London: A brain-circuit defect that triggers absence seizures- the most common form of childhood epilepsy- have been identified by the researchers at the Stanford University School of Medicine.
In a study the investigators showed for the first time how defective signalling between two key brain areas — the cerebral cortex and the thalamus — could produce, in experimental mice, both the intermittent, brief loss of consciousness.
The cortex and thalamus share an intimate relationship. The cortex, like a busy executive, assesses sensory information, draws conclusions, makes decisions and directs action.
In turn, the thalamus acts like an executive assistant, sifting through sensory inputs from the eyes, ears and skin, and translating their insistent patter into messages relayed up to the cortex. The thalamus carefully manages those messages in response to signals from the cortex.
But there is a third component to the circuit: an inhibitory nerve tract that brain scientists refer to as the nRT. This tract monitors signals from both of the other two, and responds by damping activity. The overall result is a stable, self-modulating system that reliably delivers precise packets of relevant sensory information but neither veers into a chaotic state nor completely shuts itself down.
In bioengineered mice that the Stanford team studied with Wayne Frankel, PhD, of the Jackson Laboratory in Bar Harbor, Maine, this circuit is broken because the GluA4 receptor, a protein component of cells critical to the stimulation of nRT cells, is missing. Notably, these mice were prone to intermittent absence seizures.
The study has been detailed in Nature Neuroscience.