A functional division of Drosophila sweet taste neurons that is value-based and task-specific.

Sucrose is an attractive feeding substance and a positive reinforcer for Drosophila But Drosophila females have been shown to robustly reject a sucrose-containing option for egg-laying when given a choice between a plain and a sucrose-containing option in specific contexts. How the sweet taste system of Drosophila promotes context-dependent devaluation of an egg-laying option that contains sucrose, an otherwise highly appetitive tastant, is unknown. Here, we report that devaluation of sweetness/sucrose for egg-laying is executed by a sensory pathway recruited specifically by the sweet neurons on the legs of Drosophila First, silencing just the leg sweet neurons caused acceptance of the sucrose option in a sucrose versus plain decision, whereas expressing the channelrhodopsin CsChrimson in them caused rejection of a plain option that was "baited" with light over another that was not. Analogous bidirectional manipulations of other sweet neurons did not produce these effects. Second, circuit tracing revealed that the leg sweet neurons receive different presynaptic neuromodulations compared to some other sweet neurons and were the only ones with postsynaptic partners that projected prominently to the superior lateral protocerebrum (SLP) in the brain. Third, silencing one specific SLP-projecting postsynaptic partner of the leg sweet neurons reduced sucrose rejection, whereas expressing CsChrimson in it promoted rejection of a light-baited option during egg-laying. These results uncover that the Drosophila sweet taste system exhibits a functional division that is value-based and task-specific, challenging the conventional view that the system adheres to a simple labeled-line coding scheme.

Pathogenesis of dysgeusia in COVID-19 patients: a scoping review.

OBJECTIVE: The novel coronavirus disease-19 (COVID-19) pandemic had intense social and economic effects. Patients infected with COVID-19 may present with a series of conditions. A considerable number of patients express taste and smell disturbances as a prodromal, coexistent, or as the only manifestation of COVID-19 infection. The objective of the present review is to review the hypothetical mechanisms of action and etiopathogenesis of dysgeusia in COVID-19 patients. MATERIALS AND METHODS: Multiple scientific databases were explored, including PubMed, Medline, Scopus, Cochrane-library, LILACS, Livivo and OpenGrey. All types of articles that discussed the pathogenesis of dysgeusia were included, while articles that described dysgeusia without detail about its mode of action were excluded. RESULTS: A total of 47 articles, with different designs, were included in this review. These articles suggested direct viral neural invasion to olfactory and gustatory nerves, viral cytotoxicity to taste buds, angiotensin II imbalance, augmented pro-inflammatory cytokines, and disturbances in salivary glands and sialic acid. COVID-19 induced-dysgeusia was also associated with systemic diseases, medications, zinc, chemicals, and disinfectants. CONCLUSIONS: The most likely cause of transient dysgeusia in COVID-19 is peripheral neurotropism and direct toxicity to taste buds or olfactory epithelium. Other factors may also play a contributory role in dysgeusia, such as a defect in the quality and quantity of saliva, pro-inflammatory cytokines, angiotensin II accumulation, systemic diseases, hypozincemia, and excessive use of chemicals.

Unlocking the Complex Flavors of Dysgeusia after Hematopoietic Cell Transplantation.

Dysgeusia is a frequently occurring symptom after hematopoietic cell transplantation (HCT) that has important long-term effects on physical, nutritional, and immunologic recovery, as well as on quality of life. Despite the relevance of this symptom, the study of dysgeusia in patients undergoing HCT has been limited, owing in part to its complexity. In this article, we review normal taste function and its clinical evaluation, discuss how dysgeusia uniquely affects patients undergoing HCT, and examine distinct, transplantation-related contributors to dysgeusia that may help elucidate strategies to ultimately reduce this symptom burden after transplantation.

Síndrome de boca ardiente: revisión y puesta al día / Burning mouth syndrome: a review and update

El síndrome de boca ardiente (SBA) es un cuadro clínico que padecen mayoritariamente mujeres de edad media o avanzada. Se caracteriza por una sensación muy molesta de ardor o escozor sobre la lengua o en otras zonas de la mucosa bucal. Puede estar acompañado de xerostomía y de disgeusia. Se suele presentar de forma espontánea y tiene un perfil clínico muy característico. Las molestias son continuas, pero aumentan hacia la tarde-noche. Aunque clásicamente se había atribuido a múltiples factores, en los últimos años hay evidencia para relacionarlo con una disfunción neuropática de tipo periférico (fibras C sensitivas o trigeminales) o de tipo central (sistema dopaminérgico nigroestriado). En el diagnóstico hay que descartar lesiones objetivables en la mucosa oral o alteraciones en la analítica sanguínea que puedan ser causa de ardor bucal. El manejo de los pacientes se basa en evitar focos irritativos orales y soporte psicológico. Para el tratamiento farmacológico del ardor en el SBA primario de causa periférica, se puede administrar clonacepam de uso tópico, y pacientes con SBA de tipo central parecen mejorar con el uso de antidepresivos del tipo de la duloxetina, anticonvulsionantes como la gabapentina, o la amisulprida (AU)

