For the new study, the researchers used samples from the brains of normal mice as well as living cortical brain tissue sampled with permission from six individuals undergoing surgical treatment for epilepsy. The surgical procedures were medically necessary to remove lesions from the brain’s hippocampus.

The researchers first validated the zap-and-freeze approach by observing calcium signaling, a process that triggers neurons to release neurotransmitters in living mouse brain tissues.

Next, the scientists stimulated neurons in mouse brain tissue with the zap-and-freeze approach and observed where synaptic vesicles fuse with brain cell membranes and then release chemicals called neurotransmitters that reach other brain cells. The scientists then observed how mouse brain cells recycle synaptic vesicles after they are used for neuronal communication, a process known as endocytosis that allows material to be taken up by neurons.

The researchers then applied the zap-and-freeze technique to brain tissue samples from people with epilepsy, and observed the same synaptic vesicle recycling pathway operating in human neurons.

In both mouse and human brain samples, the protein Dynamin1xA, which is essential for ultrafast synaptic membrane recycling, was present where endocytosis is thought to occur on the membrane of the synapse.

“Our findings indicate that the molecular mechanism of ultrafast endocytosis is conserved between mice and human brain tissues,” the author says, suggesting that the investigations in these models are valuable for understanding human biology.

Researchers say they have used a “zap-and-freeze” technology to watch hard-to-see brain cell communications in living brain tissue from mice and humans.

Findings from the new experiments published in Neuron, could potentially help scientists find the root causes of nonheritable forms of Parkinson’s disease, the researchers say.

Sporadic cases of Parkinson’s disease account for most cases of the neurodegenerative disorder, according to the Parkinson’s Foundation. The condition is marked by disruptions to the signaling point between two brain cells. That connection point, known as a synapse, is notoriously difficult to study, says the senior author.