A small V1a-expressing subset of appears important for robust circadian clock function in the mouse SCN.
Evidence
This mouse neurobiology study mapped AVP receptor signaling in SCN neuron populations and used a jet-lag paradigm to show VIP-neuron V1a was required for maintaining clock robustness.
Caveat
The work defines circuit mechanisms in mice and does not establish how the same VIP-GRP heterogeneity operates in humans.
Simplified
Understanding the network topology of a cluster of diverse neurons acting in concert requires a detailed expression map of ligand-receptor pairs involved in cell-cell communication. The neuropeptide arginine vasopressin (AVP) and signaling mediated by its cognate receptor V1a have been implicated in dorsal-to-ventral regional communication in the suprachiasmatic nucleus (SCN), a cluster of neurons that acts in concert to generate daily rhythms in behavior and physiology. Here, we show that among vasoactive intestinal peptide (VIP)-ergic neurons in the ventral SCN only a small subpopulation expresses V1a, and we demonstrate the requirement of V1a in these for maintaining the robustness of the circadian clock using a jet-lag paradigm. Notably, we found that V1a expression appears to be minimal in the other major ventral neuronal population expressing gastrin-releasing peptide (GRP). The identified heterogeneity between VIP and , and among VIP neurons, provides a basic map for understanding the cryptic network structure from dorsal AVP neurons to receiver ventral SCN.
Key numbers
9.0±1.1
Increase in c-Fos-positive
Average number of c-Fos/VIP double-positive cells in optogenetically activated AVP-ChR2 mice.
1.1±0.3 days
Faster re-entrainment in VIP-mice
Time taken for VIP-mice to re-entrain compared to controls (2.2±0.2 days).
25%
Proportion of receiving AVP appositions
Percentage of total assessed SCN receiving synaptic input from AVP neurons.
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