Canine Morphine Specific Direct ELISA Kit

Ventral tegmental area (VTA) dopamine (DA) neurons presynaptic glutamate release plays a very important role in the mechanism of morphine. Previously, a study from our lab found that morphine disinhibited glutamatergic input onto the VTA-DA neurons, which was an important mechanism for the morphine-induced increase in the VTA-DA neuron firing and related behaviors (Chen a al., 2015). However, what source of glutamatergic inputs is disinhibited by morphine remains to be elucidated. Using optogenetic strategy combined with whole-cell patchclamp, qRT-PCR, immunofluorescence and chemical genetic approach combined with behavioral methods, our results show that 1) morphine promotes glutamate release from glutamatergic terminals of medial prefrontal cortex (mPFC) neurons projecting to VTA-DA neurons but does not on those from glutamatergic terminals of the lateral hypothalamus (LH) neurons projecting to VTA-DA neurons; 2) different response of glutamatergic neurons projecting to VTA-DA neurons from the mPFC or the LH to morphine is related to the expression of GABA(B) receptors at terminals of these neurons; 3) inhibition of projection neurons from the mPFC to the VTA significantly reduces morphine-induced locomotor activity increase and conditioned place preference but inhibition of projection neurons from the LH to the VTA does not. These results suggest that morphine selectively promotes glutamate release of the glutamatergic input from mPFC onto VTA-DA neurons by removing the inhibition of the GABA(B) receptors in this glutamatergic input from mPFC.

Background: Intrathecal morphine prolongs analgesia after surgery, but has been implicated in postoperative respiratory depression or apnoeic episodes. However, this has not been investigated in a prospective trial using respiratory polygraphy. This randomised controlled triple-blinded trial tested the hypothesis that intrathecal morphine increases sleep apnoea severity, measured using respiratory polygraphy. Methods: Sixty subjects undergoing hip arthroplasty under spinal anaesthesia received either 15 mg isobaric bupivacaine 0.5% with 0.5 ml normal saline 0.9% (control group) or 15 mg isobaric bupivacaine 0.5% with 0.5 ml intrathecal morphine 100 mu g (intrathecal morphine group). Respiratory polygraphy was performed before surgery and on the first and third postoperative nights. The primary outcome was the apnoea-hypopnoea index in the supine position (supine AHI) on the first postoperative night. Secondary outcomes included supine AHI on the third postoperative night, oxygen desaturation index (ODI), and ventilatory frequency during the first and third postoperative nights. Results: On the first postoperative night, mean (95% confidence interval) values for supine AHI were 20.6 (13.9-27.3) and 21.2 (12.4-30.0) events h(-1)in the control and intrathecal morphine groups, respectively (P=0.90). There were no significant between-group differences for any of the secondary outcomes, except for a significantly higher central and mixed apnoea index preoperatively and significantly lower mean SpO(2) on the third postoperative night in the control group. Conclusions: Intrathecal morphine did not increase sleep apnoea severity when measured using respiratory polygraphy. Of note, all patients had an increased number of apnoeic episodes on the third postoperative night.