Interaction between TRPV1-expressing neurons in the hypothalamus

Abstract

Transient receptor potential vanilloid type 1 (TRPV1) is a ligand-gated ion channel expressed in the peripheral and central nervous systems. TRPV1-dependent mechanisms take part in a wide range of physiological and pathophysiological pathways including the regulation of homeostatic functions. TRPV1 expression in the hypothalamus has been described as well as evidence that TRPV1-dependent excitatory inputs to hypothalamic preautonomic neurons are diminished in diabetic conditions. Here we aimed to determine the functional expression of TRPV1 in two hypothalamic nuclei known to be involved in the central control of metabolism and to test the hypothesis that TRPV1-expressing neurons receive TRPV1-expressing inputs. A mouse model (TRPV1Cre/tdTom) was generated to identify TRPV1-expressing cells and determine the cellular properties of TRPV1-expressing neurons in adult mice. Our study demonstrated the functional expression of TRPV1 in the dorsomedial hypothalamic nucleus and paraventricular nucleus in adult mice. Our findings revealed that a subset of TRPV1Cre/tdTom neurons receive TRPV1-expressing excitatory inputs, indicating direct interaction between TRPV1-expressing neurons. In addition, astrocytes likely play a role in the modulation of TRPV1-expressing neurons. In summary, this study identified specific hypothalamic regions where TRPV1 is expressed and functional in adult mice and the existence of direct connections between TRPV1Cre/tdTom neurons. NEW & NOTEWORTHY Transient receptor potential vanilloid type 1 (TRPV1) is expressed in the hypothalamus, and TRPV1-dependent regulation of preautonomic neurons is decreased in hyperglycemic conditions. Our study demonstrated functional expression of TRPV1 in two hypothalamic nuclei involved in the control of energy homeostasis. Our results also revealed that a subset of TRPV1-expressing neurons receive TRPV1-expressing excitatory inputs. These findings suggest direct interaction between TRPV1-expressing neurons.

Distribution of transient receptor potential vanilloid-1 channels in gastrointestinal tract of patients with morbid obesity

“…Several animal studies and epidemiological studies have been conducted to explain the potential mechanisms of capsaicin’s anorexigenic effect. TRPV1, mainly found in neurons, has also been shown to be present in rodent adipocytes, skeletal muscle, and the hypothalamus[ 14 - 16 , 19 , 40 , 41 ]. Capsaicin has multisystemic effects via widely distributed TRPV1 expression: it promotes lipolysis, inhibits adipogenesis, and increases the transition from white adipose tissue to thermogenic brown adipose tissue in adipose tissue; in the hypothalamus, it reduces appetite and creates a feeling of satiety; it also increases intestinal blood flow and has close relations with glucose homeostasis by increasing insulin secretion in the pancreas and by increasing glucagon like peptide-1 levels[ 14 , 17 , 18 , 20 , 42 - 44 ].…”

Heat Stress Responses in Birds: A Review of the Neural Components

“…Thermoreceptors are also found in the brain, primarily the hypothalamus, and are known to elicit similar responses as signals that originated from cutaneous thermoreceptors. TRPV1 is found on cells in the paraventricular nucleus (PVN) and dorsomedial nucleus (DMN) of the hypothalamus of mice [57], as well as in the anterior (AH) and lateral hypothalamus (LH) [58], and in the PVN, DMN, LH, and arcuate (ARC) nucleus of rats Simplified representation of the mammalian thermoregulatory system. Temperature receptors in various regions relay information to the preoptic area (POA) of the hypothalamus through the release of glutamate (GLU) from warm or cold afferents.…”

Side Effects of Opioids Are Ameliorated by Regulating TRPV1 Receptors

“…It can be activated by noxious heat (≥43 °C), some endogenous lipid-derived molecules, acidic solutions (pH < 6.5), some pungent chemicals or food ingredients such as capsaicin, and toxins such as resiniferatoxin and vanillotoxins [ 16 ]. TRPV1 is mainly expressed on the peripheral and central terminals of small-diameter sensory neurons (nociceptors) in the dorsal root ganglion (DRG), trigeminal ganglion, geniculate ganglion, nodose ganglion, and jugular ganglion [ 17 , 18 ], and also expressed at the low level in the brain [ 19 , 20 ]. The activation of TRPV1 induces pain-related behaviors, and the importance of TRPV1 in nociception is also validated by deletion of the TRPV1 gene (knock-out mice) and knock-down of TRPV1 by RNA interference [ 21 ].…”