scholarly journals Amygdalofugal Influence on Processing of Taste Information in the Nucleus of the Solitary Tract of the Rat

2010 ◽  
Vol 104 (2) ◽  
pp. 726-741 ◽  
Author(s):  
Yi Kang ◽  
Robert F. Lundy

Previous studies have shown that corticofugal input to the first central synapse of the ascending gustatory system, the nucleus of the solitary tract (NST), can alter the way taste information is processed. Activity in other forebrain structures, such as the central nucleus of the amygdala (CeA), similarly influence activation of NST taste cells, although the effects of amygdalofugal input on neural coding of taste information is not well understood. The present study examined responses of 110 NST neurons to 15 taste stimuli before, during, and after electrical stimulation of the CeA in rats. The taste stimuli consisted of different concentrations of NaCl (0.03, 0.1, 0.3 M), sucrose (0.1, 0.3, 1.0 M), citric acid (0.005, 0.01 M), quinine HCl (0.003, 0.03 M), and 0.03 M MSG, 0.1 M KCl, as well as 0.1 M NaCl, 0.01 M citric acid, and 0.03 M MSG mixed with 10 μM amiloride. In 66% of NST cells sampled (73/110) response rates to the majority of effective taste stimuli were either inhibited or augmented. Nevertheless, the magnitude of effect across stimuli was often differential, which provides a neurophysiological mechanism to alter neural coding. Subsequent analysis of across-unit patterns showed that amygdalofugal input plays a role in shaping spatial patterns of activation and could potentially influence the perceptual similarity and/or discrimination of gustatory stimuli by altering this feature of neural coding.

2017 ◽  
Vol 10 (1) ◽  
pp. 116-125 ◽  
Author(s):  
D. Martínez-Vargas ◽  
A. Valdés-Cruz ◽  
V.M. Magdaleno-Madrigal ◽  
R. Fernández-Mas ◽  
S. Almazán-Alvarado

2002 ◽  
Vol 282 (4) ◽  
pp. H1278-H1287 ◽  
Author(s):  
Pedro Boscan ◽  
Julian F. R. Paton

We determined the activity of neurons within the nucleus of the solitary tract (NTS) after stimulation of the cornea and assessed whether this input affected the processing of baroreceptor and peripheral chemoreceptor inputs. In an in situ, unanesthetized decerebrate working heart-brain stem preparation of the rat, noxious mechanical or electrical stimulation was applied to the cornea, and extracellular single unit recordings were made from NTS neurons. Cornea nociceptor stimulation evoked bradycardia and an increase in the cycle length of the phrenic nerve discharge. Of 90 NTS neurons with ongoing activity, corneal stimulation excited 51 and depressed 39. There was a high degree of convergence to these NTS neurons from either baroreceptors or chemoreceptors. The excitatory synaptic response in 12 of 19 baroreceptive and 10 of 15 chemoreceptive neurons was attenuated significantly during concomitant electrical stimulation of the cornea. This inhibition was GABAA receptor mediated, being blocked by pressure ejection of bicuculline. Thus the NTS integrates information from corneal receptors, some of which converges onto neurons mediating reflexes from baroreceptors and chemoreceptors to inhibit these inputs.


Epilepsia ◽  
2002 ◽  
Vol 43 (9) ◽  
pp. 964-969 ◽  
Author(s):  
Victor M. Magdaleno-Madrigal ◽  
Alejandro Valdés-Cruz ◽  
David Martínez-Vargas ◽  
Adrián Martínez ◽  
Salvador Almazán ◽  
...  

2005 ◽  
Vol 93 (3) ◽  
pp. 1183-1196 ◽  
Author(s):  
Cheng-Shu Li ◽  
Young K. Cho ◽  
David V. Smith

