Cellular Mechanisms of a Synchronized Oscillation in the Thalamus

TLDR

Spindle waves exemplify synchronized oscillations common to thalamic and cortical neuronal activity during sleep and wakefulness. Rebound burst firing in relay cells is driven by inhibitory postsynaptic potentials from the perigeniculate nucleus, which is activated by relay neuron bursts; reducing GABA‑A inhibition amplifies GABA‑B IPSPs, producing slowed rhythmic activity similar to absence seizures. Spindle waves arise from rebound burst firing in relay cells, and while reducing GABA‑A inhibition enhances GABA‑B IPSPs to generate seizure‑like rhythmic activity, blocking GABA‑B receptors eliminates this activity without affecting normal spindles, indicating GABA‑B antagonists could treat absence seizures.

Abstract

Spindle waves are a prototypical example of synchronized oscillations, a common feature of neuronal activity in thalamic and cortical systems in sleeping and waking animals. Spontaneous spindle waves recorded from slices of the ferret lateral geniculate nucleus were generated by rebound burst firing in relay cells. This rebound burst firing resulted from inhibitory postsynaptic potentials arriving from the perigeniculate nucleus, the cells of which were activated by burst firing in relay neurons. Reduction of γ-aminobutyric acid A (GABA A ) receptor-mediated inhibition markedly enhanced GABA B inhibitory postsynaptic potentials in relay cells and subsequently generated a slowed and rhythmic population activity resembling that which occurs during an absence seizure. Pharmacological block of GABA B receptors abolished this seizure-like activity but not normal spindle waves, suggesting that GABA B antagonists may be useful in the treatment of absence seizures.