Abstract

Torpor is a peculiar mammalian behaviour, characterized by the active reduction of metabolic rate, followed by a drop in body temperature. To enter torpor, the activation of all thermogenic organs that could potentially defend body temperature must be prevented. Most of these organs, such as the brown adipose tissue, are controlled by the key thermoregulatory region of the Raphe Pallidus (RPa). Currently, it is not known which brain areas mediate the entrance into torpor. To identify these areas, the expression of the early gene c-Fos at torpor onset was assessed in different brain regions in mice injected with a retrograde tracer (Cholera Toxin subunit b, CTb) into the RPa region. The results show a network of hypothalamic neurons that are specifically activated at torpor onset and a direct torpor-specific projection from the Dorsomedial Hypothalamus to the RPa that could putatively mediate the suppression of thermogenesis during torpor.

Highlights

  • Torpor is a peculiar mammalian behaviour, characterized by the active reduction of metabolic rate, followed by a drop in body temperature

  • Since the suppression of thermogenesis is required in order to enter torpor, it is highly unlikely that Raphe Pallidus (RPa) neurons can still be active in such a condition; an inhibitory afference to RPa neurons should be activated at torpor onset

  • Combining neurons expressing the early gene c-Fos with the expression of the retrograde tracer CTb injected within the RPa, we show here a network of hypothalamic neurons that are activated at torpor onset and a direct torpor-specific projection to RPa originating in the Dorsomedial Hypothalamus (DMH) that could putatively mediate the suppression of thermogenesis of torpor itself

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Summary

Introduction

Torpor is a peculiar mammalian behaviour, characterized by the active reduction of metabolic rate, followed by a drop in body temperature. In the Torpor group, the only region showing a significant increase in c-Fos positive neurons projecting to the RPa compared to the other groups was the DMH (9.45 ± 0.29; P = 0.012 vs Cold exposure, P = 0.002 vs Fasting, P < 0.001 vs Control) (Figs 3 and 4).

Results
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