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PubMed2006

Adrenergic drugs modify the level of noradrenaline in the insular cortex and alter extinction of conditioned taste aversion in rats.

We compared the effect of conditioned taste aversion in rats by measuring the amount of sucrose that they drunk after conditioning, which differed according to whether rats had drunk the sucrose freely (SD: self drinking) during the conditioning session, or had been forced to drink it (IO: intra-oral administration through a chronically implanted cannula). The SD procedure delayed the extinction of conditioned taste aversion. Enhanced arousal, alertness, awareness or attention in the SD condition may have strengthened the memory of the taste. Brain noradrenergic networks are involved in such processes. We administered two noradrenergic drugs that produce opposite effects on noradrenaline release in the brain, methoxy-idazoxan, RX821002 (1mg/kg, i.p.), and guanfacine (0.12mg/kg, i.p.). We evaluated their effect (i) on the level of noradrenaline in the gustatory cortex using microdialysis, (ii) on glycaemia that is an essential factor of taste learning and (iii) on the comparative SD versus IO conditioned taste aversion protocol mentioned above. Injecting RX821001 increased the level of noradrenaline in the gustatory cortex up to two-fold of the baseline. This effect lasted 1h. The same dose of RX821002 did not elicit any alteration of glycaemia. It enhanced extinction of conditioned taste aversion in the SD group of rats. Injecting 0.12mg/kg of guanfacine produced the opposite effect. The noradrenaline level of the gustatory cortex decreased, but only down to 20% of the baseline. This decrease lasted 2h. Guanfacine increased glycaemia. Extinction of conditioned taste aversion was only marginally decreased by guanfacine in the SD group of rats. These results fit with Aston-Jones' point of view that the role of the noradrenergic coeruleo-cortical system may be to enhance arousal, alertness, awareness or attention to an event by a transient increase of cortical noradrenaline.

Adrenergic Agents↗

PubMed2003

Activity in the hypothalamus, amygdala, and cortex generates bilateral and convergent modulation of pontine gustatory neurons.

Evidence suggests that centrifugal modulation of brain stem gustatory cells might play a role in the elaboration of complex taste-guided behaviors like conditioned taste aversion and sodium appetite. We previously showed that activity in one forebrain area, the central nucleus of the amygdala (CeA), increased the chemical selectivity of taste cells in the parabrachial nucleus (PBN). The present study investigates how activity in 2 other similarly interconnected forebrain sites, the lateral hypothalamus (LH) and gustatory cortex (GC), might influence PBN gustatory processing in rats. The potential convergence of descending inputs from these sites, as well as the CeA, was also evaluated. After anesthesia (35 mg/kg Nembutal ip), 70 PBN gustatory neurons were tested before, during, and after electrical stimulation of these forebrain sites, while responding to 0.3 M sucrose, 0.1 M NaCl, 0.01 M citric acid, and 0.003 M QHCl. Although each forebrain site modulated taste-evoked responses, more PBN neurons were influenced by stimulation of the GC (67%) and CeA (73%) than of the LH (48%). Activation of cortex (71%) and amygdala (85%) most often produced inhibition, whereas inhibition and excitation occurred equally often during hypothalamic stimulation. Of the neurons tested for convergence (n = 60), 88% were influenced by > or =1 of the 3 sites. Twenty were modulated by stimulation at all 3 sites and another 17 by 2 of the 3 sites. The net effect of centrifugal modulation was to sharpen the across-stimulus response profiles of PBN cells, particular with regard to the NaCl- and citric acid-best cells.

Amygdala↗

PubMed2005

Excitotoxic lesions of the entorhinal cortex leave gustatory within-event learning intact.

The ability of rats with ibotenate lesions of the entorhinal cortex to form memories for events was assessed by using a gustatory within-event learning procedure. Rats first received exposure to 2 events, AX and BY, each composed of a pair of flavors. Following this exposure period, Flavor X alone was paired with the delivery of lithium chloride. Lesioned and control rats showed a greater aversion to A than to B and to AX than to BX. These results challenge theories that suppose that the entorhinal cortex plays a general role in forming representations of patterns of stimulation.

Analysis of Variance↗

PubMed1990

Brain stimulation-induced feeding alters regional opioid receptor binding in the rat: an in vivo autoradiographic study.

