scholarly journals Posterior subthalamic nucleus (PSTh) mediates innate fear-associated hypothermia in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Can Liu ◽  
Chia-Ying Lee ◽  
Greg Asher ◽  
Liqin Cao ◽  
Yuka Terakoshi ◽  
...  
Keyword(s):  
Subthalamic Nucleus ◽  
Light Chain ◽  
Heat Dissipation ◽  
Neural Mechanisms ◽  
Solitary Tract ◽  
Wild Type ◽  
Neuronal Ensembles ◽  
Fos Expression ◽  
Innate Fear ◽  
Stimulation Of

AbstractThe neural mechanisms of fear-associated thermoregulation remain unclear. Innate fear odor 2-methyl-2-thiazoline (2MT) elicits rapid hypothermia and elevated tail temperature, indicative of vasodilation-induced heat dissipation, in wild-type mice, but not in mice lacking Trpa1–the chemosensor for 2MT. Here we report that Trpa1−/− mice show diminished 2MT-evoked c-fos expression in the posterior subthalamic nucleus (PSTh), external lateral parabrachial subnucleus (PBel) and nucleus of the solitary tract (NTS). Whereas tetanus toxin light chain-mediated inactivation of NTS-projecting PSTh neurons suppress, optogenetic activation of direct PSTh-rostral NTS pathway induces hypothermia and tail vasodilation. Furthermore, selective opto-stimulation of 2MT-activated, PSTh-projecting PBel neurons by capturing activated neuronal ensembles (CANE) causes hypothermia. Conversely, chemogenetic suppression of vGlut2+ neurons in PBel or PSTh, or PSTh-projecting PBel neurons attenuates 2MT-evoked hypothermia and tail vasodilation. These studies identify PSTh as a major thermoregulatory hub that connects PBel to NTS to mediate 2MT-evoked innate fear-associated hypothermia and tail vasodilation.

scholarly journals Posterior subthalamic nucleus (PSTh) mediates innate fear-associated hypothermia

2020 ◽  
Author(s):  
Can Liu ◽  
Chia-Ying Lee ◽  
Greg Asher ◽  
Liqin Cao ◽  
Yuka Terakoshi ◽  
...  
Keyword(s):  
Body Temperature ◽  
Subthalamic Nucleus ◽  
Heat Dissipation ◽  
Neural Mechanisms ◽  
Wild Type ◽  
Neuronal Ensembles ◽  
Defensive Behaviors ◽  
Life Threatening ◽  
Acute Changes ◽  
Innate Fear

Abstract Mammals normally maintain a constant body temperature irrespective of their environmental temperature. However, emotions such as fear can trigger acute changes in body temperature accompanying defensive behaviors to enhance survival in life-threatening conditions. The neural mechanisms of fear-associated thermoregulation remain unclear. Here, we find that innate fear odor 2-methyl-2-thiazoline (2MT) evokes rapid hypothermia and elevated tail temperature, indicative of vasodilation-induced heat dissipation, in wild-type mice, but not in mice lacking Trpa1, the chemosensor for 2MT. Following 2MT exposure, wild-type but not Trpa1-/- mice exhibit high c-fos expression in the posterior subthalamic nucleus (PSTh), external lateral parabrachial subnucleus (PBel), and nucleus of the solitary tract (NTS). Tetanus toxin light chain (TeLC)-mediated inactivation of NTS-projecting PSTh neurons blunts 2MT-evoked hypothermia and abrogated tail temperature increase. Optogenetic activation of the PSTh-rostral NTS (RNTS) pathway specifically induces hypothermia and elevated tail temperature. Moreover, selective opto-stimulation of 2MT-activated PSTh-projecting PBel neurons, by capturing activated neuronal ensembles (CANE), induces hypothermia and elevated tail temperature. Conversely, chemogenetic suppression of vGlut2+ neurons in PBel and PSTh or PSTh-projecting PBel neurons attenuates 2MT-evoked hypothermia and tail temperature increment. Taken together, these results uncover a novel PBel-PSTh-NTS neural pathway that underlies 2MT-evoked innate fear-associated hypothermia and tail vasodilation.

