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PubMed1988

Alcohol aversion generalization in rats: specific disruption of taste and odor cues with gustatory neocortex or olfactory bulb ablations.

Rats with ablations of the gustatory neocortex (Experiment 1) and rats with olfactory bulb ablations (Experiment 2) were compared with normal rats for aversion generalization to both single taste solutions (sucrose, sodium chloride, quinine hydrochloride, hydrochloric acid) and compound taste solutions (pairs of the four single tastants) following alcohol aversion training. All rats acquired equal and strong alcohol aversions. Control rats showed consistent aversion generalization to both the sucrose + quinine and the sucrose + hydrochloric acid solutions; no significant generalization occurred to the single tastants except a weak generalization to sucrose in Experiment 2. Rats with gustatory neocortical ablations failed to show aversion generalization to any of the taste solutions. Rats with olfactory bulbectomies displayed the same aversion generalization functions as control rats but exhibited significantly faster extinction of the alcohol aversion than did the trained control rats. Results from the present experiments suggest that during alcohol aversion learning, rats lacking gustatory neocortex use odor cues (no taste generalization), whereas rats lacking olfactory bulbs utilize taste cues (normal taste generalization).

Afferent Pathways↗

PubMed1987

Convulsant action of morphine, [D-Ala2, D-Leu5]-enkephalin and naloxone in the rat amygdala: electroencephalographic, morphological and behavioural sequelae.

Morphine hydrochloride (25-200 nmol), [D-Ala2, D-Leu5]enkephalin (10-200 nmol) and naloxone hydrochloride (100-1000 nmol) were injected unilaterally into the rat amygdala and the following electrographic, behavioural and neuropathological responses were studied. Microinjections of low doses of morphine (25-50 nmol) resulted in behavioural alterations characterized by staring, gustatory automatisms and wet shakes, whereas higher doses additionally produced motor limbic seizures and status epilepticus. The first changes in the electroencephalogram appeared in the amygdala immediately after the administration of morphine and rapidly spread to hippocampal and cortical areas. Electrographic alterations consisted of high voltage fast activity, spiking, bursts of polyspiking, electrographic seizures and periods of postictal depression. Neuropathological analysis of frontal forebrain sections by means of light microscopy revealed widespread, seizure-related damage confined to amygdala, olfactory cortex, thalamus, hippocampal formation, neocortex and substantia nigra. Pretreatment of animals with naloxone, 2-20 mg/kg s.c., as well as simultaneous microinjection of the non-convulsant dose of naloxone, 100 nmol, with morphine, 100 nmol, into the amygdala failed to block the development of convulsant activity and seizure-related brain damage produced by the opiate. In contrast, diazepam, 10 mg/kg i.p., when administered prior to the microinjection of morphine into the amygdala, abolished the epileptogenic effects of the drug. [D-Ala2, D-Leu5]Enkephalin, 10-200 nmol, elicited electrographic and behavioural responses similar to those seen after low doses of morphine, when administered into the amygdala. High voltage fast activity, single spikes, bursts of polyspiking, electrographic seizures and periods of postictal depression were seen in the electroencephalogram, but no behavioural signs of motor limbic seizures could be detected. The only behavioural correlates of epileptiform electrographic activity were wet shakes, myoclonic head twiches and gustatory automatisms. The examination of frontal forebrain sections from rats receiving [D-Ala2, D-Leu5]enkephalin revealed no morphological changes. Pretreatment of rats with either naloxone, 2 mg/kg, or diazepam, 10 mg/kg, blocked the development of behavioural and electrographic sequelae of the peptide. Naloxone, 100-1000 nmol, when microinjected into the amygdala, produced electrographic, behavioural and morphological alterations resembling those seen after high doses of morphine.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗

PubMed1991

Time-dependent recovery of taste aversion learning by fetal brain transplants in gustatory neocortex-lesioned rats.

