Gustatory and Multimodal Neuronal Responses in the Amygdala During Licking and Discrimination of Sensory Stimuli in Awake Rats

1998 ◽  
Vol 79 (1) ◽  
pp. 21-36 ◽  
Author(s):  
Hisao Nishijo ◽  
Teruko Uwano ◽  
Ryoi Tamura ◽  
Taketoshi Ono

Nishijo, Hisao, Teruko Uwano, Ryoi Tamura, and Taketoshi Ono. Gustatory and multimodal neuronal responses in the amygdala during licking and discrimination of sensory stimuli in awake rats. J. Neurophysiol. 79: 21–36, 1998. The amygdala (AM) receives information from various sensory modalities via the neocortex and directly from the thalamus and brain stem and plays an important role in ingestive behaviors. In the present study, neuronal activity was recorded in the AM and amygdalostriatal transition area of rats during discrimination of conditioned sensory stimuli and ingestion of sapid solutions. Of the 420 responsive neurons, 227 responded exclusively to one sensory modality, 120 responded to two or more modalities, and the remaining 73 could not be classified. Among the responsive neurons, 108 responded to oral-sensory stimulation (oral-sensory neurons). In detailed analyses of 84 of these oral-sensory neurons, 24 were classified as taste responsive and were located mainly in the central nucleus of the AM. The other 60 oral-sensory neurons were classified as nontaste oral-sensory neurons and were distributed widely throughout the AM. Both the taste and nontaste oral-sensory neurons also responded to other sensory stimuli. Of the 24 taste neurons, 21 were tested at least with four standard taste solutions. On the basis of the magnitudes of their responses to these sapid stimuli, the taste neurons were classified as follows: seven sucrose-best, four NaCl-best, three citric acid-best, and six quinine HCl-best. The remaining cell responded significantly only to lysine HCl and monosodium glutamate. Multivariate analyses of these 21 taste neurons suggested that, in the AM, taste quality was processed based on palatability. Taken with previous lesion studies, the present results suggest that the AM plays a role in the evaluation of taste palatability and in the association of taste stimuli with other sensory stimuli.

2002 ◽  
Vol 19 (4) ◽  
pp. 207-219 ◽  
Author(s):  
Eynat Gal ◽  
Murray Dyck ◽  
Anne Passmore

AbstractThis study was designed to test whether there is a functional relationship between sensory stimulation and stereotyped movements (SM). Four children with autism and intellectual disability (according to DSM-IV criteria) who showed stereotyped movements were studied. The Short Sensory Profile was used to define whether a child perceived stimulation within each sensory modality as aversive, attractive, or neutral. The Stereotyped and Self-Injurious Movements Interview was used to identify each child's repetitive movements. Children were then exposed to sensory stimuli that were neutral, aversive or attractive. Results indicate that children: (a) initiate or increase stereotyped movements immediately following the onset of an aversive stimulus, (b) terminate or decrease stereotyped movements following the onset of an attractive stimulus and (c) initiate or increase stereotyped movements during periods of neutral stimulation. We conclude that stereotyped movements are functionally related to sensory stimulation; individuals who frequently engage in stereotyped movements may do so in order to cope with under-stimulation and aversive over-stimulation.


1994 ◽  
pp. 419-420
Author(s):  
Hisao Nishijo ◽  
Teruko Uwano ◽  
Makoto Yonemori ◽  
Taketoshi Ono

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 10-11
Author(s):  
J Pujo ◽  
G De Palma ◽  
J Lu ◽  
S M Collins ◽  
P Bercik

