ABSTRACT
Voice recognition (VR) technology needs improvement, but is as integral to the current practice of radiology as Radiology Information Systems and Picture Archival and Communication Systems. In the 1990s, the radiology community gave VR technology a rather lukewarm reception, but since then it has emerged as the predominant method of radiology reporting in the United States. In this article, we examine how VR technology works, outline the positive and negative aspects of VR technology on work flow, identify common VR transcription errors and review the discussion on VR adoption in the recent literature. We add to the discussion our personal experiences in an international teleradiology group.
ABSTRACT
The neural pathways through which central serotonergic systems regulate food intake and body weight remain to be fully elucidated. We report that serotonin, via action at serotonin1B receptors (5-HT1BRs), modulates the endogenous release of both agonists and antagonists of the melanocortin receptors, which are a core component of the central circuitry controlling body weight homeostasis. We also show that serotonin-induced hypophagia requires downstream activation of melanocortin 4, but not melanocortin 3, receptors. These results identify a primary mechanism underlying the serotonergic regulation of energy balance and provide an example of a centrally derived signal that reciprocally regulates melanocortin receptor agonists and antagonists in a similar manner to peripheral adiposity signals.
Subject(s)
Eating/physiology , Neurons/physiology , Receptor, Melanocortin, Type 3/physiology , Receptor, Serotonin, 5-HT1B/physiology , Receptors, Melanocortin/physiology , Serotonin/physiology , Animals , Eating/drug effects , Electric Stimulation , Male , Mice , Mice, Inbred A , Mice, Inbred C57BL , Mice, Knockout , Mice, Obese , Mice, Transgenic , Nerve Net/drug effects , Nerve Net/physiology , Neurons/drug effects , Pyridines/pharmacology , Receptor, Melanocortin, Type 4/agonists , Receptor, Melanocortin, Type 4/antagonists & inhibitors , Receptor, Melanocortin, Type 4/physiology , Receptors, Melanocortin/agonists , Receptors, Melanocortin/antagonists & inhibitors , Serotonin/pharmacology , Serotonin 5-HT1 Receptor AgonistsABSTRACT
The central neuropeptide Y (NPY) Y1 receptor (Y1-R) system has been implicated in feeding, endocrine, and autonomic regulation. In the present study, we systematically examined the brain distribution of Y1-R mRNA in rodents by using radioisotopic in situ hybridization histochemistry (ISHH) with a novel sensitive cRNA probe. Within the rat hypothalamus, Y1-R-specific hybridization was observed in the anteroventral periventricular, ventromedial preoptic, suprachiasmatic, paraventricular (PVH), dorsomedial, ventromedial, arcuate, and mamillary nuclei. In the rat, Y1-R mRNA expression was also seen in the subfornical organ, anterior hypothalamic area, dorsal hypothalamic area, and in the lateral hypothalamic area. In addition, Y1-R hybridization was evident in several extrahypothalamic forebrain and hindbrain sites involved in feeding and/or autonomic regulation in the rat. A similar distribution pattern of Y1-R mRNA was observed in the mouse brain. Moreover, by using a transgenic mouse line expressing green fluorescent protein under the control of the melanocortin-4 receptor (MC4-R) promoter, we observed Y1-R mRNA expression in MC4-R-positive cells in several brain sites such as the PVH and central nucleus of the amygdala. Additionally, dual-label ISHH demonstrated that hypophysiotropic PVH cells coexpress Y1-R and pro-thyrotropin-releasing hormone mRNAs in the rat. These observations are consistent with the proposed roles of the central NPY/Y1-R system in energy homeostasis.
Subject(s)
Brain Mapping , Hypothalamus/metabolism , RNA, Messenger/metabolism , Receptor, Melanocortin, Type 4/metabolism , Receptors, G-Protein-Coupled/metabolism , Receptors, Neuropeptide/metabolism , Animals , Appetite Regulation/physiology , Feeding Behavior/physiology , In Situ Hybridization, Fluorescence , Male , Mice , Mice, Transgenic , Prosencephalon/metabolism , RNA, Complementary/analysis , Rats , Rats, Sprague-Dawley , Receptors, G-Protein-Coupled/genetics , Receptors, Neuropeptide/genetics , Rhombencephalon , Tissue DistributionABSTRACT
The melanocortin 4 receptor (MC4-R) plays a pivotal role in maintaining energy homeostasis in rodents and humans. For example, MC4-R deletion or mutation results in obesity, hyperphagia, and insulin resistance. Additionally, subsets of leptin-induced autonomic responses can be blocked by melanocortin receptor antagonism, suggesting that MC4-R-expressing neurons are downstream targets of leptin. However, the critical autonomic control sites expressing MC4-Rs are still unclear. In the present study, we systematically examined the distribution of MC4-R mRNA in the adult rat central nervous system, including the spinal cord, by using in situ hybridization histochemistry (ISHH) with a novel cRNA probe. Autonomic control sites expressing MC4-R mRNA in the hypothalamus included the anteroventral periventricular, ventromedial preoptic, median preoptic, paraventricular, dorsomedial, and arcuate nuclei. The subfornical organ, dorsal hypothalamic, perifornical, and posterior hypothalamic areas were also observed to express MC4-R mRNA. Within extrahypothalamic autonomic control sites, MC4-R-specific hybridization was evident in the infralimbic and insular cortices, bed nucleus of the stria terminalis, central nucleus of the amygdala, periaqueductal gray, lateral parabrachial nucleus, nucleus of the solitary tract, dorsal motor nucleus of the vagus (DMV), and intermediolateral nucleus of the spinal cord (IML). By using dual-label ISHH, we confirmed that the cells expressing MC4-R mRNA in the IML and DMV were autonomic preganglionic neurons as cells in both sites coexpressed choline acetyltransferase mRNA. The distribution of MC4-R mRNA is consistent with the proposed roles of central melanocortin systems in feeding and autonomic regulation.