Although opioid antagonists block feeding behavior in a variety of animal models, the number and identity of CNS regions in which the inferred endogenous opioid activity mediates feeding have yet to be established. Furthermore, it is not yet clear whether the opioid activity that sustains feeding is a concomitant of the appetitive motivational state or the consummatory response. In an effort to address these issues, an in vivo autoradiographic method was used to visualize CNS regional changes in opioid release during appetitively motivating electrical stimulation in the lateral hypothalamus (ESLH) and during consummatory behavior elicited by such stimulation. Regional decreases in [3H]diprenorphine [(3H]Dpr) binding, suggesting increased release of an endogenous opioid peptide, were observed in the medial prefrontal cortex, medial septum, gustatory cortex, zona incerta, mediodorsal thalamus, and hippocampus of rats receiving ESLH. Decreased binding in the latter 4 structures did not appear when animals were allowed to eat during ESLH, suggesting that the inferred opioid release is associated with appetitive behaviors elicited by ESLH which are suppressed when food is available and consummatory behavior predominates. When animals were allowed to eat during ESLH, [3H]Dpr binding in anterior cingulate cortex decreased substantially, suggesting that feeding behavior specifically triggers opioid release in this region. ESLH and feeding were found to increase [3H]Dpr binding in a number of CNS regions. Alternative explanations for increased binding, including inhibition of tonic opioid release, changes in cerebral blood flow, and opioid receptor up-regulation are discussed.

Animals↗

PubMed1998

Responses of neurons in the insular cortex to gustatory, visceral, and nociceptive stimuli in rats.

Extracellular unit responses to baroreceptor and chemoreceptor stimulation, gustatory stimulation of the posterior tongue, electrical stimulation of the superior laryngeal (SL) nerve, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Forty-three neurons identified responded to stimulation by at least one of the stimuli used in the present study. Of the 43 neurons, 33 responded to tail pinch, and the remaining 10 had no response; 18 showed an excitatory response, and 15 showed an inhibitory response. Of the 43 neurons, 35 responded to electrical stimulation of the SL nerve; 27 showed an excitatory response, and 8 showed an inhibitory response. Of the 20 neurons that responded to baroreceptor stimulation by an intravenous injection of methoxamine hydrochloride (Mex), 11 were excitatory and 9 were inhibitory. Twenty-seven neurons were responsive to an intravenous injection of sodium nitroprusside (SNP); 10 were excitatory and 17 were inhibitory. Ten neurons were excited and 16 neurons were inhibited by arterial chemoreceptor stimulation by an intravenous injection of sodium cyanide (NaCN). Twenty-six neurons were responsive to at least one of the gustatory stimuli (1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose): four to six excitatory neurons and three to nine inhibitory neurons for each stimulus. A large number of the neurons (42/43) received convergent inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (38/43) were responsive to two or more stimulus groups when the natural stimuli used in the present study are grouped into three, gustatory, visceral, and nociceptive stimuli. The neurons recorded were located in the insular cortex between 2.8 mm anterior and 1.1 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.0 mm (n = 43) anterior to the AC. This indicates that most of the neurons identified in the present study were located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from baroreceptor, chemoreceptor, gustatory, and nociceptive organs and may have roles in taste aversion or in regulation of visceral responses.

Afferent Pathways↗

PubMed1989

Thalamic projections to the cortical gustatory area in the cat studied by retrograde axonal transport of horseradish peroxidase.

The thalamic projections to the cortical gustatory area in the cat were studied using the horseradish peroxidase (HRP) method. The gustatory area extends from the lateral lip of the presylvian sulcus (posterior two-thirds) to the posterior part of the orbital gyrus. It is bounded anteriorly by area 6a beta, laterally by the first somatosensory area, medially by the fundus and medial bank of the presylvian sulcus (prefrontal area), and posteriorly by the insular area. The cortical gustatory area receives fibers mainly from the medial smaller-celled part of the posteromedial ventral nucleus (VPMM). Cortical projections of the VPMM are organized topically; the anterior part of the gustatory cortex receives fibers from the anterodorsal and posteroventral portions of the anterior two-thirds of the VPMM, whereas the posterior gustatory cortex receives fibers from the anteroventral, posterodorsal and posterior portions of the posterior two-thirds of the VPMM. In addition, there appears to be a mediolateral organization of the cortical projections of the VPMM to the gustatory area. The cortical gustatory area receives a few projections from the ventral lateral, ventral medial, submedial, paracentral, lateral central, parafascicular and medial central nuclei.

Animals↗

PubMed1993

AF64A (ethylcholine mustard aziridinium) impairs acquisition and performance of a spatial, but not a cued water maze task: relation to cholinergic hypofunction.

