron abnormal neural coding in visual cortex area 17 of monocular deprivation rats

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Shanghai Research Institute of Acupuncture and Meridian and Springer-Verlag GmbH Germany
Subject
Medicine & Public Health; Acupuncture
ISSN
1672-3597
eISSN
1993-0399
D.O.I.
10.1007/s11726-017-1010-2
Publisher site
See Article on Publisher Site

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