Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin

1989 ◽  
Vol 257 (5) ◽  
pp. R1162-R1168 ◽  
Author(s):  
R. C. Ritter ◽  
S. Ritter ◽  
W. R. Ewart ◽  
D. L. Wingate
Keyword(s):  
Food Intake ◽  
Sensory Neurons ◽  
Gastric Distension ◽  
Extracellular Recordings ◽  
Cholecystokinin Octapeptide ◽  
Unmyelinated Axons ◽  
Sensory Modalities ◽  
Afferent Inputs ◽  
Dorsal Hindbrain ◽  
The Brain

Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.

Cholecystokinin octapeptide analogues suppress food intake via central CCK-A receptors in mice

1993 ◽  
Vol 265 (3) ◽  
pp. R481-R486 ◽  
Author(s):  
Y. Hirosue ◽  
A. Inui ◽  
A. Teranishi ◽  
M. Miura ◽  
M. Nakajima ◽  
...  
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Rank Order ◽  
Peripheral Circulation ◽  
Inhibitory Effect ◽  
Peripheral Tissues ◽  
Cholecystokinin Octapeptide ◽  
The Central Nervous System ◽  
The Difference ◽  
The Brain

To examine the mechanism of the satiety-producing effect of cholecystokinin (CCK) in the central nervous system, we compared the potency of intraperitoneally (ip) or intracerebroventricularly (icv) administered CCK-8 and its analogues on food intake in fasted mice. The icv administration of a small dose of CCK-8 (0.03 nmol/brain) or of Suc-(Thr28, Leu29, MePhe33)-CCK-7 (0.001 nmol/brain) suppressed food intake for 20 min, whereas CCK-8 (1 nmol/kg, which is equivalent to 0.03 nmol/brain) or Suc-(Thr28, Leu29, MePhe33)-CCK-7 (1 nmol/kg) had satiety effect after ip administration. Dose-response studies indicated the following rank order of potency: Suc-CCK-7 > or = Suc-(Thr28, Leu29, MePhe33)-CCK-7 > or = CCK-8 > or = (Nle28,31)-CCK-8 >> desulfated CCK-8 = CCK-4 = 0 in the case of ip administration and Suc-(Thr28, Leu29, MePhe33)-CCK-7 >> Suc-CCK-7 > or = CCK-8 > or = (Nle28,31)-CCK-8 >> desulfated CCK-8 = CCK-4 = 0 in the case of icv administration. The selective CCK-A receptor antagonist MK-329 reversed the inhibitory effect of the centrally as well as peripherally administered CCK-8, or of Suc-(Thr28, Leu29, MePhe33)-CCK-7, whereas the selective CCK-B receptor antagonist L-365260 did not. The icv administered CCK-8 did not appear in the peripheral circulation. These findings suggest the participation of CCK-A receptors in the brain in mediating the satiety effect of CCK and the difference in CCK-A receptors in the brain and peripheral tissues.

Postlesional Vestibular Reorganization in Frogs: Evidence for a Basic Reaction Pattern After Nerve Injury

2001 ◽  
Vol 85 (6) ◽  
pp. 2643-2646 ◽  
Author(s):  
Fumiyuki Goto ◽  
Hans Straka ◽  
Norbert Dieringer
Keyword(s):  
Nerve Injury ◽  
Vestibular Nuclei ◽  
Reaction Pattern ◽  
Similar Process ◽  
Spatial Response ◽  
Sensory Modalities ◽  
Basic Reaction ◽  
Afferent Inputs ◽  
Motor Maps ◽  
The Brain