The cholinergic neurotoxin AF64A (ethylcholine mustard aziridinium) produced alterations in a spatial but not a nonspatial cognitive task following ICV injection. AF64A impaired acquisition and performance in the standard Morris water maze task, evidenced by significantly longer latencies to find the submerged platform. However, the AF64A group exhibited shorter latencies and more direct paths to the target at the end of training, which suggests acquisition of efficient search strategies and a sparing of procedural memory. However, the AF64A group spent significantly less time in the target quadrant during the probe trial than the CSF group. This suggests a failure to learn the specific location of the target and impaired declarative memory processes. In contrast, AF64A did not affect performance of a cued MWM task that did not involve spatial memory processing, demonstrating the absence of motoric, sensory, or motivational impairments. The AF64A-induced behavioral deficits were associated with a) a significant decrease in high affinity choline transport (HAChT), b) reduced concentrations of 5-HT and 5-HIAA, and c) an increased ratio of 5-HIAA/5HT, in the HPC. There were no changes in choline uptake in the gustatory cortex, the amygdala, or the striatum. Percent time in the target quadrant during the probe trial was significantly correlated with HAChT in the HPC. There were no correlations between any of the behavioral measures and HAChT in the striatum, gustatory cortex, or the amygdala, or between serotonergic or noradrenergic parameters in the HPC. These data suggest that AF64A produces cognitive deficits in spatial tasks that are correlated with the cholinergic hypofunction induced by the compound.

Acetylcholine↗

PubMed1984

The cortical projection of the basolateral amygdaloid nucleus in the rat: a retrograde fluorescent dye study.

The fluorescent dye, retrograde labeling technique was used to determine the extent of the projection from the basolateral nucleus of the amygdala to the neocortex in the rat. Each rat received a single cortical injection of fast blue, and in one-half of the animals, a subsequent injection of nuclear yellow was placed in a different cortical region. An analysis of the results demonstrates that the projection to the midline cortex arises in the medial neurons within the caudal two-thirds of the basolateral nucleus. This projection is directed to the anterior cingulate cortex, but not to the posterior cingulate cortex. The primary motor cortex receives a basolateral amygdala projection which originates from neurons in two areas, (1) the medial part of the anterior one-third of the nucleus and (2) the center (in the lateral to medial axis) portion of the posterior two-thirds of the nucleus. The latter neurons are situated lateral to the neurons projecting to the cingulate cortex. Somatosensory cortex injections label many fewer basolateral nucleus neurons than do motor cortex injections, but these neurons are located in a position similar to that of those labeled by motor cortex injections. Finally the gustatory cortex, which lies just dorsal to the rhinal sulcus, receives a basolateral projection from neurons in the lateroventral one-half of the basolateral nucleus. These results demonstrate that the basolateral nucleus gives rise to a rather widespread and topographically organized projection to the anterior half of the neocortex of the rat.

Amidines↗

PubMed1988

Afferent projections to the parafascicular thalamic nucleus of the rat, as shown by the retrograde transport of wheat germ agglutinin.

Afferent projections to the parafascicular nucleus of the rat have been mapped using the retrograde transport of unconjugated wheat germ agglutinin and immunohistochemistry using very short survival times. Retrogradely labelled neurones were found in laminae V and V1 of primary motor cortex, lamina V1 of primary somatosensory cortex, and deep laminae of gustatory cortex; in the reticular thalamic nucleus and zona incerta; and in the caudate-putamen, entopeduncular nucleus, mesencephalic reticular formation and pretectum. Additional label was found in the laterodorsal tegmental nucleus, nucleus tegmenti pedunculopontinus, dorsal and ventral parabrachial nuclei, vestibular nuclei and the lateral cervical, medial and interpositus nuclei of the cerebellum. These results are discussed in the context of the connections of parafascicular nucleus with the motor system, particularly the basal ganglia. Of particular interest are inputs from laterodorsal tegmental nucleus, nucleus reticularis of thalamus, mesencephalic reticular formation, nucleus tegmenti pedunculopontinus, primary motor cortex and deep cerebellar nuclei. These indicate that the parafascicular nucleus lies at an interface between the reticular activating system on the one hand, and the motor system on the other. This result thus enlarges on present concepts of the parafascicular nucleus. Comparison of afferent projections to a variety of non-specific thalamic nuclei, the parafascicular, paraventricular and mediodorsal thalamic nuclei, indicate a remarkable set of topographic parallels from cortical, reticular thalamic, hypothalamic and brainstem sites. These comparisons provide clues as to the organisational principles of these non-specific thalamic nuclei, particularly in the context of the reticular activating system.

Afferent Pathways↗

PubMed2001

Cortical association areas in the gustatory system.

