Neural Protein Plays Key Role in Bipolar Disorder

July 14, 2014
Jacquelyn Gray

Researchers at Tufts University have further clarified a key protein's role in bipolar disorder.

Researchers at Tufts University have further clarified a key protein’s role in bipolar disorder.

For their study published in Science Signaling, Grace Gill, PhD, and her colleagues set out to determine whether store-operated calcium (Ca2+) channels are associated with Sp4 protein degradation.

“Understanding how transcription factors like Sp4 are regulated may provide us with ways to change neuronal gene expression to treat symptoms of mental illness, including bipolar disorder,” Gill said in a statement.

Through their work, the researchers found Ca2+ channel signaling is most active when a neuron is at rest.

“We report that maximal activation of store-operated Ca2+ entry (SOCE) occurred in cerebellar granule neurons cultured under resting conditions, and that this Ca2+ influx promoted the degradation of transcription factor Sp4, a regulator of neuronal morphogenesis and function,” the authors wrote, adding their findings “indicated that, in neurons, SOCE is induced by hyperpolarization, and suggested that this Ca2+ influx pathway is a distinct mechanism for regulating neuronal gene expression.”

Although cells are widely perceived as being inactive or active, Gill said their activity is more multifaceted in nature.

“The calcium-signaling regulation of Sp4 during the resting phase was unexpected and suggests 2 things: resting neurons are more active than we had thought, and calcium signaling influences gene expression in both active and resting neurons,” she said.

According to the statement, the findings supplement a previous study led by Gill, which reported decreased Sp4 levels in the lower brain are associated with bipolar disorder.