Abstract Background Abdominal pain is a common complaint in patients with chronic gastrointestinal disorders. Accumulating evidence suggests that gut microbiota is an important determinant of gut function, including visceral sensitivity. Germ-free (GF) mice have been shown to display visceral hypersensitivity, which normalizes after colonization. Sex also appears to play a key role in visceral sensitivity, as women report more abdominal pain than men. Thus, both gut bacteria and sex are important in the regulation of gut nociception, but the underlying mechanisms remain poorly understood. Aims To investigate the role of gut microbiota and sex in abdominal pain. Methods We used primary cultures of sensory neurons from dorsal root ganglia (DRG) of female and male conventionally raised (SPF) or germ-free (GF) mice (7–18 weeks old). To study the visceral afferent activity in vitro, calcium mobilization in DRG sensory neurons was measured by inverted fluorescence microscope using a fluorescent calcium probe Fluo-4 (1mM). Two parameters were considered i) the percentage of responding neurons ii) the intensity of the neuronal response. First, DRG sensory neurons were stimulated by a TRPV1 agonist capsaicin (12.5nM, 125nM and 1.25µM) or by a mixture of G-protein coupled receptors agonist (GPCR: bradykinin, histamine and serotonin; 1µM, 10µM and 100µM). We next measured the neuronal production of substance P and calcitonin gene-related peptide (CGRP), two neuropeptides associated with nociception, in response to capsaicin (1.25µM) or GPCR agonists (100µM) by ELISA and EIA, respectively. Results The percentage of neurons responding to capsaicin and GPCR agonists was similar in male and female SPF and GF mice. However, the intensity of the neuronal response was higher in SPF male compared to SPF female in response to capsaicin (125nM: p=0.0336; 1.25µM: p=0.033) but not to GPCR agonists. Neuronal activation was similar in GF and SPF mice of both sexes after administration of capsaicin or GPCR agonists. Furthermore, substance P and CGRP production by sensory neurons induced by capsaicin or GPCR agonists was similar in SPF and GF mice, regardless of sex. However, while the response to capsaicin was similar, the GPCR agonists-induced production of substance P was higher in SPF male mice compared to SPF females (p=0.003). The GPCR agonists-induced production of CGRP was similar in SPF male and female mice. Conclusions Our data suggest that at the level of DRG neurons, the absence of gut microbiota does not predispose to visceral hypersensitivity. The intensity of DRG neuronal responses to capsaicin and the GPCR agonists-induced production of substance P are higher in male compared to female mice, in contrast to previously published studies in various models of acute and chronic pain. Further studies are thus needed to investigate the role of sex in visceral sensitivity. Funding Agencies CIHR


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emily T. Wood ◽  
Kaitlin K. Cummings ◽  
Jiwon Jung ◽  
Genevieve Patterson ◽  
Nana Okada ◽  
...  

AbstractSensory over-responsivity (SOR), extreme sensitivity to or avoidance of sensory stimuli (e.g., scratchy fabrics, loud sounds), is a highly prevalent and impairing feature of neurodevelopmental disorders such as autism spectrum disorders (ASD), anxiety, and ADHD. Previous studies have found overactive brain responses and reduced modulation of thalamocortical connectivity in response to mildly aversive sensory stimulation in ASD. These findings suggest altered thalamic sensory gating which could be associated with an excitatory/inhibitory neurochemical imbalance, but such thalamic neurochemistry has never been examined in relation to SOR. Here we utilized magnetic resonance spectroscopy and resting-state functional magnetic resonance imaging to examine the relationship between thalamic and somatosensory cortex inhibitory (gamma-aminobutyric acid, GABA) and excitatory (glutamate) neurochemicals with the intrinsic functional connectivity of those regions in 35 ASD and 35 typically developing pediatric subjects. Although there were no diagnostic group differences in neurochemical concentrations in either region, within the ASD group, SOR severity correlated negatively with thalamic GABA (r = −0.48, p < 0.05) and positively with somatosensory glutamate (r = 0.68, p < 0.01). Further, in the ASD group, thalamic GABA concentration predicted altered connectivity with regions previously implicated in SOR. These variations in GABA and associated network connectivity in the ASD group highlight the potential role of GABA as a mechanism underlying individual differences in SOR, a major source of phenotypic heterogeneity in ASD. In ASD, abnormalities of the thalamic neurochemical balance could interfere with the thalamic role in integrating, relaying, and inhibiting attention to sensory information. These results have implications for future research and GABA-modulating pharmacologic interventions.


2021 ◽  
pp. 251660852098429
Author(s):  
Dorcas B. C. Gandhi ◽  
Ivy Anne Sebastian ◽  
Komal Bhanot

Sensory dysfunction is one of the common impairments that occurs post stroke. With sensory changes in all modalities, it also affects the quality of life and incites suicidal thoughts. The article attempts to review and describe the current evidence of various approaches of assessment and rehabilitation for post-stroke sensory dysfunction. After extensive electronic database search across Medline, Embase, EBSCO, and Cochrane library, it generated 2433 results. After screening according to inclusion and exclusion criteria, we included 11 studies. We categorized data based on type of sensory deficits and prevalence, role of sensory system on motor behavior, type of intervention, sensory modality targeted, and dosage of intervention and outcome measures used for rehabilitation. Results found the strong evidence of involvement of primary and secondary motor areas involved in processing and responding to somatosensation, respectively. We divided rehabilitation approaches into sensory stimulation approach and sensory retraining approach focused on using external stimuli and relearning, respectively. However, with varied aims and targeted sensory involvement, the study applicability is affected. Thus, this emerges the need of extensive research in future for evidence-based practice of assessments and rehabilitation on post-stroke sensory rehabilitation.


