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P S Lasiter

Publications and source records attributed to P S Lasiter.

At least 19 recordsLinked to original sources
PubMed1995

Alterations in geniculate ganglion proteins following fungiform receptor damage.

Previous anatomical studies in rat have shown that damage produced to fungiform receptors of the anterior tongue at postnatal age 2 (P2) alters the growth and ramification of primary gustatory axons in the rostral nucleus of the solitary tract (NST). Studies employing artificial rearing (AR) procedures, which functionally deprive rat pups of orochemical stimulation during critical periods of postnatal life, produce similar alterations in the development of primary gustatory axons in the NST. Therefore, orochemical stimulation during rat's early postnatal life is necessary for normal development of primary gustatory axons in the rostral NST. One hypothesis concerning receptor-damage effects and AR effects is that receptor damage during critical periods of development may alter the regulation (i.e. transcription/translation) and/or distribution (i.e. transport) of proteins in geniculate ganglion neurons, thereby affecting growth of primary gustatory axons in the rostral NST. Specific aims of the present experiments were to comprehensively examine electrophoretic profiles of geniculate ganglion proteins following P2 receptor damage and late (> P40) receptor damage. Results show that concentrations of particular geniculate ganglion proteins are differentially altered following P2 receptor damage and late receptor damage, and that early receptor damage and late receptor damage produces distinct effects on the electrophoretic profiles of particular classes of proteins. Between the ages of P7-P38, P2 receptor damage lowers ganglion concentration of an acidic membrane glycoprotein designated as A1, with an apparent M(r) of 64-67 kDa and a pI of 4.8-5.2 P2 receptor damage also lowers ganglion concentrations of GAP-43. P2 receptor damage produces transient decreases in ganglion concentrations of NF-160, NF-200, and 8 additional acidic proteins. Three of these proteins may correspond to peripheral nerve sheath proteins analyzed in previous studies of the sciatic nerve, and one of these proteins may correspond to a 24 kDa growth-associated protein characterized in regenerating optic nerve. The time-course for changes observed in ganglion proteins following P2 damage was consistent with that observed for normal anatomical development of primary gustatory axons in both the lingual epithelium and NST. Receptor damage produced at P40 and later yielded different patterns of changes in geniculate ganglion proteins. Late receptor damage produced a transient increase in ganglion concentrations of NF-160, NF-200, GAP-43 and four additional acidic proteins within the 29-57 kDa M(r) range. Late receptor damage also produced a transient decrease in the concentrations of protein A1 and a 30 kDa protein that was not affected by P2 damage. Therefore, proteins that were preferentially affected by P2 damage may be involved in the regulation of initial axonal growth within the lingual epithelium and NST, as opposed to the structural repair or maintenance of extant axons. Relationships between normal anatomical development in peripheral and central components of primary gustatory axons are discussed in relation to availability of particular cytoskeletal and growth-associated proteins.

Animals↗
PubMed1995

Effects of orochemical stimulation on postnatal development of gustatory recipient zones within the nucleus of the solitary tract.

Previous receptor damage studies and artificial rearing (AR) studies in rat have demonstrated that orochemical stimulation between the postnatal ages of P2 and P14 is necessary for development of primary gustatory axons and terminal endings in the rostral nucleus of the solitary tract (NST). Objectives of the present experiment were to evaluate the qualitative nature of orochemical stimulation and amount of orochemical stimulation that is necessary to produce normal axonal and terminal development in gustatory recipient zones of the rostral and intermediate NST. To this end, ultra-pure water, 30, 150, and 500 mM NaCl, 80 and 340 mM lactose, whole rat milk, and rat milk that had been subject to extensive dialysis (12-14 kD MWCO) was delivered to independent groups of rat pups during AR procedures. Unstimulated AR animals and matched mother-reared (MR) animals were used as controls. AR animals received experimental orochemical stimulation between the ages of P4 and P10, and were thereafter returned to lactating dams until the time of weaning; MR animals received experimental orochemical stimulation during the course of normal nursing. Following maturation, anterograde fluorescent dual-labeling experiments were conducted to map the course and distribution of primary gustatory axons within the NST. Results show that experimental stimualtion with water during AR procedures is not sufficient to produce normal development of primary gustatory axons and terminal endings in the gustatory NST. Stimulation with 30, 150, and 500 mM NaCl produced normal axonal development in the NST, as did 80 and 340 mM lactose, whole rat milk, and dialyzed rat milk.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Immunohistochemical correlates of peripheral gustatory sensitivity to sodium and amiloride.