We recently showed that fetal brain transplants produced a significant recovery in the ability of gustatory neocortex-lesioned rats to learn a conditioned taste aversion. In this report we assessed the capability of gustatory neocortex fetal brain transplants to produce behavioral recovery at different times. Four groups of male Wistar rats showing disrupted taste aversions due to gustatory neocortex lesions were studied. The lesioned animals received fetal cortical grafts, obtained from 16-day-old fetuses, and were retrained in the behavioral procedure after 15, 30, 45, or 60 days postgraft. Behavioral results showed a very good functional recuperation at 60 days, slight recovery at 45 and 30 days, and a poor recovery at 15 days postgraft. Results with HRP histochemistry revealed that at 30, 45, and 60 days postgrafting there were increased connections with the ventromedial nucleus of the thalamus and with the amygdala. At 15 days postgrafting there was an absence of HRP-labeled cells. In addition, behavioral recovery was correlated with increased acetylcholinesterase activity, detected histochemically, and with morphological neuronal maturation, revealed by Golgi staining. These results suggest that morphological maturity and reconnectivity between grafts and host tissue are important for behavioral recovery in gustatory neocortex-lesioned rats.

Acetylcholinesterase↗

PubMed1988

Harlequin syndrome: the sudden onset of unilateral flushing and sweating.

Facial flushing and sweating were investigated in five patients who complained of the sudden onset of unilateral facial flushing in hot weather or when exercising vigorously. One patient probably suffered a brainstem infarct at the time that the unilateral flush was first noticed, and was left with a subtle Horner's syndrome on the side opposite to the flush. The other four had no other neurological symptoms and no ocular signs of Horner's syndrome. Thermal and emotional flushing and sweating were found to be impaired on the non-flushing side of the forehead in all five patients whereas gustatory sweating and flushing were increased on that side in four of the five patients, a combination of signs indicating a deficit of the second sympathetic neuron at the level of the third thoracic segment. CT and MRI of this area failed to disclose a structural lesion but latency from stimulation of the motor cortex and thoracic spinal cord to the third intercostal muscle was delayed on the non-flushing side in one patient. The complaint of unilateral flushing and sweating was abolished in one patient by ipsilateral stellate ganglionectomy. The unilateral facial flushing and sweating induced by heat in all five patients was thus a normal or excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit. The onset in the four cases of peripheral origin followed strenuous exertion, which suggested that an anterior radicular artery may have become occluded at the third thoracic segment during torsion of the thoracic spine.

Adult↗

PubMed1982

Olfactory connections of substantia innominata and nucleus of the horizontal limb of the diagonal band in the rat: an electrophysiological study.

Extracellular unit recordings performed on 113 spontaneously discharging neurons in the substantia innominata-nucleus of the horizontal limb of the diagonal band region revealed that 46 (41%) were transsynaptically discharged or inhibited following stimulation of the main and accessory olfactory bulb (MOB, AOB) and the prepyriform cortex (PPC). A significantly greater number of cells were responsive to MOB and PPC than to AOB shocks. Eight (7%) neurons were antidromically invaded following MOB volleys. These findings suggest that the MOB has functional reciprocal connections with the 'ventral striatum', a region which can function, presumably as a nodal point for convergence of visual, gustatory and olfactory information relevant to feeding and drinking behavior.

Amygdala↗

PubMed1994

Increased potency and binding of mazindol to putative brain anorectic receptors in obesity-prone rats.

A class of sodium-sensitive, low affinity binding sites in the brain recognizes [3H]mazindol (MAZ). Competition for [3H]MAZ binding at these sites correlates with the anorectic potency of various phenethylamine drugs suggesting that these might be anorectic binding sites. Here [3H]MAZ binding, in the absence of sodium, was assessed by quantitative receptor autoradiography in rat brain. Binding was saturable, widespread and heterogenous with Kd = 3-229 microM and Bmax = 0.64-21.9 nmol/mg protein in various brain areas. By saturation studies, highest binding was in the somatosensory cortex, central amygdalar nucleus and bed nucleus of the stria terminalis. Hypothalamic subnuclei had intermediate and the piriform cortex had low binding. Rats were identified as prone to develop (DIO-prone) or resist (DR-prone) diet-induced obesity by their low vs. high 24 h urine norepinephrine excretion, respectively. While similar in body weight and basal 30 min intake of 4% sucrose, DIO-prone rats had 28% greater inhibition of sucrose intake by 3 mg/kg MAZ, i.p. (86 +/- 5%) than DR-prone rats (67 +/- 6%; P = 0.05). DIO-prone rats also had 23-55% higher levels of 10 nM [3H]MAZ binding in various hypothalamic and amygdalar nuclei, the somatosensory, piriform and gustatory cortices and thalamus. Given their greater sensitivity the highest dose of MAZ used and their higher binding of MAZ to putative brain anorectic receptors, DIO-prone rats might have a deficiency of an endogenous satiety factor which could predispose them to develop obesity when challenged with high energy, high sucrose diets.

