Skip to main content
. Author manuscript; available in PMC: 2009 Jun 2.
Published in final edited form as: Neuroscience. 2008 Mar 18;153(4):1268–1277. doi: 10.1016/j.neuroscience.2008.03.008

Figure 3. Estrogen attenuates whereas testosterone is required for the expression of antinociception produced by clonidine.

Figure 3

A. Intrathecal administration of clonidine (7 µg/ 5 µl) produced a significant increase in tail withdrawal latencies in OVX and male groups, but not in OVX+E groups. Clonidine significantly increased the latencies in the male and OVX groups, and maintained its effects for the period of testing (90 min). However, there was no effect of clonidine in the OVX+E group. B. In normally cycling females, clonidine significantly increased the tail withdrawal latencies at the diestrous stage, but not at the proestrous stage. C. Clonidine was completely ineffective in castrated males. Estradiol treatment did not alter this absence of effect, however, testosterone replacement in GDX males restored the antinociceptive effects of clonidine. D. The cumulative effect of clonidine over time was determined using area under the curve analysis. AUC was significantly higher in the male, OVX, diestrous and GDX+T groups in comparison to the OVX+E, proestrous, GDX, GDX+E and vehicle control groups. *p<0.05