Dian‑Dian Wang1,2 · Run‑Zhou Yang1  · Song‑Tang Sun3  · Ya‑Lun Sun4  · Rui‑Yu Wang1,2 · Xiao‑Yan Meng1,2 · Sen‑Miao Li1,2 · Jia‑Kang Li1,2 · Pei‑Pei Liu1  · Shu‑Ang Li1  · Jian‑Sheng Kang1,2

1 Clinical Systems Biology Laboratories, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China 

2 The First Clinical School of Medicine, Zhengzhou University, Zhengzhou 450052, China 

3 Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou University People’s Hospital, Zhengzhou 450003, China 

4 Department of Neurology, Henan Provincial People’s Hospital, Henan University People’s Hospital, Zhengzhou 450003, China

Abstract

Thermal homeostasis is critical for mammalian physiology. The hypothalamic preoptic area (POA) is a key center for thermoregulation and contains calcium/calmodulin-dependent protein kinase type I (CaMKI)-positive temperature-insensitive neurons, whose functional roles remain unclear. Here, we found that calcium oscillations of CaMKI-positive POA (POA^CaMKI) neurons decreased during adenosine monophosphate (AMP)-induced hypothermia via the adenosine A1 receptor, with the power spectral density of the delta-band exhibiting a power-scaling law associated with changes in core body temperature (~ΔTcore³). This suggests that POA^CaMKI neurons encode Tcore reference information via delta-band dynamics. The observed power-law scaling indicated a robust association between POA^CaMKI neuronal activity and thermoregulatory dynamics, suggesting that these neurons may contribute to both body temperature sensing and control. This study reveals a negative feedback mechanism for thermal homeostasis and provides a paradigm shift for decoding information in the frequency domain and understanding the neural regulation of physiological homeostasis.

Keywords

POA^CaMKI neurons; Information encoding in frequency domain; Minimal negative feedback loops; Power-law scaling relationship; Adenosine A₁ receptor; AMP

[SpringerLink]