Amygdala↗

PubMed1993

Organization of cortical afferent input to orbitofrontal areas in the rhesus monkey.

Odorant signal processing takes place in a diverse group of primary olfactory areas which receive direct input from the olfactory bulb. Orbitofrontal cortices participate in olfactory functions, but the pathways through which they receive olfactory or other input have not been clearly defined. The retrograde tracers horseradish peroxidase and fluorescent dyes were injected in orbital cortices to study their afferent cortical connections. Labeled neurons in primary olfactory areas (prepiriform cortex, anterior olfactory nucleus and olfactory tubercle) were directed mainly to a posterior orbitofrontal region and to a lesser extent the neighboring caudal part of area 13. There was no evidence of direct projections from primary olfactory areas to the rostral parts of area 13, or to areas 12 or 11. Most labeled neurons in primary olfactory areas were directed to agranular cortices, fewer projected to dysgranular areas, and there was no evidence that any reached granular cortices. The areas which received the most robust olfactory projections showed the lowest degree of laminar organization among prefrontal cortices. Early processing in the olfactory system thus takes place in areas which differ sharply on structural grounds from "early" eulaminate post-Rolandic sensory cortices. In addition to olfactory cortical projections, numerous labeled neurons in transitional (limbic) cortices were directed to orbital areas, and fewer but still substantial numbers of afferent neurons were found in eulaminate cortices. Unlike post-Rolandic unimodal sensory areas, which seems to be committed to the processing of input from one sensory modality via sequential and/or parallel pathways, caudal orbital areas received highly distributed input from primary olfactory areas, and in addition, from gustatory, visual, auditory and somatosensory areas. The structural and connectional features of olfactory recipient orbital cortices thus differ markedly from those observed in other sensory association areas and suggest a mode of processing adapted early in cortical evolution.

Animals↗

PubMed1983

Intraamygdaloid morphine produces seizures and brain damage in rats.

Behavioral and neuropathological responses to increasing doses of morphine hydrochloride (10-75 micrograms) administered into the rat amygdala were studied. Unilateral microinjections of morphine in doses of 40 and 75 micrograms produced a sequence of behavioral alterations including staring spells, gustatory automatisms, wet dog shakes, motor limbic seizures and limbic status epilepticus. Lower doses of morphine (10 and 20 micrograms) showed different threshold for these behavioral phenomena but a similar time course of development. Histological examination of frontal forebrain sections revealed widespread, apparently seizure-mediated pattern of brain damage. Neuropathological alterations were observed in the olfactory cortex, thalamus, neocortex, hippocampal formation and amygdaloid complex. Pretreatment of animals with diazepam (10 mg/kg i.p.) prevented the development of sustained limbic seizures and brain damage caused by morphine, while pretreatment with naloxone hydrochloride (2-20 mg/kg i.p.) failed to affect morphine-induced convulsant activity and brain damage. These results may suggest that morphine elaborates sustained limbic seizures and widespread brain damage by mechanism underlying the antagonism of inhibitory amino acid neurotransmission and opioid receptors do not seem to be involved.

Amygdala↗

PubMed1983

Afferent interactions of cranial nerves involved in ingestion.

Substantial behavioral evidence implicates visceral afferent activity in the regulation of feeding behavior. One mechanism often suggested for this influence involves visceral afferent activity interacting with oral or gustatory afferent activity. This brief review summarizes the anatomical and electrophysiological evidence that indicates that such interactions might in fact take place. The available evidence for interactions between visceral and gustatory afferent messages is far from convincing, but perhaps only because the issue has seldom been addressed. The most direct tests suggested by the hypothesis advanced remain to be carried out.

Afferent Pathways↗

PubMed1998

Structure and function of gustatory neurons in the nucleus of the solitary tract. III. Classification of terminals using cluster analysis.

