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Michigan State UniversityBreedlove Jordan lab at MSU

The Role of Co-Factors in Steroid-Mediated Neural Plasticity

For the first two model systems described above (the SNB and the medial amygdala), you read about how gonadal hormones (androgens and/or estrogens) are capable of changing neuronal morphology. You also read that in some cases we know where hormones act to alter neuronal morphology. For example, we know that androgens induce adult SNB motoneuronal cell bodies to grow by activating androgen receptors in SNB motoneurons, and that without functional androgen receptors, SNB motoneurons do not grow in response to androgens. We also know that normally only some adult SNB motoneurons grow in response to adult androgens (increasing cell body size), while others do not. However, just about all motoneurons have androgen receptors, indicating that whether or not a motoneuron has androgen receptors can not explain why some motoneurons grow in response to androgens, while others do not. Thus, we have become interested in steroid receptor cofactors and whether they will explain these differences in androgen-responsiveness. Steroid receptor cofactors can be viewed as 'helper proteins' that are recruited to the AR after androgens bind and activate the receptor. Such cofactors are thought to play an essential role in the regulation of gene transcription by steroid receptors. We would like to know whether differences in steroid receptor cofactors exist that might account for differences in androgen-responsiveness among motoneurons.

Recall that the medial amygdala in Siberian hamsters exposed to short days loses its responsiveness to hormones, failing to grow in response to hormones as it does in hamsters exposed to long days. We are also interested in whether steroid receptor cofactors have a role in the change in hormone responsiveness that we observe in this model system.