What a great Titisee Conference! “Warm, cold, and life” brought together brilliant minds exploring how temperature shapes the brain, physiology, and behaviour — from mice, wild animals to humans. Thanks to Boehringer Ingelheim Fonds for the support!

We modeled mouse behavior with a drift-diffusion model: Trpv1-KO mice have less fidelity in detecting warm temp differences but compensate with higher sampling rate leading to an overall preference similar to wildtype mice. Trpm2-KOs fail to accumulate temp evidence, losing 31°C preference.

In agreement with this idea: in mice overexpressing Trpv1, neurons respond to warmth faster—and in the behavior assay the mice quickly lock onto 31°C, switching rooms less than wildtypes (purple: Trpv1 overexpressor mice; grey wildtypes).

Calcium imaging of cultured neurons reveals Trpv1 mediates the rapid neuronal response to warming, and less the steady-state signal. This suggests that the rate of temperature increase might be encoded by Trpv1 (each triangle is the responds onset to the warmth stimulus; x-axis: time in seconds)

Tracking data shows Trpv1-KOs switch rooms more often—possibly compensating for difficulty sensing warmth.. (Yellow = TRPV1 KO mice)

Trpm2-KO mice no longer prefer 31°C and spend equal time at 34–38°C, suggesting Trpm2 is key for selecting innocuous warm temps.

Compared to floor-only tests, the chamber assay better detects subtle warm temp differences. Mice prefer temps nearer their thermoneutral zone (~31°C). Pink = chamber; black = classic plate assay.

So we built a chamber-based assay where we can precisely control full-room temps (including floor) via Peltier elements. Mice choose between two rooms via a tunnel (but don’t linger there!).

On February 12, shortly before “High noon”, scientists at German research campuses, including here in Heidelberg, will stand up for Democracy: “facts, not fake news are needed for democracy”. See aufstehenfuerdemokratie.de/englisch/ – there is also find a Petition related to the cause. Get involved.

(10/n) In summary, we identified a slowly evolving plasticity mechanism in a specific subset of hypothalamic preoptic neurons. This mechanism, triggered by long-term heat exposure, facilitates thermal acclimation and enhances heat tolerance in mice.

(9/n) Wojciech further analyzed the underlying cellular mechanism, revealing that a persistent sodium current mediated by Nav1.3 (SCN3a) drives the neurons’ tonic and temperature-sensitive pacemaker activity.

(6/n) Remarkably, these neurons do more than just increase tonic (static) firing. They develop intrinsic temperature sensitivity, becoming bona fide warm-sensitive neurons!

(3/n) We started with a simple hypothesis: long-term exposure to heat might induce neuronal plasticity, much like other strong or sustained sensory stimuli.