Abstract
The release of GABA from local interneurons in the dorsal lateral geniculate nucleus (dLGN-INs) provides inhibitory control during visual processing within the thalamus. It is commonly assumed that this important class of interneurons originates from within the thalamic complex, but we now show that during early postnatal development Sox14/Otx2-expressing precursor cells migrate from the dorsal midbrain to generate dLGN-INs. The unexpected extra-diencephalic origin of dLGN-INs sets them apart from GABAergic neurons of the reticular thalamic nucleus. Using optogenetics we show that at increased firing rates tectal-derived dLGN-INs generate a powerful form of tonic inhibition that regulates the gain of thalamic relay neurons through recruitment of extrasynaptic high-affinity GABAA receptors. Therefore, by revising the conventional view of thalamic interneuron ontogeny we demonstrate how a previously unappreciated mesencephalic population controls thalamic relay neuron excitability.
Highlights
The release of GABA from local interneurons in the dorsal lateral geniculate nucleus provides inhibitory control during visual processing within the thalamus
Using optogenetics we demonstrate that GABA released from Sox[14] þ dorsal lateral geniculate nucleus (dLGN)-INs generates a frequency-dependent form of tonic inhibition, which depends on the activation of extrasynaptic
In 9 out of 12 paired recordings increasing the action potentials (APs) firing of the Gfp þ putative dLGN-IN resulted in a clear increase in the tonic conductance recorded from the Gfp À thalamic relay neuron (Fig. 1f)
Summary
The release of GABA from local interneurons in the dorsal lateral geniculate nucleus (dLGN-INs) provides inhibitory control during visual processing within the thalamus. According to the prosomeric model[11,12], thalamic progenitors are specified within the second ( known as dorsal thalamus) and third ( known as ventral thalamus or prethalamus) diencephalic prosomere (p2 and p3) Inhibitory progenitors, including those of the RTN, are found in p3; whilst excitatory neurogenesis takes place in p2 (refs 13,14). Using optogenetics we demonstrate that GABA released from Sox[14] þ dLGN-INs generates a frequency-dependent form of tonic inhibition, which depends on the activation of extrasynaptic
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