Nerve injury induces a reorganization of subcortical and cortical sensory or motor maps in mammals. A similar process, vestibular plasticity 2 mo after unilateral section of the ramus anterior of N. VIII was examined in this study in adult frogs. The brain was isolated with the branches of both N. VIII attached. Monosynaptic afferent responses were recorded in the vestibular nuclei on the operated side following ipsilateral electric stimulation either of the sectioned ramus anterior of N. VIII or of the intact posterior vertical canal nerve. Excitatory and inhibitory commissural responses were evoked by separate stimulation of each of the contralateral canal nerves in second-order vestibular neurons. The afferent and commissural responses of posterior vertical canal neurons recorded on the operated side were not altered. However, posterior canal-related afferent inputs had expanded onto part of the deprived ramus anterior neurons. Inhibitory commissural responses evoked from canal nerves on the intact side were detected in significantly fewer deprived ramus anterior neurons than in controls, but excitatory commissural inputs from the three contralateral canal nerves had expanded. This reactivation might facilitate the survival of deprived neurons and reduce the asymmetry in bilateral resting activities but implies a deterioration of the original spatial response tuning. Extensive similarities at the synaptic and network level were noted between this vestibular reorganization and the postlesional cortical and subcortical reorganization of sensory representations in mammals. We therefore suggest that nerve injury activates a fundamental neural reaction pattern that is common between sensory modalities and vertebrate species.

Capsaicin pretreatment attenuates suppression of food intake by cholecystokinin

1985 ◽  
Vol 248 (4) ◽  
pp. R501-R504 ◽  
Author(s):  
R. C. Ritter ◽  
E. E. Ladenheim
Keyword(s):  
Food Intake ◽  
Sensory Neurons ◽  
Fourth Ventricle ◽  
Small Diameter ◽  
Red Pepper ◽  
Afferent Neurons ◽  
Cholecystokinin Octapeptide ◽  
Vagal Afferent

Capsaicin, the pungent principal in red pepper, has been shown to damage small-diameter peptide-containing sensory neurons. Suppression of feeding by cholecystokinin octapeptide (CCK OP) was attenuated after systemic pretreatment with capsaicin. Capsaicin pretreatment did not attenuate suppression of food intake by intragastric preloads. Pretreatment of rats with microgram quantities of capsaicin injected into the fourth ventricle, near the sites of vagal afferent termination, also attenuated CCK OP-induced suppression of food intake. These results suggest that the satiety-inducing effects of CCK OP are mediated, at least in part, by capsaicin-sensitive afferent neurons.

scholarly journals Food-induced brain responses and eating behaviour

2012 ◽  
Vol 71 (4) ◽  
pp. 511-520 ◽  
Author(s):  
Paul A.M. Smeets ◽  
Lisette Charbonnier ◽  
Floor van Meer ◽  
Laura N. van der Laan ◽  
Maartje S. Spetter
Keyword(s):  
Food Intake ◽  
Eating Behaviour ◽  
Sensory Stimulation ◽  
Nutrient Sensing ◽  
Self Control ◽  
Gastric Distension ◽  
Brain Responses ◽  
Gut Hormone ◽  
Advanced Analysis ◽  
The Brain

The brain governs food intake behaviour by integrating many different internal and external state and trait-related signals. Understanding how the decisions to start and to stop eating are made is crucial to our understanding of (maladaptive patterns of) eating behaviour. Here, we aim to (1) review the current state of the field of ‘nutritional neuroscience’ with a focus on the interplay between food-induced brain responses and eating behaviour and (2) highlight research needs and techniques that could be used to address these. The brain responses associated with sensory stimulation (sight, olfaction and taste), gastric distension, gut hormone administration and food consumption are the subject of increasing investigation. Nevertheless, only few studies have examined relations between brain responses and eating behaviour. However, the neural circuits underlying eating behaviour are to a large extent generic, including reward, self-control, learning and decision-making circuitry. These limbic and prefrontal circuits interact with the hypothalamus, a key homeostatic area. Target areas for further elucidating the regulation of food intake are: (eating) habit and food preference formation and modification, the neural correlates of self-control, nutrient sensing and dietary learning, and the regulation of body adiposity. Moreover, to foster significant progress, data from multiple studies need to be integrated. This requires standardisation of (neuroimaging) measures, data sharing and the application and development of existing advanced analysis and modelling techniques to nutritional neuroscience data. In the next 20 years, nutritional neuroscience will have to prove its potential for providing insights that can be used to tackle detrimental eating behaviour.

