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Catherine Wilson

Publications and source records attributed to Catherine Wilson.

3 recordsLinked to original sources
PubMed2004

5-HT7 receptor subtype as a mediator of the serotonergic regulation of luteinizing hormone release in the zona incerta.

5-Hydroxytryptamine (5-HT) and the 5-HT(1A/7) receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralinHBr (8-OH-DPAT), injected into the zona incerta (an area in the dorsal hypothalamus) of the female rat, inhibit the release of luteinizing hormone (LH) and the effects of both are blocked by the 5-HT(2/7) receptor antagonist, ritanserin. As both 8-OH-DPAT and ritanserin have moderate activity at the 5-HT7 receptor subtype, the possibility that this subtype might mediate their effects in the zona incerta has been investigated. Ovariectomised rats were primed with 5 microg oestradiol benzoate followed at 48 h by 0.5 mg progesterone, which induces an LH surge. 5-Carboxamidotryptamine (5-CT), a potent but non-selective agonist at 5-HT7 receptors, like 5-HT and 8-OH-DPAT, inhibited the LH surge at 5 and 1.25 nmol injected bilaterally into the zona incerta. The non-selective 5-HT(2/7) receptor antagonist ritanserin and the selective 5-HT7 receptor antagonist, (R)-3-(2-(2-(4-methyl-piperidin-1-yl)-pyrrolidine-1-sulfonyl)-phenol (SB-269970-A) at 0.5 microg/side blocked all three receptor agonists when injected concurrently into the zona incerta. However, lower (0.2 microg) and higher doses (2 and 5 microg) of SB-269970-A were less effective, indicating a bell-shaped dose-response curve. SB-269970-A was also inhibitory when administered systemically (1 mg/kg intraperitoneally (i.p.)). When LH release was suppressed by 5 microg oestradiol benzoate, SB-269970-A (0.5 and 2 microg) did not elevate levels, indicating it is unlikely that 5-HT7 receptors mediate a tonic inhibition on release but rather are involved in terminating the pre-ovulatory LH surge. These data demonstrate that 5-HT7 receptors play a role in the regulation of LH by the zona incerta in rat brain.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2004

Parallel genetic basis for repeated evolution of armor loss in Alaskan threespine stickleback populations.

Most adaptation is thought to occur through the fixation of numerous alleles at many different loci. Consequently, the independent evolution of similar phenotypes is predicted to occur through different genetic mechanisms. The genetic basis of adaptation is still largely unknown, however, and it is unclear whether adaptation to new environments utilizes ubiquitous small-effect polygenic variation or large-effect alleles at a small number of loci. To address this question, we examined the genetic basis of bony armor loss in three freshwater populations of Alaskan threespine stickleback, Gasterosteus aculeatus, that evolved from fully armored anadromous populations in the last 14,000 years. Crosses between complete-armor and low-armor populations revealed that a single Mendelian factor governed the formation of all but the most anterior lateral plates, and another independently segregating factor largely determined pelvic armor. Genetic mapping localized the Mendelian genes to different chromosomal regions, and crosses among these same three widely separated populations showed that both bony plates and pelvic armor failed to fully complement, implicating the same Mendelian armor reduction genes. Thus, rapid and repeated armor loss in Alaskan stickleback populations appears to be occurring through the fixation of large-effect variants in the same genes.

Animals↗