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Different effects of dynorphin A on in vitro guinea pig hippocampal CA3 pyramidal cells with various degrees of paired-pulse facilitation
Authors:T Iwama  K Ishihara  M Satoh  H Takagi
Affiliation:1. Department of Rehabilitation Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China;2. Center for Human Movement Sciences, University Medical Center Groningen, University of Groningen, Groningen 9713, the Netherlands;3. Institute of Medical Research, Northwestern Polytechnical University, Xi’an 710072, PR China;1. Department of Pharmacy, The Second Affiliated (Xinqiao) Hospital, The Army (Third Military) Medical University, Chongqing, China;2. Department of Pain and Rehabilitation, The Second Affiliated (Xinqiao) Hospital, The Army (Third Military) Medical University, Chongqing, China;3. Department of Wound Infection and Drug, State Key Laboratory of Trauma, Burn and Combined Injury, The Third Affiliated (Daping) Hospital, The Army (Third Military) Medical University, Chongqing, China;4. Department of Neurology, The Second Affiliated (Xinqiao) Hospital, The Army (Third Military) Medical University, Chongqing, China;5. Department of Neurology, The Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing, China
Abstract:We investigated the effects of dynorphin A (Dyn A), a heptadecapeptide, on the population spikes of the guinea pig hippocampal CA3 pyramidal neurons, in vitro, using paired-pulse stimulation of the mossy fibers. Dyn A produced facilitatory and inhibitory effects on the population spikes in the preparations with lower and higher degrees of paired-pulse facilitation, respectively. Morphine and D-Ala2, D-Leu5-en-kephalin, mu- and delta-agonist, respectively, predominantly potentiated the population spikes, while kappa-agonists such as U-50, 488H and bremazocine mainly caused an inhibition. These results suggest that Dyn A has two separate (excitatory and inhibitory) effects on the guinea pig hippocampal CA3 neurons through mu-(delta) and kappa-opioid receptors, respectively.
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