Morphine is thought to produce reinforcement phenomena via stimulation of mu, delta, and kappa opioid receptors that regulate stress perception, pain control, reward behavior, and neurohormone secretion in reward-relevant brain systems. It has the highest affinity for mu, followed by delta and kappa. Rapid activation of the mu opioid receptor by morphine results in a euphoric phenotype, thus conferring the reinforcing effects of the drug. This activation is accompanied by extracellular dopamine release, which alters several events related to the cAMP signal transduction pathway. Of particular significance is that CREB seems to be modified by morphine, thereby affecting addictive behavioral phenomena, such as withdrawal symptoms.
Clonality:
Monoclonal
Concentration:
1ug/ul
Clone Designation:
[2F11]
Buffer:
Aqueous buffered solution containing 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Source:
KLH conjugated Morphine molecular modified
Target:
Morphine
Application Dilute:
WB(WB=1:500-2000), IF(IF=1:100-500)
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