In mammals, transduction of sodium stimuli occurs via amiloride-sensitive sodium channels. In rat, gustatory physiological sensitivity to sodium stimuli develops gradually during the early postnatal period. In addition, if pregnant rats are subjected to dietary sodium restriction during gestation, their offspring fail to develop normal gustatory physiological responses to sodium and sensitivity to amiloride. In the present study, we used polyclonal antibodies raised against amiloride-sensitive sodium channels to ascertain whether gustatory function is correlated with the immunological presence of the transduction apparatus for sodium stimuli in the taste buds of neonatal rats and adult offspring of sodium-restricted dams. The results indicate that antiamiloride-sensitive sodium channel antisera bind cells within taste buds of neonatal and adult rats, regardless of maternal dietary condition. Therefore, despite the functional absence of taste system amiloride-sensitive sodium channels, the antigenic determinants of these channels are expressed. These data suggest that the onset of normal gustatory sodium sensitivity in neonatal normal rats results from the progressive activation of existing, quiescent channels. Furthermore, they rule out the possibility that the failure to synthesize channel protein underlies the lack of gustatory sodium and amiloride sensitivity in the offspring of sodium-restricted rats.

Amiloride↗
PubMed1992

Postnatal development of gustatory recipient zones within the nucleus of the solitary tract.

Previous studies have examined pre- and postsynaptic development of the first-order central gustatory relay, located in the rostral nucleus of the solitary tract (NST). This region of the NST is innervated by primary gustatory axons arising from the facial-intermediate nerve. However, a large portion of the gustatory NST is innervated by axons arising from the glossopharyngeal nerve, and although the time course for development of N.VII recipient zones has been defined development of glossopharyngeal afferent terminal fields has not been examined. Moreover, the time course for development of projection neurons located postsynaptic to gustatory afferent axons has not been examined in any portion of the NST. The objectives of the present study were to 1) define the time course for development of N.VII and N.IX terminal fields and 2) examine temporal relationships between development of afferent terminal fields and development of projection neurons located postsynaptic to gustatory afferent axons. To this end, triple fluorescent labeling procedures were used to simultaneously visualize developing axons and projection neurons. Results show that afferent terminal fields develop along the rostrocaudal axis of the NST. Axons of the N.VII terminal field are present in the rostral NST at P1 and develop to approximately P25. Axons and terminal endings of N.IX do not enter the NST until approximately P9-P10, and these terminal fields develop within the intermediate NST until approximately P45. Many NST neurons destined to project axons to the second-order central gustatory relay, located in the caudal parabrachial nucleus (PBN), do not possess axonal connections with the PBN during the first 2-3 weeks of postnatal life. As afferent terminal fields develop, these neurons establish connections with the PBN between the ages of approximately P7 and P45-P60. The delay between afferent terminal field development and development of PBN projection neurons in the N.VII terminal field is approximately 3 weeks. The delay between pre- and postsynaptic development in the N.IX terminal field is approximately 1 week. Potential relationships between pre- and postsynaptic development are discussed, in addition to relationships between anatomical development in the NST and the emergence of taste-guided behaviors.

Afferent Pathways↗
PubMed1991

Effects of early postnatal receptor damage on dendritic development in gustatory recipient zones of the rostral nucleus of the solitary tract.

