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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Anesthesiology. 2019 Apr;130(4):592–608. doi: 10.1097/ALN.0000000000002615

Fig.4. Pretreatment with endogenous TRPV1 agonist N-oleoyldopamine attenuates capsaicin-induced enhancement in glutamate transmission and firing in LHb neurons.

Fig.4.

Representative traces showing enhancement of sEPSCs induced by N-oleoyldopamine (OLDA,10 μM) followed by capsaicin (3 μM) in a Naive (A1) and an EtOH-WD (B1) neuron. (A2-B2) Exemplar current traces were acquired in A1 and B1, before and during OLDA application, and OLDA/capsaicin co-application. Application of a high concentration OLDA (10 μM) enhanced sEPSC frequency (C) in LHb neurons of naïve but not in EtOH-WD rats. (D) OLDA did not alter sEPSC amplitude. (E) In the presence of 10 μM OLDA, capsaicin (3μM) produced a weaker increase on sEPSC frequency in naïve rats. (F) Representative traces showing enhancement of firing induced by OLDA alone or OLDA/capsaicin co-application in neurons of Naïve and EtOH-WD rats. (G) OLDA (10 μM) activated the LHb neurons of naïve rats but not that of EtOH-WD rats. (H) With the pretreatment of OLDA (10 μM), capsaicin (3 μM) produced a weaker increase in firing in naïve rats. *P < 0.05, **P < 0.01 relative to respective 0.2μM OLDA. ##P < 0.01, Naïve in comparison with EtOH-WD rats. @P < 0.05, @@P < 0.01, capsaicin-induced change within OLDA comparison to without OLDA (aCSF).