The lateral hypothalamus (LH) and the central nucleus of the amygdala (CeA) exert an influence on ingestive behavior and are reciprocally connected to gustatory and viscerosensory areas, including the nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN). We investigated the effects of LH and CeA stimulation on the activity of 101 taste-responsive neurons in the hamster PbN. Eighty three of these neurons were antidromically activated by stimulation of these sites; 57 were antidromically driven by both. Of these 83 neurons, 21 were also orthodromically activated—8 by the CeA and 3 by the LH. Additional neurons were excited ( n = 5) or inhibited ( n = 8) by these forebrain nuclei but not antidromically activated. Taste stimuli were: 0.032 M sucrose, 0.032 M sodium chloride (NaCl), 0.032 M quinine hydrochloride (QHCl), and 0.0032 M citric acid. Among the 34 orthodromically activated neurons, more sucrose-best neurons were excited than inhibited, whereas the opposite occurred for citric-acid- and QHCl-best cells. Neurons inhibited by the forebrain responded significantly more strongly to citric acid and QHCl than cells excited by these sites. The effects of electrical stimulation were mimicked by microinjection of dl-homocysteic acid, indicating that cells at these forebrain sites were responsible for these effects. These data demonstrate that many individual PbN gustatory neurons project to both the LH and CeA and that these areas modulate the gustatory activity of a subset of PbN neurons. This neural substrate is likely involved in the modulation of taste activity by physiological and experiential factors.


2001 ◽  
Vol 85 (2) ◽  
pp. 770-783 ◽  
Author(s):  
Robert F. Lundy ◽  
Ralph Norgren

Visceral signals and experience modulate the responses of brain stem neurons to gustatory stimuli. Both behavioral and anatomical evidence suggests that this modulation may involve descending input from the forebrain. The present study investigates the centrifugal control of gustatory neural activity in the parabrachial nucleus (PBN). Extracellular responses were recorded from 51 single PBN neurons during application of sucrose, NaCl, NaCl mixed with amiloride, citric acid, and QHCl with or without concurrent electrical stimulation in the ipsilateral central nucleus of the amygdala (CeA). Based on the sapid stimulus that evoked the greatest discharge, 3 neurons were classified as sucrose-best, 32 as NaCl-best, and 16 as citric acid-best. In most of the neurons sampled, response rates to an effective stimulus were either inhibited or unchanged during electrical stimulation of the CeA. Stimulation in the CeA was without effect in two sucrose-best neurons, nine NaCl-best neurons, and one citric acid-best neuron. Suppression was evident in 1 sucrose-best neuron, 18 NaCl-best neurons, and 15 citric acid-best neurons. In NaCl-best neurons inhibited by CeA stimulation, the magnitude of the effect was similar for spontaneous activity and responses to the five taste stimuli. Nonetheless, the inhibitory modulation of gustatory sensitivity increased the relative effectiveness of NaCl resulting in narrower chemical selectivity. For citric acid–best neurons, the magnitude of inhibition produced by CeA activation increased with an increase in stimulus effectiveness. The responses to citric acid were inhibited significantly more than the responses to all other stimuli with the exception of NaCl mixed with amiloride. The overall effect was to change these CA-best neurons to CA/NaCl-best neurons. In a smaller subset of NaCl-best neurons ( n = 5), CeA stimulation augmented the responsiveness to NaCl but was without effect on the other stimuli or on baseline activity. It appears that electrical stimulation in the CeA modulates response intensity, as well as the type of gustatory information that is transmitted in a subset of NaCl-best neurons. These findings provide an additional link between the amygdala and the PBN in the control of NaCl intake, modulating the response and the chemical selectivity of an amiloride-sensitive Na+-detecting input pathway.


1980 ◽  
Vol 59 (s6) ◽  
pp. 255s-257s ◽  
Author(s):  
Karen L. Barnes ◽  
C. M. Ferrario

1. The mechanism by which the area postrema augments central sympathetic drive during electrical stimulation is presently unknown. This pathway may involve either direct facilitation of brain-stem vasomotor neurons or inhibition of the sympatho-inhibitory baroreceptor relay in the nucleus tractus solitarii. 2. The present study employed selective lesions within the solitary tract nucleus to assess the participation of the primary baroreceptor relay in the pressor response during electrical stimulation of the area postrema. 3. The magnitude of the pressor response was unchanged after destruction of the solitary tract and lateral solitary nucleus which centrally interrupted the baroreceptor reflex. However, microknife cuts through the medial solitary nucleus, which spared the carotid sinus reflex, significantly reduced the magnitude of the area postrema pressor response. 4. Previous anatomical studies support these results and confirm that, although the area postrema pressor pathway traverses the most medial portion of the solitary complex, it does not produce augmented sympathetic outflow by inhibition of the primary baroreflex relay.


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