Loss of cholecystokinin and glucagon-like peptide-1-induced satiation in mice lacking serotonin 2C receptors

2009 ◽  
Vol 296 (1) ◽  
pp. R51-R56 ◽  
Author(s):  
Lori Asarian
Keyword(s):  
Neural Mechanisms ◽  
Wild Type ◽  
Gut Peptides ◽  
Serotonin Signaling ◽  
The Central Nervous System ◽  
Fos Expression ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

To investigate the role of serotonin 2C receptors (2CR), which are expressed only in the central nervous system, in the satiating actions of the gut peptides CCK and glucagon-like peptide 1 (GLP-1), we examined 1) the effect of null mutations of serotonin 2CR (2CR KO) on the eating-inhibitory potencies of dark-onset intraperitoneal injections of 0.9, 1.7, or 3.5 nmol/kg (1, 2, or 4 μg/kg) CCK and 100, 200, and 400 nmol/kg (33, 66, or 132 μg/kg) GLP-1, and 2) the effects of intraperitoneal injections of 1.7 nmol//kg CCK and 100 nmol/kg GLP-1 on neuronal activation in the brain, as measured by c-Fos expression. All CCK and GLP-1 doses decreased 30-min food intake in wild-type (WT) mice, but none of them did in 2CR KO mice. CCK increased the number of cells expressing c-Fos in the nucleus tractus solitarii (NTS) of WT, but not 2CR KO mice. CCK induced similar degrees of c-Fos expression in the paraventricular (PVN) and arcuate (Arc) nuclei of the hypothalamus of both genotypes. GLP-1, on the other hand, increased c-Fos expression similarly in the NTS of both genotypes and increased c-Fos expression more in the PVN and Arc of 2CR KO mice, but not WT mice. These results indicate that serotonin signaling via serotonin 2CR is necessary for the full satiating effects of CCK and GLP-1. In addition, they suggest that the satiating effects of the two peptides are mediated by different neural mechanisms.

Fos expression in ferret dorsal vagal complex after peripheral emetic stimuli

1994 ◽  
Vol 266 (4) ◽  
pp. R1118-R1126 ◽  
Author(s):  
F. M. Boissonade ◽  
K. A. Sharkey ◽  
J. S. Davison
Keyword(s):  
Electrical Stimulation ◽  
Hypertonic Saline ◽  
Area Postrema ◽  
Dorsal Vagal Complex ◽  
Solitary Tract ◽  
Communicating Branch ◽  
Nuclear Phosphoprotein ◽  
Fos Expression ◽  
Hypertonic Saline Injection ◽  
Stimulation Of

The aim of this study was to investigate neuronal activation in the dorsal vagal complex of the halothane-anesthetized ferret after peripheral emetic stimuli. Neuronal activity was studied by examining the distribution of the nuclear phosphoprotein Fos using immunohistochemistry. The emetic stimuli used were electrical stimulation of the supradiaphragmatic vagal communicating branch (SVCB) or intraduodenal injection of hypertonic saline. Electrical stimulation of the SVCB induced the densest Fos expression within the medial subnucleus of the nucleus of the solitary tract. After hypertonic saline injection, the greatest density of Fos-positive nuclei was observed within the area postrema and also in the medial subnucleus of the nucleus of the solitary tract. It was concluded that the emetic response to hypertonic saline involves neurons in both the area postrema and the nucleus of the solitary tract, especially the medial subnucleus, and that the medial subnucleus is important in the emetic response to SVCB stimulation.

scholarly journals Critical roles of the immunoglobulin intronic enhancers in maintaining the sequential rearrangement of IgH and Igk loci

2006 ◽  
Vol 203 (7) ◽  
pp. 1721-1732 ◽  
Author(s):  
Matthew A. Inlay ◽  
Tongxiang Lin ◽  
Heather H. Gao ◽  
Yang Xu
Keyword(s):  
B Cells ◽  
Developmental Stage ◽  
Heavy Chain ◽  
Light Chain ◽  
Matrix Attachment Region ◽  
Cis Elements ◽  
Wild Type ◽  
Intronic Enhancer ◽  
Attachment Region

V(D)J recombination of immunoglobulin (Ig) heavy (IgH) and light chain genes occurs sequentially in the pro– and pre–B cells. To identify cis-elements that dictate this order of rearrangement, we replaced the endogenous matrix attachment region/Igk intronic enhancer (MiEκ) with its heavy chain counterpart (Eμ) in mice. This replacement, denoted EμR, substantially increases the accessibility of both Vκ and Jκ loci to V(D)J recombinase in pro–B cells and induces Igk rearrangement in these cells. However, EμR does not support Igk rearrangement in pre–B cells. Similar to that in MiEκ−/− pre–B cells, the accessibility of Vκ segments to V(D)J recombinase is considerably reduced in EμR pre–B cells when compared with wild-type pre–B cells. Therefore, Eμ and MiEκ play developmental stage-specific roles in maintaining the sequential rearrangement of IgH and Igk loci by promoting the accessibility of V, D, and J loci to the V(D)J recombinase.

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