The existence, location and interrelationships of cortical gustatory association areas in primates and rodents are discussed. Based on previous proposals, and on anatomical, physiological and lesion data, we propose that in addition to primary gustatory cortex, located in primate opercular cortex and rodent granular insular cortex, three association areas exist. A secondary area is located in dysgranular insular cortex, a tertiary area in agranular insular cortex, and the terminus of the cortical gustatory analyzer is located in perirhinal cortex. We propose that the subjective awareness of flavor is most probably due to neuronal activities in agranular insular cortex.

Animals↗

PubMed1996

Carbachol mimics effects of sensory input on tyrosine phosphorylation in cortex.

We have recently shown that in the gustatory cortex of the rat, taste learning enhances protein tyrosine phosphorylation and taste memory is blocked by muscarinic antagonists. A major protein whose tyrosine phosphorylation is stimulated by taste learning in cortex is a 180 kDa synaptic glycoprotein identified as the NMDA receptor subunit 2B (NR2B). Here we report that microinjection of carbachol into the taste cortex modulates protein tyrosine phosphorylation similarly to the effect of unfamiliar taste, and that a 180 kDa protein whose tyrosine phosphorylation is enhanced in vivo by carbachol is NR2B. These data, combined with our previous findings, are in line with the hypothesis that muscarinic input plays a role in encoding new items in memory, and that tyrosine phosphorylation of NR2B is involved in this process.

Amino Acid Sequence↗

PubMed1997

Rat gustatory memory requires protein kinase C activity in the amygdala and cortical gustatory area.

We have studied the physiological involvement of protein kinase C (PKC) in the formation of conditioned taste aversion (CTA) by means of microinjections of PKC inhibitors into the gustatory cortex (GC), amygdala (AMY) and thalamic gustatory area at various time-windows of the CTA paradigm. Rats injected between the CS-US interval with PKC inhibitors into the GC and AMY, but not into the thalamic gustatory area, failed to acquire CTA. Injections of PKC inhibitors 4 h after the US presentation or just before the retention test elicited no disruptive effect. Injections of PKC inhibitor into the AMY, but not into the GC, 30 min after the CS-US pairing impaired CTA formation. These results show that PKC activity in the GC and AMY has a key role in the acquisition phase of CTA, but not in the retrieval phase. The findings also suggest that the GC is concerned with information processing of the CS, and that the AMY is involved in the CS-US association.

Amygdala↗

PubMed2026

Locus coeruleus activation transforms cortical taste representations.

Noradrenergic neurons in the locus coeruleus (LC) shape sensory processing, yet how LC activity influences population taste coding remains unclear. Using optogenetic LC activation with miniscope imaging in the gustatory cortex (GC), we examined LC modulation of multiple taste attributes. Phasic LC activation strengthens correlations between neuronal responses and palatability and expands the dynamic range of stimulus representations along a palatability axis. This expansion is driven by an aversive shift in the representations of all tastants except sucrose, the most palatable stimulus. For mixture ratio and concentration, phasic activation expands and rotates attribute axes, potentially reflecting dependencies between these attributes and palatability. These transformations likely arise from multiplicative gain modulation and more flexible tuning changes. Tonic LC activation affects fewer neurons and does not expand attribute axes. Together, the findings show that LC activation reorganizes GC population geometry in a pattern-dependent manner, linking neuromodulation with feeding behavior and affective processing.

CP: neuroscience↗

PubMed1992

Taste neurons in the cortex of the alert cynomolgus monkey.

The activity of single neurons in the gustatory cortex of alert cynomolgus monkeys was analyzed. Taste-evoked activity in response to the four prototypical taste stimuli was recorded from a cortical gustatory area comprising the frontal operculum and adjoining anterior insula. Spontaneous activity for 364 gustatory neurons was 3.9 +/- 4.9 (mean +/- SD) spikes/s. Mean net (gross minus spontaneous) discharge rates for all gustatory neurons were: 1.0 M glucose = 4.9 +/- 11.6, 0.3 M NaCl = 3.2 +/- 7.1, M quinine HCl = 2.6 +/- 5.8, and 0.01 M HCl = 1.7 +/- 4.6. The results from intensity-response functions imply that the perception of each basic taste quality in the nonhuman primate is based on the activity of the appropriate neural subgroup rather than on the mean activity of all taste cells. Therefore a more meaningful index of the effectiveness of a stimulus may be the discharge rate it evokes from the subset of gustatory neurons for which it is the best stimulus. Glucose was the best stimulus for 142 cells (including ties), from which it elicited a mean net response of 10.3 spikes/s; NaCl was best for 107 neurons which gave a mean 8.7 spikes/s; quinine HCl evoked 6.2 spikes/s from the 74 cells that responded best to it; HCl elicited 5.9 spikes/s from the 49 neurons for which it served as best stimulus. The response characteristics of cortical taste cells indicate heterogeneous features, and significantly different patterns from those reported in other nonchemical sensory systems.