The rostral gustatory zone of the nucleus of the solitary tract (NST) exhibits extensive anatomical development during the first 3 weeks of postnatal life, and this development requires the presence of intact gustatory receptors during a critical period. We have previously shown that unilateral damage induced to fungiform papillae of the anterior tongue at postnatal day 2 (P2) alters normal migration and ramification of chorda tympani (CT) axons in the rostral NST. In addition to alterations of axonal development, P2 receptor damage decreases the intraneuronal distance between neurons that project axons to the second-order central gustatory relay, located in the caudal parabrachial nucleus (PBN). This observation suggested that P2 receptor damage may alter both axonal development and dendritic development in the rostral gustatory NST. The present study evaluated potential changes in dendritic development of PBN projection neurons following either P2 or P10 receptor damage. Morphological studies were first conducted to quantitatively define somatic characteristics of neurons that project axons to the PBN. Independent experiments used fluorescent labeling combined with subsequent Golgi-impregnation to study dendritic architecture of identified PBN projection neurons. Results confirmed that P2 receptor damage alters dendritic development of PBN projection neurons located in CT terminal fields. Anterior tongue receptor damage at P2 (1) reduces planar length of first- and second-order dendritic branches, (2) reduces the mean number of second-order branches per neuron, and (3) reduces the density of spine processes on second-order dendritic branches. A critical period exists for these effects, similar to that reported for axonal development, insofar as P2 receptor damage alters dendritic development of PBN projection neurons, whereas P10 receptor damage does not. Dendrites of identified PBN projection neurons located in regions of the NST that receive primary afferent axons from the glossopharyngeal nerve are not affected by anterior tongue damage at P2. These results show that early postnatal receptor damage influences both pre- and postsynaptic development in the rostral gustatory NST. These anatomical changes are undoubtedly related to alterations in taste-guided behaviors that are observed following P2 receptor damage.

Animals↗
PubMed1990

Effects of early postnatal receptor damage on development of gustatory recipient zones within the nucleus of the solitary tract.

The temporal correspondence between neuroanatomical and neurophysiological development of peripheral and central gustatory neurons has suggested that morphological development of the first-order central gustatory relay, located in the rostral nucleus of the solitary tract (NST), may be dependent on afferent input from peripheral gustatory pathways. The objective of the present study was to determine the effects of perinatal receptor damage on development of gustatory recipient zones within the rostral and intermediate NST. Results show that damage induced to fungiform receptors of the anterior tongue at postnatal day 2 (P2) alters normal development of NST terminal fields associated with the chorda tympani nerve (CT) and greater superficial nerve (GSP), and that alterations in the CT/GSP terminal field persist in adulthood after peripheral gustatory receptors have regenerated. Damage induced to fungiform receptors at P2 does not alter the normal development of glossopharyngeal terminal fields in the intermediate NST. Receptor damage produced at P10 and P20 is without effect on normal development of the CT/GSP terminal field. Thus, fungiform receptor damage at P2 produces specific alterations in the development of NST terminal fields that receive projections from the facial-intermediate nerve, and receptor damage effects are only obtained during a critical period of postnatal development. P2 receptor damage has the overall effect of eliminating caudally directed migration of CT/GSP axons to additional projection neurons that establish connections with the second-order central gustatory relay located in the parabrachial nucleus (PBN). Behavioral studies were conducted to determine the functional consequences of early receptor damage. Results from behavioral studies show that bilateral damage to fungiform papillae at P2 alters normal adult preferences to low and intermediate concentrations of NaCl and sucrose tastes, yet aversions to citric acid and quinine HCl are not obviously affected. Therefore, anatomical alterations in the CT/GSP terminal field produced by P2 receptor damage are accompanied by specific changes in adult taste preference responses.

Animals↗
PubMed1990

Murine strain differences in taste responsivity and organization of the rostral nucleus of the solitary tract.

