scholarly journals Effect of Electrical Stimulation of the Nucleus of the Solitary Tract on the Development of Electrical Amygdaloid Kindling in the Cat

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


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.


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.


2011 ◽  
Vol 91 (2) ◽  
pp. 215-220 ◽  
Author(s):  
A. Braud ◽  
A. Vandenbeuch ◽  
F. Zerari-Mailly ◽  
Y. Boucher

The aim of this study was to investigate the inferior alveolar nerve (IAN) and chorda tympani (CT) projections onto gustatory neurons of the nucleus of the solitary tract (NST) in the rat by immunochemical and electrophysiological techniques. IAN afferents were retrogradely labeled. NST neurons were labeled either by retrograde tracer injection into the parabrachial nucleus (PBN) or by c-Fos mapping after CT activation. NST neurons responding to tastant stimulation were recorded in vivo before and after electrical stimulation of the IAN. Results from the immunolabeling approach showed IAN boutons “en passant” apposed to retrogradely labeled neurons from PBN and to CT-activated neurons in the NST. Recordings of single NST neurons showed that the electrical stimulation of the IAN significantly decreased CT gustatory responses. Analysis of these data provides an anatomical and physiological basis to support trigeminal dental and gustatory interactions within the brainstem.


1989 ◽  
Vol 257 (2) ◽  
pp. R405-R409
Author(s):  
D. J. McKitrick ◽  
F. R. Calaresu

As microinjection of atrial natriuretic factor (ANF) into the nucleus of the solitary tract (NTS) has been shown to elicit depressor responses [D. J. McKitrick and F. R. Calaresu. Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R182-R187, 1988], we investigated the possibility that these responses might be facilitated either by electrical stimulation of arterial baroreceptor fibers in the aortic depressor nerve (ADN) or by simultaneous microinjection of L-glutamate (Glu) into the same sites in the NTS. Male Wistar rats (n = 51) were anesthetized with urethan (1.4 g/kg ip), artificially ventilated, and the dorsal medulla was exposed. The ADN was isolated, cut distally, and the central end was placed on bipolar stimulating electrodes. Threshold doses of 10(-7) M ANF microinjected into the NTS were combined with threshold electrical stimulation of the ADN (n = 37) or threshold doses of 0.13-0.5 M Glu (n = 14) microinjected into the NTS. There was a significant interaction between ANF microinjection and ADN stimulation in producing changes in mean arterial pressure (MAP) and heart rate [HR; P less than 0.05; -20.2 +/- 2.3 (SE) mmHg and -30.8 +/- 6.9 (SE) beats/min, respectively; n = 18]. There was also a significant interaction between ANF and Glu in producing changes in MAP and HR [P less than 0.05; -16.3 +/- 1.8 (SE) mmHg and -15.0 +/- 3.0 (SE) beats/min, respectively; n = 8]. These results indicate that ANF influences neurons in the NTS, which are also influenced by activation of arterial baroreceptors, and ANF and Glu interact in the NTS to produce facilitated cardiovascular responses.


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