Welcome to the Neuroendocrinology Lab!!!
Members of my laboratory and I are curious about the interactions among hormones, the brain, and behavior. More specifically, we study the spatial and temporal precision of hormone provision, and how this precision results in complex behaviors like learning and memory.
Here’s the deal – some hormones are synthesized in many different tissues, affect many different targets, and modulate many different behaviors. How then, is the right hormone provided to the right target at the right time?
Estrogens, like estradiol (E2) is one such hormone. It is synthesized in the ovary, placenta, adipose tissue, the pituitary, and in the brain itself. E2 can affect parts of the forebrain, midbrain, hindbrain, and the spinal cord to influence behaviors as distinct as balance, mood, energy balance, aggression, memory, and sex. To make things even more interesting, E2 is a steroid (oil soluble, not water soluble), and thus has potential access to every cell in the body (every cell has a fat membrane). So, how can E2 be provided to just the right target tissue at just the right time and at just the right dose, to affect any one particular behavior while excluding effects on others?
Our laboratory studies E2 synthesis in the brains of songbirds. The zebra finch has been a resilient animal model in neuroendocrinology for many reasons, one of which is that these birds make high levels of E2 in many different parts of the brain. This is accomplished by expressing the enzyme aromatase at high levels. Aromatase is the enzyme that converts testosterone to estradiol.
We study two distinct phenomena:
- Aromatase expression in presynaptic boutons and postsynaptic dendrites
- Aromatase expression in astrocytes
The Synaptocrine Hypothesis
Almost twenty years ago, we located the aromatase protein in presynaptic boutons in the zebra finch brain using immunocytochemistry and electron microscopy (Peterson et al., 2005). We corroborated these results by measuring aromatase activity and expression in synaptosomes (Rohmann et al. 2007). Along with our collaborators we termed this form of signaling, “synaptocrine,” since it is very different from other forms of secreted signaling (Remage-Healey et al., 2011; Saldanha et al., 2011). Since then we have learned that synaptic aromatase may be regulated differently from that in other parts of the neuron (Cornil et al., 2012) and that synaptic aromatase may be a critical modulator of memory function (Bailey et al., 2013; 2017). Current projects explore the interactions among electrical activity, synaptic aromatase and neurotransmitter release.
Induced aromatase in astrocytes
Also about twenty years ago, we discovered that injury to the zebra finch brain results in the induction of aromatase expression in a cell type that normally does not express this protein. Astrocytes around the site of brain injury begin transcribing and translating the aromatase gene and transcript within hours of brain damage (Peterson et al., 2001). We now know that this induction of aromatase expression limits the size of brain damage (Wynne & Saldanha, 2004; Saldanha et al., 2005; Wynne et al., 2008) and increases cytogenesis and neurogenesis (Walters & Saldanha, 2008; Walters et al., 2011). Interestingly, it is the inflammation that results from brain trauma that induces aromatase expression in astrocytes (Pedersen et al., 2017) and the E2 synthesized by astrocytes reduces chronic inflammation (Pedersen et al., 2016). Current projects involve understanding the generality of this phenomena in transgenic mice.