Animals↗

PubMed1991

Insular cortex and amygdala lesions differentially affect acquisition on inhibitory avoidance and conditioned taste aversion.

These experiments examined the effects of NMDA-induced lesions of the amygdala and insular (gustatory) cortex (IC) on inhibitory avoidance learning and conditioned taste aversion (CTA) in rats. IC lesions, but not amygdala lesions, disrupted CTA. In contrast, lesions of either brain region disrupted inhibitory avoidance learning. These findings support the view that the IC is strongly involved in the acquisition of external as well as visceral aversively motivated behavior. Despite extensive functional interconnections, these 2 brain regions appear to have different roles in mediating different forms of aversively based learning.

Amygdala↗

PubMed2004

Imaging of olfaction and gustation.

Positron emission tomographic (PET) scanning can be used to assess the cortical processing of responses to different odorants in man. The olfactory bulb receives the first projections on an ipsilateral basis from the nose, but then the cortex and the limbic system respond bilaterally. More irritating, burning odors (e.g., acetone) project via the trigeminal rather than the olfactory nerve and induce changes in the brain stem and the cortex. Sweet and salty tastes are readily distinguishable, but a bitter or painful stimulus leads to a deactivation of the primary gustatory cortex, which is in keeping with the need to focus on an avoidance response. The complex discrimination of odors, however, seems to involve the insula cortex, cerebellum, and hypothalamus, with pheromones seemingly sensed via the olfactory system in humans.

Animals↗

PubMedDate not supplied

[Gustatory nervous pathway syndromes].

Although the lingual nerve and the chorda tympani are the components of the classic peripheral gustatory pathway, loss of taste in patients after surgery for trigeminal neuralgia supports for the existence of an accessory gustatory pathway through the trigeminal sensory root and the gasserian ganglion. Bell's palsy is the most common pathology of the peripheral gustatory pathway. The central gustatory pathway ascends from the solitary tract nucleus in the medulla up to the upper pons in the ipsilateral central tegmental tract, rather than in the medial lemniscus as proposed in the past. It is not possible to specify whether the central gustatory pathway decussates or not at the lower midbrain level. Interruption of the gustatory pathway in the brainstem usually occurs with stroke or demyelination. The thalamic gustatory relay is located in the most medial aspect of the ventroposteromedial nucleus, immediately adjacent to the somatosensory area for the oral cavity and fingers. Therefore, ageusia associated with the sensory cheiro-oral syndrome may occur with a thalamic lesion. The laterality of the gustatory representation in the thalamus remains unresolved. Studies on epileptic gustatory aura have demonstrated that the insula and the anteromedial temporal lobe are the primary and secondary gustatory cortex, respectively. Taste perception results in patients with corpus callosum section and strokes or tumors involving the insula support the hypothesis that there is a gustatory representation of both hemitongues in the left cerebral hemisphere, whereas only the right hemitongue is represented in the right hemisphere.

Afferent Pathways↗

PubMed1988

Double dissociations of the effects of amygdala and insular cortex lesions on conditioned taste aversion, passive avoidance, and neophobia in the rat using the excitotoxin ibotenic acid.

The results in this article show that although electrolytic amygdala lesions disrupt learning of a conditioned taste aversion (CTA), ibotenic acid-induced, axon-sparing lesions of the amygdala do not. However, ibotenic acid lesions of the insular cortex do disrupt learning of a CTA. Electrolytic, but not ibotenic acid lesions of the amygdala, interrupt axons running between the insular (gustatory) cortex and the brain stem/hypothalamus. It is the destruction of these projections which appear to underly CTA deficits after amygdala lesions. Other results revealed that ibotenic acid lesions of the insular cortex attenuated the reaction to the novel taste of saccharin in a familiar environment but failed to affect the ingestion of a novel food in a novel environment or passive avoidance learning. Conversely, ibotenic acid lesions of the amygdala did not affect the reaction to novel saccharin in a familiar environment but did impair both the reaction to novel food in a novel environment and passive avoidance learning. We conclude that the insular cortex is involved in reactions to the novelty and associative salience exclusively of taste stimuli, whereas the amygdala is probably more concerned with the reaction to more general aspects of novelty in the environment and in fear-motivated behavior.

Amygdala↗