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Interaction of Taste and Ingestion
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
Gustatory neurons in the PBN project at least as massively to a second series of targets independent of the thalamocortical axis: those situated throughout the ventral forebrain.45,57,58 The densest termini include the lateral hypothalamus, central nucleus of the amygdala, and bed nucleus of the stria terminalis, although other ventral forebrain sites are also implicated. These structures are associated with motivation, emotion, reinforcement, and, in particular, ingestion. Their damage disrupts normal responsiveness to exteroceptive input, a syndrome known as sensory neglect, which may contribute to the aphagia consequent to hypothalamic lesions.59,60 Lesions also interfere with taste-mediated interoceptive functions, such as sodium appetite61 and the acquisition62,63 or retention64,65 of conditioned taste aversions. Thus, there appears to be a functional distinction between the two major targets of PBN fibers in the rat. Projections to the thalamocortical axis may mediate the discriminative capacity of the taste system, an exteroceptive function in the same category as oral somesthesis whose mediating fibers accompany those of taste. Connections to the ventral forebrain may permit the integration of taste with interoceptive and exteroceptive information to guide and regulate feeding behavior.65 Such a hypothesis, now implied primarily by lesion studies, awaits electrophysiological confirmation.
Nuclei of the Solitary Tract and Regulation of Glycemia
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Cesar Timo-Iaria, Edson Carlos Fraga da Silva, Naomi Shinomiya Hell
It has been repeatedly demonstrated that bilateral lesion of the lateral hypothalamus in several species provokes aphagia. However, rats subjected to such lesion recover the capacity to eat spontaneously if artificially fed during a few weeks;57,58 cats recover from the lesion in about two months if kept alive by forced feeding.24 Considering that the hypothalamic glucoreceptors trigger more potent mechanisms than the NTS and hepatic glucoreceptors, in that order,27 and that the hypothalamic area containing glucoreceptors has to be destroyed to cause aphagia, it is probable that recovery from aphagia occurs because the NTS (and possibly the hepatic) glucoreceptors take over the linkage of feeding behavior with regulation of glycemia.
Gastrointestinal tract
Published in Brian J Pollard, Gareth Kitchen, Handbook of Clinical Anaesthesia, 2017
Tumours of the oesophagus are usually present with dysphagia which may be partial or complete at the time of surgery. Residual food particles may remain in the oesophagus as may liquid in the case of complete aphagia. Where obstruction is complete the patient will not be able to clear saliva.
Vitamin D attenuated 6-OHDA-induced behavioural deficits, dopamine dysmetabolism, oxidative stress, and neuro-inflammation in mice
Published in Nutritional Neuroscience, 2022
Adedamola Bayo-Olugbami, Abdulrazaq Bidemi Nafiu, Abdulbasit Amin, Olalekan Michael Ogundele, Charles C. Lee, Bamidele Victor Owoyele
6-OHDA lesions are commonly induced unilaterally, as bilateral dopamine denervation is associated with aphagia, adipsia, and weight loss [19]. Also, unilateral intrastriatal injections with 6-OHDA causes progressive loss of dopaminergic neurons, simulating nigrostriatal damage [20]. At different levels of the nigrostriatal tract, injection of 6-OHDA causes different degrees of DA degeneration [21] and these have different impacts behaviourally and histochemically. Striatal injection of 6-OHDA causes a graded and progressive loss of substantia nigra neurons [22], which is useful as a partial DA depletion model in studies of functional recovery [21]. It therefore mimics the earlier stage of the disorder [23].