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Effects of lesions of the gustatory necortex on taste aversion learning in the rat.

Normal rats and rats with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal rats and rats with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Rats with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal rats and rats with GN lesions. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normal rats again learned specific aversions to all four solutions, but rats with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of rats with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration; and it was proposed that the data could be accounted for by postulating a change in the threshold for taste-illness associations following GN lesions.

Animals↗

Changes in neurotrophin-3 messenger RNA expression patterns in the prenatal rat tongue suggest guidance of developing somatosensory nerves to their final targets.

While brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) has been localized in the developing gustatory epithelium, little information is available about neurotrophin-3 (NT-3) mRNA expression pattern in the prenatal developing gustatory and lingual epithelium. In the present study, using in situ hybridization histochemistry, we report on NT-3 mRNA expression in the tongue of rats. At embryonic day (E) 13-17, NT-3 mRNA was expressed subepithelially in the periphery of the developing tongue, as well as among developing muscle. At E19, there was a shift in the expression of NT-3 mRNA. It was then expressed in the surface epithelium of the developing tongue in the developing filiform papillae and, in higher concentrations, in top-surface and fringe epithelium of the developing circumvallate papillae, and top- and lateral-surface epithelium of the developing fungiform papillae. NT-3 mRNA expression in areas rich in somatosensory innervation of the tongue, as well as its specific expression in defined regions compared with BDNF, and the decreased labeling noted from prenatal and early postnatal animals to adults indicate a specific role for NT-3 in the development of lingual somatosensory innervation, as well as for maintenance of this innervation.

Afferent Pathways↗

The development of parvalbumin-immunoreactivity in the neocortex of the mouse.

In the present study the postnatal development of parvalbumin-immunoreactivity was examined in the neocortex of the mouse. Postnatal mice were processed at different developmental stages using a well-characterized monoclonal antibody against parvalbumin, and immunocytochemistry. The first immunoreactive neurons appeared in the first parietal and retrosplenial cortices at postnatal day 10 (P10). From P11 to P12, immunoreactivity emerged in the second parietal, cingular, frontal, hindlimb-forelimb, first temporal, primary and secondary occipital and gustatory cortices, and at P14, parvalbumin-positive cells were present in the remaining regions. In general, parvalbumin-immunoreactivity appeared first in the primary sensory/motor areas, and then in second sensory/motor or associative areas. The maturation of parvalbumin-immunoreactivity, however, was a long-lasting process, which was not completed until adult stages. In all cortical regions, parvalbumin-immunoreactive cells were present first in layer V, from which immunoreactivity expanded to the upper and inner cortical layers at subsequent developmental stages. This pattern of maturation differed from the usual 'inside-out' gradient of neocortical neurogenesis and maturation. At the cellular level, parvalbumin-immunoreactivity appeared first in cell somata, and staining of dendrites and boutons was apparent two days later. From the second postnatal week onwards, an immunoreactive axonal system was observed in the neocortical white matter and the corpus callosum. We conclude that the emergence and maturation of parvalbumin-immunoreactivity in the mouse neocortex shows marked area-specific differences, but proceeds following a similar center-to-outside radial gradient. These features may reflect the acquisition of certain physiological properties by a subset of GABAergic inhibitory neurons.

Animals↗

Neonatal ablations of the gustatory neocortex in the rat: taste aversion learning and taste reactivity.

Rats sustaining ablations of gustatory neocortex (GN) at 2, 10, 20, or 60 days of age were compared with control rats in the acquisition and extinction of a learned taste aversion; in addition, these rats were tested for taste preference across five concentrations of sodium chloride solution. Results indicated that GN ablation disrupted aversion acquisition and extinction regardless of age at surgery. Taste response functions for the sodium chloride solutions shown by all GN groups of rats mirrored those of control rats: preference (relative to water baseline) for middle concentrations and rejection of the strongest salt concentration. There was a suggestion that the 20- and 60-day-old GN rats were hyperresponsive to the suprathreshold concentrations of NaCl (except the strongest concentration). The increased response to salt solutions in the 20- and 60-day GN rats may have been related to the significant decreases in water consumption relative to that of normal rats. Water consumption of control rats and GN rats in the 2-day and 10-day groups was essentially equal. It is concluded that infant ablation of the GN does not spare normal taste aversion learning and that rats with GN ablations, regardless of age at surgery, respond in a normal manner to the hedonic aspects of sodium chloride solutions.

