Representations of the Texture of Food in the Primate Orbitofrontal Cortex: Neurons Responding to Viscosity, Grittiness, and Capsaicin

2003 ◽  
Vol 90 (6) ◽  
pp. 3711-3724 ◽  
Author(s):  
Edmund T. Rolls ◽  
Justus V. Verhagen ◽  
Mikiko Kadohisa
Keyword(s):  
Food Intake ◽  
Orbitofrontal Cortex ◽  
Silicone Oil ◽  
Food Selection ◽  
Single Neurons ◽  
Cortical Areas ◽  
Food Texture ◽  
A Site ◽  
The Brain ◽  
Somatosensory Cortical Areas

The primate orbitofrontal cortex (OFC) is a site of convergence from taste, olfactory, and somatosensory cortical areas. We describe a population of single neurons in the macaque OFC that responds to the texture of food in the mouth. Use of oral viscosity stimuli consisting of carboxymethylcellulose (CMC) in the range 1–10,000 centipoise showed that the responses of one subset of these neurons were related to stimulus viscosity. Some of the neurons had increasing responses to increasing viscosity, some had decreasing responses, and some neurons were tuned to a range of viscosities. These neurons are a different population to oral fat-sensitive neurons, in that their responses to fats (e.g., safflower oil), to silicone oil [(Si(CH3)2O)n], and to mineral oil (hydrocarbon) depended on the viscosity of these oils. Thus there is a dissociation between texture channels used to sense viscosity and fat. Some of these viscosity-sensitive single neurons were unimodal (somatosensory; 25%) and some received convergent taste inputs (75%). A second subpopulation of neurons responded to gritty texture (produced by microspheres suspended in CMC). A third subpopulation of neurons responded to capsaicin. These results provide evidence about the information channels used to represent the texture and flavor of food in a part of the brain important in appetitive responses to food and are relevant to understanding the physiological and pathophysiological processes related to food intake, food selection, and the effects of variety of food texture in combination with taste and other inputs that affect food intake.

Neurons in the Primate Orbitofrontal Cortex Respond to Fat Texture Independently of Viscosity

2003 ◽  
Vol 90 (3) ◽  
pp. 1514-1525 ◽  
Author(s):  
Justus V. Verhagen ◽  
Edmund T. Rolls ◽  
Mikiko Kadohisa
Keyword(s):  
Orbitofrontal Cortex ◽  
Carboxymethyl Cellulose ◽  
Silicone Oil ◽  
Somatosensory System ◽  
Fat Intake ◽  
System Use ◽  
A Site ◽  
Similar Texture ◽  
Separate Population ◽  
Somatosensory Cortical Areas

The primate orbitofrontal cortex (OFC) is a site of convergence from primary taste, olfactory, and somatosensory cortical areas. We describe the responses of a population of single neurons in the OFC that respond to orally applied fat (e.g., safflower oil) and to substances with a similar texture but different chemical composition, such as mineral oil (hydrocarbon) and silicone oil [(Si(CH3)2O)n]. These findings provide evidence that the neurons respond to the oral texture of fat, sensed by the somatosensory system. Use of an oral viscosity stimulus consisting of carboxymethyl-cellulose in the range 1–10,000 centipoise (cP) showed that the responses of these fat-sensitive neurons are not related to stimulus viscosity. Thus a textural component independent of viscosity and related to the slick or oily property is being used to activate these oral fat-sensitive neurons. Moreover, a separate population of neurons responds to viscosity (produced, e.g., by the carboxymethyl-cellulose series), but not to fat with the same viscosity. Thus there is a dissociation between texture channels used to sense fat viscosity and non–fat-produced viscosity. Further, free fatty acids such as linoleic acid do not activate these neurons, providing further evidence that the oral fat-sensing mechanism through which these OFC neurons are activated is not gustatory but textural. Most of this population of fat-sensitive neurons receive convergent taste inputs. These results provide evidence about how oral fat is sensed and are relevant to understanding the physiological and pathophysiological processes related to fat intake.

scholarly journals Primate Insular/Opercular Taste Cortex: Neuronal Representations of the Viscosity, Fat Texture, Grittiness, Temperature, and Taste of Foods