1997 ◽  
Vol 92 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Gervais Tougas ◽  
Markad Kamath ◽  
Geena Watteel ◽  
Debbie Fitzpatrick ◽  
Ernest L. Fallen ◽  
...  

1. The heart and the oesophagus have similar sensory pathways, and sensations originating from the oesophagus are often difficult to differentiate from those of cardiac origin. We hypothesized that oesophageal sensory stimuli could alter neurocardiac function through autonomic reflexes elicited by these oesophageal stimuli. In the present study, we examined the neurocardiac response to oesophageal stimulation and the effects of electrical and mechanical oesophageal stimulation on the power spectrum of beat-to-beat heart rate variability in male volunteers. 2. In 14 healthy volunteers, beat-to-beat heart rate variability was compared at rest and during oesophageal stimulation, using either electrical (200 μs, 16 mA, 0.2 Hz) or mechanical (0.5 s, 14 ml, 0.2 Hz) stimuli. The power spectrum of beat-to-beat heart rate variability was obtained and its low- and high-frequency components were determined. 3. Distal oesophageal stimulation decreased heart rate slightly (both electrical and mechanical) (P < 0.005), and markedly altered heart rate variability (P < 0.001). Both electrical and mechanical oesophageal stimulation increased the absolute and normalized area of the high-frequency band within the power spectrum (P < 0.001), while simultaneously decreasing the low-frequency power (P < 0.005). 4. In humans, oesophageal stimulation, whether electrical or mechanical, appears to amplify respiratory-driven cardiac vagoafferent modulation while decreasing sympathetic modulation. The technique provides access to vagoafferent fibres and thus may yield useful information on the autonomic effects of visceral or oesophageal sensory stimulation.


1996 ◽  
Vol 270 (6) ◽  
pp. R1371-R1379 ◽  
Author(s):  
K. L. Teff ◽  
K. Engelman

In animals, bypassing the oropharyngeal receptors by intragastric administration of glucose results in glucose intolerance. To determine whether the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after intragastric administration of glucose, with and without subjects tasting food. Plasma glucose area under the curve (AUC) was significantly lower after oral sensory stimulation (3,433 +/- 783 vs. 5,643 +/- 1,397 mg.dl-1. 195 min-1; P < 0.03; n = 8). Insulin and C-peptide AUCs were higher during the first one-half of the sampling period (insulin, 5,771 +/- 910 vs. 4,295 +/- 712 microU. ml-1.75 min-1; P < 0.05; C-peptide, 86 +/- 10 vs. 66 +/- 9 ng.ml-1. 75 min-1; P < 0.03) and lower during the second one-half of the sampling period compared with the control condition (1,010 +/- 233 vs. 2,106 microU.ml-1. 120 min-1; P < 0.025; 31 +/- 8 vs. 56 +/- 18 ng.ml-1. 120 min-1; P < 0.05; insulin and C-peptide, respectively). Oral sensory stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 pg.ml-1. 195 min-1; P < 0.002). These data provide evidence in humans that oral sensory stimulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.


GYMNASIUM ◽  
2019 ◽  
Vol XIX (1) ◽  
pp. 42
Author(s):  
Mihaela Anghel

One of the reasons behind the choice of the topic is that this problem of sensory-motor development in children with physical and mental deficiencies, especially in children with Down syndrome, is not sufficiently known and studied, sensory-motor development representing an important factor in their physical and social development. The reason I chose this theme and the theoretical basis from which I started was to improve the psychomotor behaviors through sensory stimulation. The assumptions we went into the research were: 1. If we use different sensory combination strategies, the Down Syndrome will be able to compensate for the psycho-motor disorders; 2. If we apply sensory stimuli to the Down Syndrome child, then there will be ameliorations of the underlying motor conduction. The research presents a case study of a 6 year and six mouth old child diagnosed with Down syndrome. The location of the study was carried out at the "Delfinul" day center of the Betania Association.


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