In sensory systems, insight into synaptic arrangements on cells of known physiological response properties has helped our understanding of the structural basis for these properties. To carry out these types of studies, however, synaptic types in the region of interest must be defined. Unfortunately, defining synaptic types in the brainstem has proved to be a challenging enterprise. Our study was done to classify synapses in the gustatory part of the nucleus solitarius using objective quantitative criteria and a cluster analysis procedure. Cluster analysis allows classification of a population of objects, such as synaptic terminals, into groups that exhibit similar characteristics. Six terminal types were identified using cluster analysis and subsequent analyses of variance and post hoc tests. Unlike classification schemes used for the cerebral cortex, where synaptic apposition density thickness and shape of vesicles is useful (Gray's Type I and II synapses), the concentration of vesicles in a terminal was a more useful measurement with which to classify terminals in the nucleus solitarius. To validate that vesicle density (vesicles/microm2) is a useful defining characteristic to classify terminals in the nucleus solitarius, terminals of a known type were used. GABAergic terminals were identified using postembedding immunohistochemical techniques, and their vesicle density was determined. GABAergic terminals fall into the range of two of the terminal types defined by the cluster analysis and, based on vesicle density, two types of GABAergic terminals were identified. We conclude that vesicle density is a helpful means to identify synapses in this brainstem nucleus.

Analysis of Variance↗

PubMed2005

A tentative proposal on physiological polymorphism and its experimental approaches.

The purpose of this paper is to propose a tentative concept of physiological polymorphism and experimental approaches to it. We think that the concept of physiological polymorphism is to categorize the diversified phenomena into various types with statistical methods and to explain the differences among the categorized types from the viewpoint of their physiological mechanisms. Furthermore, it is necessary to take into consideration the fact that physiological polymorphism is observed as a phenotype, and the phenotype results from a genotype modified by culture and environment. As an experimental approach, we studied the effects of gustatory stimulation by chocolate on the activities of the prefrontal area and found that the activities were increased in some cases and decreased in other cases. Therefore, to begin with, when we divided them into an "increasing group" and a "decreasing group," we found that the increasing group had many subjects of Type B and High anxiety, and the decreasing group had many subjects of Type A and Normal anxiety. By the chi-square test for independence, it was found that the ratio of "increase" and "decrease" was related to the trait anxiety and type A personality, respectively. Next, we divided the activities of the prefrontal area into Type A and Type B, as well as a high anxiety group and a low anxiety group. As a result, the Type B and high anxiety groups showed significantly increased activities, while the Type A and normal anxiety groups showed no changes in their activities. Consequently, this data enabled us to explain the difference in activities of the prefrontal area from the viewpoint of personality characteristics. To conclude, we were able to categorize diversified changes in the prefrontal area into certain types when a gustatory stimulus was applied, and to explain them by using personality characteristics (State Trait Anxiety Inventory, Type A behavioral pattern) that are commonly known for their reflection of genotypes.

Anxiety↗

PubMed1989

Taste responses of cortical neurons in freely ingesting rats.