Burning mouth syndrome (BMS) is mainly found in middle aged or elderly women and is characterized by intense burning or itching sensation of the tongue or other regions of the oral mucosa. It can be accompanied by xerostomia and dysgeusia. The syndrome generally manifests spontaneously, and the discomfort is typically of a continuous nature but increases in intensity during the evening and at night. Although BMS classically has been attributed to a range of factors, in recent years evidence has been obtained relating it peripheral (sensory C and/or trigeminal nerve fibers) or central neuropathic disturbances (involving the nigrostriatal dopaminergic system). The differential diagnosis requires the exclusion of oral mucosal lesions or blood test alterations that can produce burning mouth sensation. Patient management is based on the avoidance of causes of oral irritation and the provision of psychological support. Drug treatment for burning sensation in primary BMS of peripheral origin can consist of topical clonazepam, while central type BMS appears to improve with the use of antidepressants such as duloxetine, antiseizure drugs such as gabapentin, or amisulpride (AU)

Expression levels of genes encoding melanin concentrating hormone (MCH) and MCH receptor change in taste aversion, but MCH injections do not alleviate aversive responses.

Melanin concentrating hormone (MCH) stimulates feeding driven by energy needs and reward and modifies anxiety behavior. Orexigenic peptides of similar characteristics, including nociceptin/orphanin FQ, Agouti-related protein and opioids, increase consumption also by reducing avoidance of potentially tainted food in animals displaying a conditioned taste aversion (CTA). Herein, using real-time PCR, we assessed whether expression levels of genes encoding MCH and its receptor, MCHR1, were affected in CTA in the rat. We also investigated whether injecting MCH intracerebroventricularly (ICV) during the acquisition and retrieval of LiCl-induced CTA, would alleviate aversive responses. MCHR1 gene was upregulated in the hypothalamus and brain stem of aversive animals, MCH mRNA was significantly higher in the hypothalamus, whereas a strong trend suggesting upregulation of MCH and MCHR1 genes was detected in the amygdala. Despite these expression changes associated with aversion, MCH injected prior to the induction of CTA with LiCl as well as later, during the CTA retrieval upon subsequent presentations of the aversive tastant, did not reduce the magnitude of CTA. We conclude that MCH and its receptor form an orexigenic system whose expression is affected in CTA. This altered MCH expression may contribute to tastant-targeted hypophagia in CTA. However, changing the MCH tone in the brain by exogenous peptide was insufficient to prevent the onset or facilitate extinction of LiCl-induced CTA. This designates MCH as one of many accessory molecules associated with shaping an aversive response, but not a critical one for LiCl-dependent CTA to occur.

A primary large cholesterol cyst of the mastoid presenting with dysgeusia.

The occurrence of postoperative secondary cholesterol cysts in the mastoid has been previously reported, however the occurrence of a primary large cholesterol cyst in the mastoid with bony destruction of the facial nerve has rarely been reported. The case report of a 17-year-old female patient with a primary large cholesterol cyst with dysgeusia is presented. Computed tomography and magnetic resonance imaging findings for the lesion distinguish a cholesterol granuloma, cholesteatoma and vascular tumor. The patient underwent a canal wall down mastoidectomy with mastoid obliteration. A dehiscent portion of the mastoid segment of the facial nerve was visible within the cavity; the gross finding of the facial nerve was edematous in appearance. Five years later, there has been no recurrence of disease.

Non-oral etiologies of oral malodor and altered chemosensation.

A number of non-oral causes for oral malodor have been discussed. Several well documented etiologies for non-oral malodor include renal failure, cirrhosis of the liver, and diabetes mellitus. Each of these conditions has been examined using analytical instrumentation. In addition there appear to be several other metabolic conditions involving enzymatic and transport anomalies (such as trimethylaminuria) which lead to the systemic production of volatile malodors that manifest themselves as halitosis and/or altered chemoreception. Our studies include patients who have been referred to us after being examined by numerous clinical specialists with no identification or relief from their problem. This is due in part to the intermittent nature of many of these problems as well as an apparent lack of knowledge concerning many of these metabolic problems and their relation to oral symptoms.