Brain stem melanocortinergic modulation of meal size and identification of hypothalamic POMC projections

2005 ◽  
Vol 289 (1) ◽  
pp. R247-R258 ◽  
Author(s):  
Huiyuan Zheng ◽  
Laurel M. Patterson ◽  
Curtis B. Phifer ◽  
Hans-Rudolf Berthoud
Keyword(s):  
Food Intake ◽  
Brain Stem ◽  
Fourth Ventricle ◽  
Nucleus Tractus Solitarius ◽  
Meal Size ◽  
Gastric Distension ◽  
Dorsal Vagal Complex ◽  
Melanocortin 4 Receptor ◽  
Brown Adipose ◽  
The Brain

Metabolic, cognitive, and environmental factors processed in the forebrain modulate food intake by changing the potency of direct controls of meal ingestion in the brain stem. Here, we behaviorally and anatomically test the role of the hypothalamic proopiomelanocortin (POMC) system in mediating some of these descending, indirect controls. Melanotan II (MTII), a stable melanocortin 4 receptor (MC4R) and melanocortin 3 receptor (MC3R) agonist injected into the fourth ventricle near the dorsal vagal complex, potently inhibited 14-h food intake by decreasing meal size but not meal frequency; SHU9119, an antagonist, increased food intake by selectively increasing meal size. Furthermore, MTII injected into the fourth ventricle increased and SHU9119 tended to decrease heart rate and body temperature measured telemetrically in freely moving rats. Numerous α-melanocyte-stimulating hormone-immunoreactive axons were in close anatomical apposition to nucleus tractus solitarius neurons showing c-Fos in response to gastric distension, expressing neurochemical phenotypes implicated in ingestive control, and projecting to brown adipose tissue. In retrograde tracing experiments, a small percentage of arcuate nucleus POMC neurons was found to project to the dorsal vagal complex. Thus melanocortin signaling in the brain stem is sufficient to alter food intake via changing the potency of satiety signals and to alter sympathetic outflow. Although the anatomical findings support the involvement of hypothalamomedullary POMC projections in mediating part of the descending, indirect signal, they do not rule out involvement of POMC neurons in the nucleus tractus solitarius in mediating part of the direct signal.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Interaction of GLP-1 with gastric distension in regulating food intake and satiety in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A208-A208
Author(s):  
L DEGEN ◽  
D MATZINGER ◽  
B FISCHER ◽  
F ZIMMERLI ◽  
M KNUPP ◽  
...  
Keyword(s):  
Food Intake ◽  
Gastric Distension

scholarly journals Reduction of food intake by cholecystokinin requires activation of hindbrain NMDA-type glutamate receptors

2011 ◽  
Vol 301 (2) ◽  
pp. R448-R455 ◽  
Author(s):  
Jason Wright ◽  
Carlos Campos ◽  
Thiebaut Herzog ◽  
Mihai Covasa ◽  
Krzysztof Czaja ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Food Intake ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Fourth Ventricle ◽  
Nmda Receptor Antagonist ◽  
Behavioral Pattern ◽  
Vagal Afferents ◽  
Nmda Receptor Antagonists ◽  
The Brain

Intraperitoneal injection of CCK reduces food intake and triggers a behavioral pattern similar to natural satiation. Reduction of food intake by CCK is mediated by vagal afferents that innervate the stomach and small intestine. These afferents synapse in the hindbrain nucleus of the solitary tract (NTS) where gastrointestinal satiation signals are processed. Previously, we demonstrated that intraperitoneal (IP) administration of either competitive or noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists attenuates reduction of food intake by CCK. However, because vagal afferents themselves express NMDA receptors at both central and peripheral endings, our results did not speak to the question of whether NMDA receptors in the brain play an essential role in reduction of feeding by CCK. We hypothesized that activation of NMDA receptors in the NTS is necessary for reduction of food intake by CCK. To test this hypothesis, we measured food intake following IP CCK, subsequent to NMDA receptor antagonist injections into the fourth ventricle, directly into the NTS or subcutaneously. We found that either fourth-ventricle or NTS injection of the noncompetitive NMDA receptor antagonist MK-801 was sufficient to inhibit CCK-induced reduction of feeding, while the same antagonist doses injected subcutaneously did not. Similarly fourth ventricle injection of d-3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphoric acid (d-CPPene), a competitive NMDA receptor antagonist, also blocked reduction of food intake following IP CCK. Finally, d-CPPene injected into the fourth ventricle attenuated CCK-induced expression of nuclear c-Fos immunoreactivity in the dorsal vagal complex. We conclude that activation of NMDA receptors in the hindbrain is necessary for the reduction of food intake by CCK. Hindbrain NMDA receptors could comprise a critical avenue for control and modulation of satiation signals to influence food intake and energy balance.