1. Activities of 35 taste-responsive neurons in the cortical gustatory area were recorded with chronically implanted fine wires in freely ingesting Wistar rats. Quantitative analyses were performed on responses to distilled water, food solution, and four taste stimuli: sucrose, NaCl, HCl, and quinine hydrochloride. 2. Taste-responsive neurons were classified into type-1 and type-2 groups according to the response patterns to licking of the six taste stimuli. Type-1 neurons (n = 29) responded in excitatory or inhibitory directions to one or more of the taste stimuli. Type-2 neurons (n = 6) showed responses in different directions depending upon palatability of the liquids to rats: neurons showing excitatory (or inhibitory) responses to palatable stimuli exhibited inhibitory (or excitatory) responses to unpalatable stimuli. 3. Correlation coefficients of responses to pairs of stimuli across neurons suggested that palatable stimuli (water, food solution, sucrose, and NaCl) and unpalatable stimuli (HCl and quinine) elicited reciprocal (excitatory vs. inhibitory) responses in type-2 neurons, whereas type-1 neurons showed positively correlated responses to specific combinations of stimuli such as food solution and NaCl, sucrose and HCl, NaCl and quinine, and HCl and quinine. 4. A tendency toward equalization of effectiveness in eliciting responses among the four basic taste stimuli was detected on the cortex. The ratios of mean evoked responses in 29 type-1 neurons in comparison with spontaneous rate (4.4 spikes/s) were 1.7, 1.9, 1.8, and 1.9 for sucrose, NaCl, HCl, and quinine, respectively. 5. The breadth of responsiveness to the four basic taste stimuli was quantified by means of the entropy measure introduced by Smith and Travers (33). The mean entropy value was 0.540 for 29 type-1 neurons, which was similar to 0.588 previously reported for rat chorda tympani fibers, suggesting that breadth of tuning is not more narrowly tuned in a higher level of the gustatory system in the rat. 6. Convergent inputs of other sensory modalities were detected exclusively in type-1 neurons. Thirteen (45%) of 29 type-1 neurons also responded to cold and/or warm water, but none of 6 type-2 neurons responded to thermal stimuli. Two (7%) of 29 type-1 neurons responded to almond and acetic acid odors, but the 6 type-2 neurons did not. Two (13%) of 16 type-1 neurons responded to interperitoneal injection of LiCl, which is known to induce gastrointestinal disorders, with a latency of approximately 5 min, but 4 type-2 neurons tested were not responsive to this stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1989

Fetal brain grafts induce recovery of learning deficits and connectivity in rats with gustatory neocortex lesion.

Three groups of rats showing disrupted taste aversion due to gustatory neocortex lesions, were studied. One group received a transplant of homotopic cortical tissue, another of heterotopic tectal tissue, obtained from 17-day-old fetuses. The third group remained without transplant as a lesioned control group. Comparisons of the taste aversion scores before and after graft, revealed that cortical grafted animals significantly improved the taste aversion, whereas those which received tectal grafts, and the cortical-lesioned controls did not. Moreover, results with horseradish peroxidase (HRP) histochemistry revealed that the homotopic, but not the heterotopic, brain transplants were able to re-establish connections with amygdala and with the ventromedial nucleus of the thalamus areas who normally kept connectivity with the gustatory neocortex. These results support the hypothesis that fetal brain transplants can reestablish cognitive functions, as well as connectivity with its host tissue.

Amygdala↗

PubMedDate not supplied

[Role of licking and concomitant changes in the excitability of nerve centers in the elaboration of gustatory information in rats].

The mechanism of nervous control of licking was studied in the frame work of the electrophysiological analysis of conditioned taste aversion. The licking rhythm is so stable that the rats are unable to slow it down by 20 percent. If the solution which was previously used for establishing the conditioned taste aversion, appears in the drinking spout, the rat stops drinking after one or two licks. Analysis of temporal relationships between afferent and efferent impulse activity of licking shows that the comparison of gustatory signals with memory traces and the corresponding decision occurs within 80 to 120 ms after lick onset. Electrical stimulation of the hypothalamic centres through implanted electrodes has shown that the amplitude of evoked responses and the impairment of licking increases, in proportion to the delay between lick onset and stimulus application. Isolated discharges of epileptic foci in the frontal cortex and the hypothalamus cause an omission of one or several licks, without interfering with the activity of the licking generator.

Animals↗

PubMed1988

Distribution of muscarinic receptor subtypes within architectonic subregions of the primate cerebral cortex.

The regional distributions of muscarinic receptor subtypes (M1 and M2) in the macaque brain were investigated by in vitro receptor autoradiography. Putative muscarinic receptor subtypes were distinguished by their differential affinities for pirenzepine and carbachol in competition with [3H]-quinuclidinyl benzilate. Autoradiographic visualization of muscarinic receptor subtypes demonstrated marked regional and laminar variations that respected architectonic boundaries. The M1 receptor subtype was widely distributed throughout most cortical areas and was most intense over the superficial layers. Almost all limbic and paralimbic regions including the amygdala, hippocampus, orbitofrontal, temporopolar, parahippocampal, cingulate, and parolfactory areas displayed peak densities of the M1 receptor subtype. The M2 receptor subtype was selectively elevated in the primary sensory areas of all five sensory modalities, including the visual (area 17, V1), auditory (A1), and somatosensory (3b, S1) koniocortices, the anterior olfactory nucleus, and the gustatory area. The primary motor area also displayed a relative peak of M2 receptor subtype labeling. In the hippocampal formation, M1, M2, and nicotine receptors were distributed differentially, with each subdivision having a specific complement of cholinergic receptor subtype. The M1 receptor subtype was prevalent in the dentate gyrus, the CA4-CA3 region, and the CA1 ammonic sector. The M2 receptor subtype was concentrated in the CA2 sector, the subiculum, the rhinal cortices, and the parasubiculum. Putative neural nicotinic receptors, tagged with L-[3H]-nicotine, were most concentrated within the presubiculum.