Age Factors↗

[Botulinum toxin in oromaxillofacial surgery].

BACKGROUND: The muscular system of the jaw and face is characterized by highly differential dynamics due to its strong presence within the motoric region of the cerebral cortex. Abnormal activity of the masticatory or mimic muscular system, whether acquired or congenital, leads to aesthetic and/or functional impairments for the patient. Subsequently, pathological changes of the tissue structure caused by persistent dysfunction can entail chronic pain and progressive aesthetic reduction can induce psychopathological conditions in a patient. OPERATIVE THERAPY: Inherently, surgical techniques for the treatment of muscular imbalances are inadequately differentiated, resulting in the destruction of nerve and muscular structures and are thus irreversible. PHARMACEUTICAL THERAPY: Use of botulinum toxin A can achieve short-term correction of muscular activities with very few side effects if applied in an accurate and controlled manner. This survey presents both established treatments as well as newly developed applications in craniomaxillofacial surgery: (1) the treatment of dysfunctions of the masticatory muscular system, (2) the correction of marked imbalances of the mimic muscular system resulting from surgical treatment, (3) the therapy of salivary gland-associated malfunctions, such as hypersalivation or Frey's syndrome, (4) aesthetic corrections with botulinum toxin A as a single therapy or in combination with collagen injections, (5) EMG-controlled injection of botulinum toxin A as an alternative to surgical treatment of recurrent dislocation of the TMJ, (6) prophylaxis to prevent relapse after mandibular advancement by EMG-controlled paralysis of the geniohyoid muscles.

Botulinum Toxins, Type A↗

Gustatory and multimodal neuronal responses in the amygdala during licking and discrimination of sensory stimuli in awake rats.

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.

Acoustic Stimulation↗

Gustatory responses of cortical neurons in rats. II. Information processing of taste quality.

The present report was designed to investigate neural coding of taste information in the cerebral cortical taste area of rats. The magnitude and/or type (excitatory, inhibitory, or no-response) of responses of 111 cortical neurons evoked by single concentrations of the four basic taste stimuli (sucrose, NaCl, HCl, and quinine HCl) were subjected to four types of analyses in the context of the four proposed hypotheses of taste-quality coding: across-neuron response-pattern, labeled-line, matrix-pattern, and across-region response-pattern notions (88 histologically located neurons). An across-neuron response-pattern notion assumes that taste quality is coded by differential magnitudes of response across many neurons. This theory utilizes across-neuron correlation coefficients as a metric for the evaluation of taste quality coding. Across-neuron correlations between magnitudes of responses to any pairs of the four basic taste stimuli across 111 cortical neurons were very high and were similar. However, calculations made with net responses (spontaneous rate subtracted) resulted in less positive correlations but still similar values among the various pairs of taste stimuli. This finding suggests that across-neuron response patterns of cortical neurons become less discriminating among taste qualities compared with those of the lower-order neurons. A labeled-line notion assumes that there are identifiable groups of neurons and that taste quality is coded by activity in these particular sets of neurons. Some investigators have classified taste-responsive neurons into best-stimulus categories, depending on their best sensitivity to any one of the four basic stimuli, such as sucrose-best, NaCl-best, HCl-best, and quinine-best neurons; they have suggested that taste can be classified along four qualitative dimensions that correspond to these four neuron types (i.e., four labeled lines). The present study shows that responsiveness of each of the four best-stimulus neurons had similar profiles between peripheral and cortical levels. That is, when the stimuli were arranged along the abscissa in the order of sucrose, NaCl, HCl, and quinine, there is a peak response in one place, and the responses decreased gradually from the peak. However, such response characteristics do not favor the labeled-line theory, since they can be explained in the context of the across-neuron pattern theory. A matrix-pattern notion assumes that taste quality is coded by a spatially arranged matrix pattern of activated neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Corticofugal influence on taste responses in the nucleus of the solitary tract in the rat.

