The sensation of pain is important for the survival of an organism. In humans, persistent pain can often have debilitating consequences leading to both financial and emotional destruction. Opioid-based drugs represent the most commonly prescribed medication for the treatment of pain. The reason for the popularity of opioids is based on their superior efficacy compared to other compounds. However, it is not fully known why opioids have such a powerful antinociceptive effect. Previous research has suggested that opioids may work through inhibition of ascending circuitry that transmits pain into the brain as well as activation of endogenous descending antinociceptive circuitry. The precise identity of the endogenous circuitry involved in either the transmission or inhibition of pain is not known. Previous studies indicate that the amygdala has a role in not only receiving nociceptive information, but also directly activating the descending antinociceptive circuity. The proposed experiments will examine how mu opioid receptor activation in one nucleus of the amygdala (basolateral) can effect nociceptive input and result in antinociceptive output in another amygdaloid nucleus (central). This information is important for understanding the mechanisms of opioid analgesic action.
| Finnegan, Thomas F; Chen, Shao-Rui; Pan, Hui-Lin (2006) Mu opioid receptor activation inhibits GABAergic inputs to basolateral amygdala neurons through Kv1.1/1.2 channels. J Neurophysiol 95:2032-41 |
| Finnegan, Thomas F; Chen, Shao-Rui; Pan, Hui-Lin (2005) Effect of the {mu} opioid on excitatory and inhibitory synaptic inputs to periaqueductal gray-projecting neurons in the amygdala. J Pharmacol Exp Ther 312:441-8 |