2004 ◽  
Vol 92 (3) ◽  
pp. 1685-1699 ◽  
Author(s):  
Justus V. Verhagen ◽  
Mikiko Kadohisa ◽  
Edmund T. Rolls
Keyword(s):  
Fatty Acids ◽  
Food Intake ◽  
Carboxymethyl Cellulose ◽  
Cortical Area ◽  
Food Selection ◽  
Primate Brain ◽  
Information Channels ◽  
The Brain

It is shown that the primate primary taste cortex represents not only taste but also information about many nontaste properties of oral stimuli. Of 1,122 macaque anterior insular/frontal opercular neurons recorded, 62 (5.5%) responded to oral stimuli. Of the orally responsive neurons, some (53%) represented the viscosity, tested using carboxymethyl-cellulose in the range 1–10,000 cP. Other neurons (8%) responded to fat in the mouth by encoding its texture (as shown similar responses to nonfat oils), and 8% responded to gritty texture. Some neurons (35%) responded to the temperature of the liquid in the mouth. Some neurons responded to capsaicin, and others to fatty acids. Some neurons (56%) had taste responses. Some (50%) of these neurons were unimodal, responding to one of these types of stimulus, and the majority combined responsiveness to these types of stimulus, with 23% responding for example to both taste and temperature. Some neurons respond to taste, texture, and temperature unimodally, but others combine these inputs. None of these orally responsive neurons responded to odor or to the sight of food. These results provide fundamental evidence about the information channels used to represent the taste, texture, and temperature of food in the first cortical area involved in taste in the primate brain. The results are relevant to understanding the physiological and pathophysiological processes related to how the properties of oral stimuli are represented in the brain and thus to the control of food intake and food selection.

The Brain Doesn’t Work by Logic

2018 ◽  
Author(s):  
James A. Anderson
Keyword(s):  
Lateral Inhibition ◽  
Horseshoe Crab ◽  
Compound Eye ◽  
Visual Image ◽  
Neural Computation ◽  
Single Neurons ◽  
Moving Image ◽  
Cortical Areas ◽  
Lateral Eye ◽  
The Brain

This chapter gives three examples of real neural computation. The conclusion is that the “brain doesn’t work by logic.” First, is the Limulus (horseshoe crab) lateral eye. The neural process of “lateral inhibition” tunes the neural response of the compound eye to allow crabs to better see other crabs for mating. Second, the retina of the frog contains cells that are selective to specific properties of the visual image. The frog responds strongly to the moving image of a bug with one class of selective retinal receptors. Third, experiments on patients undergoing neurosurgery for epilepsy found single neurons in several cortical areas that were highly selective to differing images, text strings, and spoken names of well-known people. In addition, new selective responses could be formed quickly. The connection to concepts in cognitive science seems inevitable. One possible mechanism is through associatively linked “cell assemblies.”

Effect of ammonia via prepyriform cortex on regulation of food intake in the rat

1976 ◽  
Vol 231 (4) ◽  
pp. 1263-1266 ◽  
Author(s):  
K Noda ◽  
K Chikamori
Keyword(s):  
Amino Acid ◽  
Food Intake ◽  
Basal Diet ◽  
Ammonium Ions ◽  
Cortical Areas ◽  
Keto Acids ◽  
Amino Acid Mixtures ◽  
Bilateral Lesions ◽  
The Brain ◽  
Prepyriform Cortex

Studies were made on whether ammonia, which is an obligatory intermediate of amino acid metabolism, depresses the food intake of rats fed a low-casein (basal) diet containing imbalanced amino acid mixtures (imbalanced diets). Bilateral lesions in the prepyriform cortex caused normalization of food intake of rats fed amino acid-imbalanced diets, confirming the work of Leung and Rogers (Am. J. Physiol. 221:929-935, 1971). Unlike normal rats, animals with prepyriform cortical lesions consumed as much of a diet containing 3% NH4Cl as they did of the basal diet. However, like normal rats, they rejected a diet containing a mixture of keto acids. Unilateral injection of NH4Cl into prepyriform cortical areas reduced the food intake to a greater extent than injection of NaCl into these areas or injection of NH4Cl into other parts of the brain. These results suggest that ammonium ions influence the appetite through their effect on prepyriform cortical areas.

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.

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.

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