Animals↗

PubMed2003

Dissociation of neural representation of intensity and affective valuation in human gustation.

We used a 2 x 2 factorial design to dissociate regions responding to taste intensity and taste affective valence. Two intensities each of a pleasant and unpleasant taste were presented to subjects during event-related fMRI scanning. The cerebellum, pons, middle insula, and amygdala responded to intensity irrespective of valence. In contrast, valence-specific responses were observed in anterior insula/operculum extending into the orbitofrontal cortex (OFC). The right caudolateral OFC responded preferentially to pleasant compared to unpleasant taste, irrespective of intensity, and the left dorsal anterior insula/operculuar region responded preferentially to unpleasant compared to pleasant tastes equated for intensity. Responses best characterized as an interaction between intensity and pleasantness were also observed in several limbic regions. These findings demonstrate a functional segregation within the human gustatory system. They also show that amygdala activity may be driven by stimulus intensity irrespective of valence, casting doubt upon the notion that the amygdala responds preferentially to negative stimuli.

Adult↗

PubMed1995

Brain mechanisms of satiety and taste in macaques.

Flavor is the primary reinforcer of eating. As satiety is induced, the reinforcement of flavor is lost. Since flavor derives largely from taste, one might expect gustatory responsiveness to decline with increasing satiety. However, no such loss of sensitivity occurs in humans, even as the reinforcing value of taste declines with satiety. Thus, we explored the effect of satiety on taste responses at several levels of the macaque's nervous system to determine where is influence began. Taste-evoked activity in the NTS and primary taste cortex was unaffected by the induction of satiety through or administration of glucose. Taste cortex projects to amygdala and orbitofrontal cortex (OFC). In amygdala, satiety reduced responsiveness by 58%; in OFC, neurons were fully suppressed. Both amygdala and OFC project to the hypothalamus, where taste responsiveness was also suppressed. Thus, the neural impact of food is reduced not in area devoted to quality analysis, but in those concerned with motivation and reinforcement.

Administration, Oral↗

PubMed1996

Differential expression of brain-derived neurotrophic factor and neurotrophin 3 mRNA in lingual papillae and taste buds indicates roles in gustatory and somatosensory innervation.

Although many studies have demonstrated the dependency of taste bud function and/or survival on intact innervation, relatively few have dealt with the development of taste bud innervation. Using in situ hybridization histochemistry, we show that brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) mRNA are expressed in a specific pattern in the taste buds, tongue papillae, and lingual epithelium during development and that expression persists into adulthood. BDNF mRNA is expressed in a fraction of the taste cells of the developing and adult taste buds in rats, showing different labeling intensities among the labeled cells. NT3 and mRNA seems to be located in areas other than those where BDNF mRNA is expressed, mainly in the superior epithelial surfaces of circumvallate papillae, the outer surface epithelium of foliate papilae, the superior surface and the lateral epithelium of the fungiform papillae, and the epithelium of the filiform papillae. NT3 mRNA labeling is also observed among muscle and connective tissue of the tongue. The morphological appearance, expression of NT3 mRNA, and ramification of nerve fibers in defined epithelial structures in the posterior wall of the anterior filiform papillae suggest the existence of a mechanosensory apparatus in these papillae. Nerve growth factor and neurotrophin 4 probes did not give rise to selective labeling in tongue, although their presence cannot be totally excluded. Based on present and prior studies, we suggest that BDNF is needed during initiation and for maintenance of gustatory innervation of taste buds and gustatory papillae and that NT3 is mainly needed for somatosensory innervation of the tongue.

Animals↗