Taste responsivity and organization of fungiform papillae, geniculate ganglion neurons and gustatory recipient zones of the nucleus of the solitary tract (NST) were examined in C57BL/6NCrlBR (C57) mice, BALB/c6NCrlBR (BALB/c) mice and CB6F1/CrlBr (CB6) mice, an F1 hybrid cross between BALB/c and C57 mice. Results from behavioral studies confirm that C57 and CB6 mice exhibit higher preferences to sucrose and lower preferences to NaCl, as compared to BALB/c mice. No strain differences were confirmed for aversion responses to citric acid or quinine HCl taste stimuli. Anatomical analyses show that the number and organization of fungiform papillae do not reliably differ between C57, BALB/c, and CB6 mice, nor do volumes of glossopharyngeal terminal fields in the NST. However, strain-specific differences exist in the number of neurons contained in the geniculate ganglion, volume of chorda tympani (CT) terminal fields in the rostral NST, and number of NST neurons contained in CT terminal fields. BALB/c and CB6 mice possess a greater number of geniculate ganglion neurons and larger CT terminal fields, as compared to C57 mice. However, strain differences in the number of geniculate ganglion neurons and terminal field volume are not obviously correlated with strain differences in gustatory responsivity. The only reliable relationship confirmed between taste responsivity and neuroanatomical organization of the rostral NST relates to the absolute number of neurons contained in CT terminal fields, and corresponding neuronal density within CT terminal fields. Chorda tympani terminal fields of C57 and CB6 mice contain an average of 379 neurons, whereas CT terminal fields of BALB/c mice contain an average of 531 neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Postnatal development of protein P-38 ('synaptophysin') immunoreactivity in pontine and medullary gustatory zones of rat.

Neurons located in gustatory zones of the nucleus of the solitary tract (NST) and parabrachial nucleus (PBN) exhibit extensive morphological development during the first 5-7 weeks of rat's postnatal life. The present study examined the time course for development of protein P-38 ('synaptophysin'), a specific integral membrane glycoprotien of clear synaptic vesicles, in the rostral NST and PBN. Results show that volumetric fractions of P-38 immunoreactions increase in the NST from P1 to P10, and are adult-like in the NST after approximately P11. In contrast, volumetric fractions of P-38 immunoreactivity increase in the PBN between approximately P11 and P30. Because we have previously demonstrated that dendritic growth in the rostral gustatory NST precedes dendritic growth in the PBN, these results confirm that maturation of both presynaptic and postsynaptic constituents of brainstem gustatory relays develop in a temporally sequential manner. Relationships between neurological development of brainstem gustatory relays and the ontogeny of taste-guided responses are discussed.

Aging↗
PubMed1989

Postnatal development of the rostral solitary nucleus in rat: dendritic morphology and mitochondrial enzyme activity.

Morphological and metabolic development of the gustatory zone of the rostral nucleus of the solitary tract (NST) was examined in rat. Transganglionic transport of horseradish peroxidase (HRP) was used to visualize the organization of gustatory projections to the rostral gustatory NST in rats aged postnatal day 1 (P1) to P34. Golgi impregnation studies were performed to analyze morphological development of dendrites in regions of the rostral NST that were identified as anterior tongue terminal fields. Results demonstrate that afferent fibers of the anterior tongue project to the rostral NST in rats as young as P1. The volume of NST terminal fields increased from P1 to approximately P16-P20, and was adult-like after approximately P20. Developmental increases in terminal field volume resulted from a preferential expansion in the rostrocaudal plane. Planar length of first-order dendrites associated with fusiform, multipolar, and ovoid neurons, and second-order dendrites of fusiform and ovoid neurons, increased approximately three-fold between P4 and P16-20. First-order dendritic length for all morphological types was adult-like after approximately 20-25 days of age, whereas second-order dendritic length of multipolar neurons increased significantly between P30 and P60-70. Histochemical studies confirmed that activity of the mitochondrial respiratory enzymes cytochrome c oxidase (EC 1.9.3.1), succinate dehydrogenase (EC 1.3.99.1), and NADH-dehydrogenase (EC 1.6.99.3) increased monotonically during the developmental period in which planar growth of first-order dendrites was observed. The present results, in combination with results from previous studies, indicate that morphological and metabolic development fo the NST occurs concomitantly with morphological development of taste receptors and peripheral gustatory nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Elevated NADH-dehydrogenase activity characterizes the rostral gustatory zone of the solitary nucleus in rat.