1. Previous work has revealed a pervasive influence of the gustatory neocortex (GN) on the electrophysiological responses to taste in the parabrachial nucleus of the pons (PbN), the second synapse in the central pathway for gustation. Subsequent experiments have further suggested that direct projections from the GN to the PbN are not sufficiently dense to account for the widespread effects of cortical input. Because the main source of input to the PbN, i.e., the nucleus of the solitary tract (NTS), also receives input from the GN, the present experiment was conducted to test the hypothesis that changes in taste responses in the PbN after temporary elimination of GN input may be a normal reaction to altered input originating in the NTS. 2. Fourty-three taste-responsive neurons in the NTS were isolated initially in urethan-anesthetized rats. Single units were then classified as "relay" (n = 12) or "nonrelay" (n = 13) on the basis of their electrophysiological response to electrical shocks delivered to the taste-responsive portion of the PbN. After histological analyses, 18 units were classified as "unknown" because the PbN stimulating electrode was found to be outside the anatomically defined taste area in the pons. 3. Electrophysiological responses to sapid solutions of the NaCl (0.1 M), HCl (0.01 M), quinineHCl (0.01 M), sucrose (0.5 M), and Na-saccharin (0.004 M) were then recorded before and after recovery from infusions of procaineHCl into the GN. Both the ipsilateral and contralateral sides of the GN, in that order, received procaine infusions separated by a recovery period of at least 45 min. 4. Analysis of across-unit patterns of response was accomplished with the use of a vector space analysis. With this approach, the response of a given neuron to a given tastant is considered as a coordinate in n-dimensional space, where n is the number of neurons tested. The responses to each stimulus generate vectors whose length relates to the overall magnitude of response across the sample and whose relative directionality indicates similarity to other across-unit patterns. Measures derived from this type of analysis were used as input in a multidimensional scaling (MDS) analysis designed to summarize the organization of the across-unit patterns of response generated by the taste stimuli. This type of analysis creates a "taste space" in which similar across-unit patterns of response are placed close together and dissimilar patterns are placed far apart.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthetics, Local↗

Brain gamma-aminobutyric acid levels are decreased in patients with phantageusia and phantosmia demonstrated by magnetic resonance spectroscopy.

BACKGROUND: Olfactory and gustatory hallucinations (phantosmias and phantageusias, respectively) are sensory distortions that commonly follow losses of olfactory and gustatory acuity (hyposmia and hypogeusia, respectively). The biochemical basis of these hallucinations is unclear. Functional magnetic resonance imaging has been used previously to demonstrate widespread and robust central nervous system (CNS) activation to memories of these sensory distortions in patients with these symptoms. In this study, possible CNS mechanisms responsible for these distortions were evaluated using magnetic resonance spectroscopy, because this technique has been used to measure various CNS metabolites in patients with neurologic disorders. METHODS: Forty-seven subjects were studied: 28 normal volunteers (13 men and 15 women) and 19 patients (8 men and 11 women) with persistent oral global phantageusia and/or birhinal phantosmia studied before any treatment. Four patients (1 man and 3 women) were studied before and after pharmacologic treatment that reduced the severity of their sensory distortions. All subjects were studied in a Signa 1.5-T magnetic resonance scanner with a quadrature head coil using a modified standard 2-dimensional J-point resolved excitation in the steady state (PRESS) sequence by which gamma-aminobutyric acid (GABA), glutamic acid, choline, N-acetylaspartate, and creatine (Cre) were measured in various CNS regions. Results were expressed using Cre as a denominator to determine ratios for each measurement. Differences were defined between normal subjects and patients before treatment and in patients before and after successful pharmacologic treatment. RESULTS: Before treatment, GABA levels in several CNS regions were lower in patients than in normal volunteers and were the only biochemical changes found; significantly lowered GABA levels were found in the cingulate, right and left insula, and left amygdala. No differences between patients and normal volunteers were found in any of the metabolites in the posterior occipital region. After treatment that inhibited sensory distortions, CNS GABA levels increased in the cingulate, insula, and amygdala but significantly only in the left insula and in the right and left amygdala. After this successful treatment, no change in any biochemical parameter was found in the posterior occipital region. CONCLUSIONS: These results indicate that decreased brain GABA levels can serve as biochemical markers of phantageusia and/or phantosmia in patients with these distortions and are the first biochemical changes in the CNS that reflect these sensory changes. After successful treatment of these distortions, CNS GABA levels increased to levels at or near normal, consistent with functional remission of these symptoms. These results substantiate a role for CNS GABA in the generation and inhibition of these sensory hallucinations. Although the underlying biochemical mechanism(s) for the generation of these decreased GABA levels are complex, because similar types of sensory hallucinations occur as auras or prodromata of epileptic seizure and migraine activity, these results suggest that there may be common biochemical changes among these disorders.

Adult↗