Astrocyte cells can both dampen and boost the flow of nerve signals. This finding was reported by the press service of the RNF.
The human nervous system includes more than just neurons; it relies on a host of supporting cells as well. Neurons branch into many processes and connect through networks built by synapses. Astrocytes help regulate the chemical environment around neurons and supply essential nutrients. Beyond these roles, they influence impulse transmission by releasing gliotransmitters into the tissue surrounding synapses, which can either enhance or suppress signals. The formation of these gliotransmitters depends on calcium ions entering astrocytes from outside the cell and mobilizing internal stores.
Researchers from the Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences in Moscow, along with colleagues in Russia and the United States, explored how a calcium source can shape the timing and strength of neural activity during astrocyte stimulation. Their experiments used animals and involved astrocytes and brain tissue from mice and rats engineered to express light-responsive proteins. These proteins render cells sensitive to light, enabling optical control of cellular activity. Illumination allows these cells to uptake calcium from the extracellular space or release it from intracellular reservoirs through ion channels or receptor activation.
The study showed that activating light-sensitive proteins that function as ion channels decreased nerve impulse transmission by as much as 54 percent in mice and 15 percent in rats. This suppression occurs because the astrocytes release two inhibitory gliotransmitters, ATP and GABA, in response to light and rising calcium levels. When the cells were additionally subjected to electrical stimulation, ATP and GABA production increased further, amplifying the dampening effect. Conversely, triggering receptors that promote calcium release from internal stores led to a stronger signal, with a 62 percent increase observed under light stimulation conditions.
These results suggest that astrocytes can steer the activity of entire neural networks by modulating impulse flow. Such control holds potential for both basic research and future therapies aimed at correcting neural dysfunctions. The researchers plan to extend their work by testing different cell types to uncover how learning and memory processes are shaped by glial involvement and calcium signaling in the brain.
Beyond the immediate implications for neuroscience, these findings open doors to novel strategies for studying how the brain adapts to new tasks and experiences. Understanding how glial cells contribute to synaptic changes could inform approaches to treat disorders where neural communication is compromised, and might guide methods to enhance rehabilitation after injury. As the science advances, the goal is to map how calcium dynamics within astrocytes interface with neuronal circuits, shedding light on the complex dialogue that underpins perception, decision making, and lasting memory.
The broader vision includes developing techniques to modulate neural activity in a controlled manner, not only for research but also for clinical applications. While the current work centers on animal models, the underlying principles offer a roadmap for translating glial-targeted interventions into therapies that support brain health and cognitive function. Ongoing investigations will continue to unravel how distinct gliotransmitters shape signal timing, error correction, and synchronization across brain networks, enabling a more precise understanding of how the brain learns and adapts over time.
In this evolving field, scientists emphasize the importance of carefully balancing excitation and inhibition within neural circuits. The ability to tune this balance via astrocytes could lead to breakthroughs in treating conditions characterized by excessive or insufficient neuronal activity. As research progresses, the hope is to harness glial mechanisms for improving neural plasticity and resilience, while also safeguarding against unintended disruptions to brain function.