The regional distribution of NADH-dehydrogenase (NADH-DH; EC 1.6.99.3) activity was examined in the nucleus of the solitary tract (NST) in the rat, with specific emphasis given to the rostral gustatory zone. Activity of NADH-DH in the rostral gustatory zone was compared to intermediate and caudal divisions of the NST which receive projections from the glossopharyngeal and vagus nerves. Animals received injections of horseradish peroxidase (HRP) in the anterior tongue, or applications of HRP crystals to the cut chorda tympani nerve to visualize chorda tympani terminal fields in the rostral NST. Tissue was subsequently reacted for NADH-dehydrogenase and transported HRP using sequential histochemical procedures. Results show that relative activity of NADH-DH is highest in areas of the NST that receive projections from the chorda tympani nerve. Lateral divisions of the NST, which receive projections from the lingual-trigeminal nerve, show moderate enzymatic activity, but such activity is quantitatively lower than that observed in the chorda tympani terminal field. Intermediate and caudal portions of the NST show the lowest NADH-DH activity of all NST regions examined. These results confirm that histochemistry for NADH-dehydrogenase can serve as an endogenous marker for chorda tympani terminal fields in the rostral NST.

Animals↗
PubMed1988

Postnatal development of the parabrachial gustatory zone in rat: dendritic morphology and mitochondrial enzyme activity.

Previous studies have shown that behavioral and neurophysiological responses to tastes develop during rat's postnatal life. The present experiments evaluated morphological and metabolic development of neurons in the gustatory zone of the caudal parabrachial nucleus (PBNc) of rat. Histological reconstruction studies were conducted to establish coordinate systems for PBNc gustatory zones in developing rats. Reliability of coordinate systems were evaluated in separate experiments following infusions of horseradish peroxidase in the thalamic taste area. Morphological and Golgi impregnation studies were performed to characterize neuronal and dendritic architecture in PBNc gustatory zones defined by coordinates. Conventional histochemical studies were performed for the mitochondrial respiratory enzymes cytochrome C oxidase (CO; EC 1.9.3.1) succinate dehydrogenase (SDH; EC 1.3.99.1), and NADH-dehydrogenase (NADH-DH; EC 1.6.99.3). Results show that two somatic morphologies can be statistically characterized in PBNc gustatory zones: Multipolar somatic types and fusiform somatic types. Multipolar and fusiform neurons of neonatal and adult rats project axons to the thalamic taste area, and dendrites of these neurons grow extensively between approximately 16 days after birth to approximately 35 days after birth. Activity of CO, SDH, and NADH-DH increases in the PBNc gustatory zones during the period of dendritic growth, and continues to increase slightly to approximately 45 days. These results provide the first demonstration of postnatal morphological and metabolic developmental in a central gustatory relay. Postnatal development of gustatory system therefore appears similar to that reported for other sensory systems, to the extent that morphological and metabolic development accompanies the ontogeny of taste responses.

Aging↗
PubMed1988

Organization of GABA and GABA-transaminase containing neurons in the gustatory zone of the nucleus of the solitary tract.

Previous cytoarchitectural and electron micrographic studies have indicated that the gustatory zone of the nucleus of the solitary tract (NST) may contain local circuit neurons. It is known that neurons of the caudal "visceroceptive" NST contain GABA, glutamic acid decarboxylase (EC 4.1.1.15), and GABA-transaminase (GABA-T; 4-aminobutyrate: 2-oxoglutarate aminotransferase; EC 2.6.1.19). The present study was conducted to determine whether or not neurons in the gustatory zone of the NST of rat contain GABA and the principle degradative enzyme of GABA, GABA-T. Transganglionic transport of horseradish peroxidase (HRP) was used to identify chorda tympani (CT) nerve terminal fields. Immunohistochemical studies were combined with transport experiments to evaluate the organization of GABA immunoreactive neurons in CT terminal fields. Results show that GABA immunoreactive neurons and puncta are located within CT terminal fields. These neurons evince small ovoid morphologies resembling Golgi interneurons, and comprise an average of 18% of total neurons in CT terminal fields. Independent histochemical studies reveal that approximately 82% of GABA immunoreactive neurons within CT terminal fields exhibit GABA-T activity. Retrograde transport of HRP was used in additional studies to evaluate whether or not axons of putative GABAergic neurons project to the second-order central gustatory relay located in the caudal parabrachial nucleus (PBNc), to the caudal NST, or to regions surrounding the rostral or caudal NST. Combined studies indicate that GABA immunoreactive neurons in the gustatory NST do not project axons to the PBNc, to the caudal NST, or to regions adjacent to the rostral or caudal NST.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobutyrate Transaminase↗
PubMed1985

Involvement of the anterior insular gustatory neocortex in taste-potentiated odor aversion learning.

