PI3K/Akt inhibition suppressesexcitatory synaptic transmission in substantia gelatinosa neurons in an inflammatory pain model in rats [Sıçanlarda bir yangısal ağrı modelinde substantia gelatinosa tabakasında pi3k/akt İnhibisyonu eksitatör sinaptik geçişi süprese eder]

Pi3k/aktsignaling pathway has been shown to contribute to thermal and mechanical hyperalgesia. nociceptive excitatory synaptic transmission is a critical factor to pain behavior responses. however,it is unclear whether pi3k/akt pathway is involved in the modulation of excitatory synaptic transmission within the spinal cord. in this study,two inhibitors of the pi3k/akt pathway,ly294002 and wortmannin,were used to test the potential functional roles in the excitatory synaptic transmission. ly294002 and wortmannin did not change the frequency or amplitude of spontaneous excitatory postsynaptic current (sepsc) in the spinal slice preparedfrom adult rats by injection of saline,but bothof them decreased the frequency and amplitude of sepsc in the spinal slice preparedfrom adult rats by injection of a complete freund's adjuvant (cfa). further studyshowed thatly294002 or wortmannin treatment attenuatedcfa-inducedincreased expression of p-aktin the spinal dorsal horn. thus,the present study showed that pi3k/akt pathway played an important role in themaintenance ofthe nociceptive transmission in hypersensitive state,contributing to behavioral nociceptive responses. © 2015,ege university press. all rights reserved.