| First Author | Slugg RM | Year | 2000 |
| Journal | Neuroendocrinology | Volume | 72 |
| Issue | 4 | Pages | 208-17 |
| PubMed ID | 11070424 | Mgi Jnum | J:65685 |
| Mgi Id | MGI:1927047 | Doi | 10.1159/000054589 |
| Citation | Slugg RM, et al. (2000) Effect of the &mgr;-opioid agonist DAMGO on medial basal hypothalamic neurons in beta-endorphin knockout mice. Neuroendocrinology 72(4):208-17 |
| abstractText | The endogenous opioid neurotransmitter beta-endorphin (beta-END), a product of the proopiomelanocortin (POMC) gene, is strongly implicated in the control of the female reproductive cycle, stress responses, and antinociception. Using selective gene targeting, we have generated a strain of mice that do not express any beta-END. These mice exhibit both normal reproduction and normal basal and stress-induced hypothalamic-pituitary-axis activity, but exhibit a significantly attenuated opioid-mediated stress-induced analgesia. To further understand the cellular bases of these responses, we have studied mediobasal hypothalamic (MBH) neurons, including POMC neurons, using whole-cell patch recording in an in vitro slice preparation. Twenty-seven MBH cells were recorded in wild-type and 25 MBH cells were recorded in beta-END knockout mice. Neurons from both genotypes showed a significant positive correlation between DAMGO concentration (from 30 nM to 10 &mgr;M) and the induced outward K(+) current. The genotypes did not differ, however, in either the DAMGO-induced maximum outward current response or EC(50), or for the maximal response to the GABA(B) agonist baclofen. Furthermore, quantitative receptor autoradiography utilizing (3)H-DAMGO did not reveal any differences in total &mgr;-opioid receptor binding between genotypes. Therefore, we conclude that the complete absence of beta-END throughout development did not alter either the expression of &mgr;-opioid receptors or their coupling to K(+) channels in MBH neurons. Copyright 2000 S. Karger AG, Basel |