When an odor conditioned stimulus (CS) precedes illness (unconditioned stimulus; UCS), rats acquire relatively weak odor aversions. Conversely, when a compound odor-taste (flavor) CS precedes illness, rats acquire robust aversions both to the odor and to the taste components of a compound flavor CS. Thus, tastes potentiate odor-illness aversions during toxiphobic conditioning. Such conditioning effects have been referred to as taste-potentiated odor aversion learning (POA). Previous neurobehavioral experiments have shown that the anterior insular gustatory neocortex contributes to conditioned taste aversion (CTA) learning. The present experiment examined the involvement of the anterior insular gustatory neocortex in CTA learning and POA learning. To that end, four distinct groups of rats received bilateral electrolytic lesion placements in the orbitofrontal neocortex, the "somatic" gustatory neocortex, the anterior insular gustatory neocortex or the posterior insular neocortex. Control animals received anesthesia only. Subgroups of animals thereafter received aversion conditioning using either an odor (almond) CS or a compound odor-taste (almond-saccharin) CS. Aversions to the almond odorant and/or saccharin tastant were evaluated during extinction. Results indicated that animals lacking orbitofrontal neocortex or posterior insular neocortex acquired normal CTAs and POAs. Animals lacking somatic gustatory neocortex exhibited impaired CTA learning, yet those animals showed normal POA learning. Lesions centered in the anterior insular neocortex impaired both CTA learning and POA learning. These results demonstrate that the insular gustatory neocortex is uniquely involved in the higher-order integration of odors, tastes and illness.

Animals↗
PubMed1985

Taste discriminations in rats lacking anterior insular gustatory neocortex.

Previous neurobehavioral investigations have demonstrated that the anterior insular gustatory neocortex (AIGN) mediates taste-illness learning. The present experiment evaluated taste discriminations in rats lacking AIGN. Two groups of rats received distinct surgical treatments. One-half of the animals received bilateral electrolytic lesion placements in the AIGN: Remaining animals received anesthesia and scalp incisions only. Following postoperative recovery animals received standard two-bottle preference tests with various concentrations of sucrose to evaluate gustatory reactivity. Animals thereafter received two-bottle discrimination tests with selected sucrose concentrations. At the conclusion of preference tests and discrimination tests with sucrose, preference tests and discrimination tests were conducted with sodium chloride. Following those tests animals received taste aversion conditioning to determine whether or not AIGN lesions impaired taste-illness learning. Results of two-bottle taste tests indicated that AIGN lesions do not obviously alter taste reactivity nor taste discriminations to preferred concentrations of sucrose and NaCl. Anterior insular lesions did, however, impair normal taste aversion learning. These results, in combination with those of previous investigators, provide further evidence that the AIGN preferentially contributes to taste learning functions.

Animals↗
PubMed1985

Cortical substrates of taste aversion learning: involvement of dorsolateral amygdaloid nuclei and temporal neocortex in taste aversion learning.