scholarly journals Polymodal Functionality of C. elegans OLL Neurons in Mechanosensation and Thermosensation

2021 ◽  
Author(s):  
Yuedan Fan ◽  
Wenjuan Zou ◽  
Jia Liu ◽  
Umar Al-Sheikh ◽  
Hankui Cheng ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Sensory Neurons ◽  
Molecular Mechanisms ◽  
Temperature Sensitive ◽  
Cold Sensation ◽  
Cold Response ◽  
C Elegans ◽  
Sensory Modalities ◽  
A Cell ◽  
Bona Fide

AbstractSensory modalities are important for survival but the molecular mechanisms remain challenging due to the polymodal functionality of sensory neurons. Here, we report the C. elegans outer labial lateral (OLL) sensilla sensory neurons respond to touch and cold. Mechanosensation of OLL neurons resulted in cell-autonomous mechanically-evoked Ca2+ transients and rapidly-adapting mechanoreceptor currents with a very short latency. Mechanotransduction of OLL neurons might be carried by a novel Na+ conductance channel, which is insensitive to amiloride. The bona fide mechano-gated Na+-selective degenerin/epithelial Na+ channels, TRP-4, TMC, and Piezo proteins are not involved in this mechanosensation. Interestingly, OLL neurons also mediated cold but not warm responses in a cell-autonomous manner. We further showed that the cold response of OLL neurons is not mediated by the cold receptor TRPA-1 or the temperature-sensitive glutamate receptor GLR-3. Thus, we propose the polymodal functionality of OLL neurons in mechanosensation and cold sensation.

scholarly journals The path from trigeminal asymmetry to cognitive impairment: a behavioral and molecular study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria Paola Tramonti Fantozzi ◽  
Giulia Lazzarini ◽  
Vincenzo De Cicco ◽  
Angela Briganti ◽  
Serena Argento ◽  
...  
Keyword(s):  
Pupil Size ◽  
Muscle Spindles ◽  
Molecular Study ◽  
Contralateral Side ◽  
Acute Effects ◽  
Adult Rats ◽  
Afferent Inputs ◽  
Acute And Chronic Effects ◽  
The Brain ◽  
Mandibular Branch

AbstractTrigeminal input exerts acute and chronic effects on the brain, modulating cognitive functions. Here, new data from humans and animals suggest that these effects are caused by trigeminal influences on the Locus Coeruleus (LC). In humans subjects clenching with masseter asymmetric activity, occlusal correction improved cognition, alongside with reductions in pupil size and anisocoria, proxies of LC activity and asymmetry, respectively. Notably, reductions in pupil size at rest on the hypertonic side predicted cognitive improvements. In adult rats, a distal unilateral section of the trigeminal mandibular branch reduced, on the contralateral side, the expression of c-Fos (brainstem) and BDNF (brainstem, hippocampus, frontal cortex). This counterintuitive finding can be explained by the following model: teeth contact perception loss on the lesioned side results in an increased occlusal effort, which enhances afferent inputs from muscle spindles and posterior periodontal receptors, spared by the distal lesion. Such effort leads to a reduced engagement of the intact side, with a corresponding reduction in the afferent inputs to the LC and in c-Fos and BDNF gene expression. In conclusion, acute effects of malocclusion on performance seem mediated by the LC, which could also contribute to the chronic trophic dysfunction induced by loss of trigeminal input.

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