Scientists stop rats' stroke-induced seizures with pulse of light
Baku, November 19 (AZERTAC). Stanford University School of Medicine scientists have shown that a structure deep within the brain is a crucial component of recurring seizures that can arise as a delayed consequence of a cerebral stroke. This structure, called the thalamus, is known as a relay station routing inputs from the senses to the brain’s higher cognitive processing centers in the cerebral cortex. But the thalamus has never before been implicated in post-stroke seizures.
In a study published online Nov. 7 in Nature Neuroscience, the investigators proved that the thalamocortical tract — a nerve bundle that among other things conveys sensory information from the thalamus to many parts of the more-expansive cerebral cortex, the outermost layer of the mammalian brain — is intimately involved in post-cerebral-stroke seizures.
The researchers first induced strokes to a small spot in rats’ somatosensory cortex, the part of the cortex that processes information such as touch and pain. This rendered the rats vulnerable to seizures starting within weeks. Employing a combination of sophisticated techniques, the scientists engineered a method of remotely detecting electrical activity in the thalamocortical tract that accompanied the rats’ seizures and, at the press of a button, shutting down the activity in the tract. Doing this invariably stopped a rat’s seizure.
“If we prevent the thalamus from participating in the seizure, we actually block the seizure — instantly,” said John Huguenard, PhD, professor of neurology and neurological sciences and of molecular and cellular physiology. Huguenard is the senior author of the study. In 2011, he and his colleagues published a study, also in Nature Neuroscience, implicating the thalamus in absence, or petit mal, epilepsy, the most common form of epilepsy among children. Strokes, on the other hand, are much more likely to afflict older people.
“The current thinking in the field,” Huguenard said, “has been that the thalamus isn't an integral part of the brain circuitry that goes haywire during the recovery phase after a cortical stroke.” After all, he noted, in humans the thalamus and the cerebral cortex are several inches apart — in the central nervous system, that’s considered a long distance.
But the thalamus and the cortex are intimate partners in an ongoing two-way communication in which the thalamus receives signals from the outside world, tunes and bundles these signals into packets that it perpetually punts to relevant parts of the cortex, and then receives feedback from the cortex — such as, “I’m busy now, so I’m ignoring you,” or “Whoa, what did you just say?” Constant communication requires sturdy transmission lines, and the thalamus and cortex are connected by nerve bundles that transmit in opposite directions. The thalamocortical tract is the output line from the thalamus to the cortex.
The researchers’ first exploration in the stroke-affected rats, according to Jeanne Paz, PhD, a research associate in Huguenard’s laboratory and the lead author of the new study, took place in the part of the thalamus that corresponds to the cortical area where the stroke had occurred. “Not surprisingly, we saw cell death there,” Paz said. Huguenard, Paz and their teammates had correctly assumed the rats’ strokes, although they were occurring far from the thalamus, would damage not only brain cells resident in the somatosensory cortex but also the tips of nerve fibers ascending from the thalamic area that bundles touch-related inputs and routes them to the somatosensory cortex. Injury to its tip is often enough to cause an entire nerve cell to die.
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