Studies in systems ranging from humans to lower vertebrates have demonstrated that neural circuits can be modulated by steroid hormones. Many organs in the body are receptive to steroid hormones, which exert their actions either indirectly via the circulation or directly via local production in tissues, including the brain. Two classic neuroethological model systems, the songbird and midshipman fish, have demonstrated that neurons in auditory circuits possess both the capability to produce 17β-estradiol (E2), a potent estrogen, as well as E2 receptors. E2 was first shown to act via a nuclear receptor, known as estrogen receptor alpha (ERα), resulting in transcriptional modifications. However, rapid effects of E2 have also been demonstrated which occur in a time period too short to be accounted for by genomic mechanisms. Currently, little is known about the mechanisms through which estrogens exert their rapid actions.
The research focus of my lab is understanding how steroid hormones modulate neuronal function acutely and chronically using a well-described sensory system, the Mauthner cell circuit of the goldfish, which controls the escape response. The Mauthner cell receives massive input from the auditory branch of the VIIIth cranial nerve and the circuit has been described over many decades anatomically, physiologically and behaviorally. Given the identifiably of the few cells involved in the circuit, it provides an ideal model for studying evolutionarily conserved cellular and circuit interactions in an intact vertebrate central nervous system. The Mauthner cell circuit also permits correlation of a well-defined behavior with its underlying physiological, anatomical and biochemical processes.
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