A groundbreaking study published today in the Journal of Neuroscience provides new insights into how brain cells relay critical information from their extremities to their nucleus, activating genes essential for learning and memory.
Researchers have identified a key pathway that links how neurons send signals to each other, or synaptic activity, to the expression of genes necessary for long-term changes in the brain. This discovery offers crucial insights into the molecular processes underlying memory formation.
“These findings illuminate a critical mechanism that connects local synaptic activity to the broader gene expression changes necessary for learning and memory,” said Mark Dell’Acqua, professor of pharmacology at the University of Colorado Anschutz Medical Campus and senior author of the study. “This paper is mainly a basic science finding of a fundamental process of what nerve cells do. Understanding this relay system not only enhances our knowledge of brain function but could also better inform therapeutic treatments for cognitive disorders.”
The nucleus, where genes that modify neuron function are controlled, is located far from the synapses, which receive input at distant dendrites extending from the neuron cell body. This study focuses on the cAMP-response element binding protein (CREB), a transcription factor that regulates genes vital for dynamic changes at synapses, which are essential for neuronal communication. While CREB’s role in supporting learning and memory is well-documented, the exact mechanisms that lead to its activation during neuronal activity have remained unclear.
Using advanced microscopy techniques, graduate student Katlin Zent, under Dr. Dell’Acqua’s guidance, uncovered a crucial relay mechanism. This mechanism involves the activation of receptors and ion channels that generate calcium signals, which rapidly communicate from synapses in the distant dendrites to the nucleus in the neuron cell body.
“Going forward, this research will enable us to better examine how these pathways are utilized in different disease states,” Dell’Acqua explained. “We could see exactly which parts of this new mechanism are disrupted, helping us understand how this pathway impacting learning and memory is affected. This discovery highlights potential targets for interventions aimed at conditions like Alzheimer’s disease and other memory-related disorders.”
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