The amygdaloid complex is functionally implicated in conditioned taste aversion (CTA) learning. Results of previous neurobehavioral studies have provided equivocal evidence concerning the involvement of specific amygdaloid nuclei in CTA learning. The present study was conducted to examine the involvement of the central (CE), lateral (LA), and basolateral (BL) amygdaloid nuclei and the temporal neocortices (area 20) in CTA learning. To that end, distinct groups of rats received bilateral electrolytic lesion placements in the CE, LA, BL, or the temporal neocortices. Control animals received scalp and meningeal incisions only. Following recovery, animals were habituated to a restricted drinking schedule with distilled water. Animals then received CTA conditioning, with LiCl used both as the conditioned stimulus and as the unconditioned stimulus. Anterograde degeneration histologies were performed on all brain tissue to evaluate relations between CTA learning deficits and axonal pathology induced by lesion placements. Results of behavioral manipulations indicated that destruction of the CE, LA, or temporal neocortex impaired CTA acquisition, but damage induced to the basolateral amygdaloid nucleus did not. Anatomical observations indicated that degeneration of amygdalofugal and/or corticofugal projections to the convolutions of the olfactory tubercle (medial), subthalamic nucleus, and the parabrachial complex is correlated with CTA learning deficits. These results indicate that destruction of the dorsolateral amygdaloid nuclei and/or the temporal neocortices may produce CTA learning deficits by affecting olfactory, gustatory, and/or gastrointestinal processing in various portions of the forebrain.

Amygdala↗
PubMed1985

Thalamocortical relations in taste aversion learning: I. Involvement of gustatory thalamocortical projections in taste aversion learning.

The anterior insular gustatory neocortex (AIGN) has been implicated as a functional substrate of conditioned taste aversion (CTA) learning. Results of previous neuroanatomical and neurobehavioral experiments indicate that projections from gustatory-responsive neurons in the posterior ventromedial thalamic nuclei (parvicellular division; VPMpc) may provide relevant input to the AIGN during CTA learning. In rat, gustatory thalamocortical projections from VPMpc thalamus traverse the ventrolateral neostriatum (VLS) enroute to the AIGN. In these experiments, various neuroanatomical and neurobehavioral manipulations in the VLS were used to examine the contribution of presumed gustatory thalamocortical projections to CTA learning. These experiments demonstrate that projections from VPMpc thalamus to the AIGN are essential for normal CTA learning. Because both VPMpc thalamus and the AIGN each have been implicated as functional substrates of CTA learning, the present results suggest that the gustatory thalamocortical relay per se is necessary for normal taste-illness learning.

Afferent Pathways↗
PubMed1985

Thalamocortical relations in taste aversion learning: II. Involvement of the medial ventrobasal thalamic complex in taste aversion learning.

Previous neurobehavioral studies have implicated the gustatory thalamocortical relay as a functional substrate of conditioned taste aversion (CTA) learning. These experiments were conducted to examine the involvement of the gustatory thalamic nuclei in fundamental taste reactivity, gastrointestinal reactivity, and CTA learning. In Experiment 1, bilateral electrolytic lesions were produced in the medial ventrobasal thalamic complex (VBm), including the thalamic gustatory nuclei, in one group of rats. A separate group of rats received control lesion placements in the mediodorsal-periventricular (MD-PV) thalamic nuclei. Animals then received preference-aversion taste tests followed by CTA conditioning. At the conclusion of conditioning, lesions were produced in the anterior insular gustatory neocortex (AIGN) to evaluate whether or not the AIGN contributed to CTA learning in animals lacking VBm thalamus. Results of Experiment 1 indicated that control lesions did not disrupt taste reactivity, gastrointestinal reactivity, or CTA learning. Destruction of VBm thalamus attenuated taste reactivity to sucrose, citric acid, and quinine hydrochloride; however, such lesions did not impair normal taste reactivity to sodium chloride. Lesion placements in VBm thalamus also did not reliably impair gastrointestinal reactivity to ingested LiCl. Elimination of VBm thalamus markedly attenuated CTA learning. Results of neocortical lesion manipulations showed that the AIGN contributed to initial CTA learning in animals lacking MD-PV thalamus but that the AIGN did not mediate initial CTA learning in animals lacking VBm thalamus. Whether animals lacking VBm thalamus used olfactory cues associated with drinking solutions to acquire CTAs was evaluated in Experiment 2. Results of Experiment 2 demonstrated that animals lacking VBm thalamus and the olfactory bulbs could not acquire aversions to ingested LiCl following eight conditioning trials. These experiments demonstrate that destruction of VBm thalamus, including the gustatory thalamic nuclei, is sufficient to prevent CTA learning.

Afferent Pathways↗