Integration of cornea and cardiorespiratory afferents in the nucleus of the solitary tract of the rat

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.

2009 ◽  
Vol 296 (1) ◽  
pp. R80-R87 ◽  
Author(s):  
Miroslav Rozloznik ◽  
Julian F. R. Paton ◽  
Mathias Dutschmann

Hallmarks of the mammalian diving response are protective apnea and bradycardia. These cardiorespiratory adaptations can be mimicked by stimulation of the trigeminal ethmoidal nerve (EN5) and reflect oxygen-conserving mechanisms during breath-hold dives. Increasing drive from peripheral chemoreceptors during sustained dives was reported to enhance the diving bradycardia. The underlying neuronal mechanisms, however, are unknown. In the present study, expression and plasticity of EN5-bradycardias after paired stimulation of the EN5 and peripheral chemoreceptors was investigated in the in situ working heart-brain stem preparation. Paired stimulations enhanced significantly the bradycardic responses compared with EN5-evoked bradycardia using submaximal stimulation intensity. Alternating stimulations of the EN5 followed by paired stimulation of the EN5 and chemoreceptors (10 trials, 3-min interval) caused a progressive and significant potentiation of EN5-evoked diving bradycardia. In contrast, bradycardias during paired stimulation remained unchanged during repetitive stimulation. The progressive potentiation of EN5-bradycardias was significantly enhanced after microinjection of the 5-HT3 receptor agonist (CPBG hydrochloride) into the nucleus tractus solitarii (NTS), while the 5-HT3 receptor antagonist (zacopride hydrochloride) attenuated the progressive potentiation. These results suggest an integrative function of the NTS for the multimodal mediation of the diving response. The potentiation or training of a submaximal diving bradycardia requires peripheral chemoreceptor drive and involves neurotransmission via 5-HT3 receptor within the NTS.


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

1963 ◽  
Vol 204 (4) ◽  
pp. 667-672 ◽  
Author(s):  
F. Morin ◽  
S. T. Kitai ◽  
H. Portnoy ◽  
C. Demirjian

The lateral cervical nucleus was explored with microelectrodes in lightly anesthetized cats. Extracellular responses were recorded from 160 neurons following physiological stimulation of the ipsilateral side of the body from the neck to the tail. The stimuli activating the neurons were touch, pressure, and joint movement. Neurons responding to touch were more prevalent than neurons responding to pressure on the skin or on deep structures; those responding to joint movements were a small fraction of the neuronal sample studied. For the three stimuli tested, the limbs were more prominently represented than the trunk. Tactile and pressure peripheral fields activating single neurons were of three types: restricted (a few hairs, small areas within one segment of a limb), large (wide areas of the trunk, whole limb), and very large (whole ipsilateral aspect of the body, both limbs). Restricted fields were less numerous than the large fields. One-third of the fields activating single neurons following tactile stimulation was of the very large type. The existence of the very large fields indicated a high degree of convergence of afferents onto neurons of the cervical nucleus.


1988 ◽  
Vol 66 (3) ◽  
pp. 380-384 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Reginald Nadeau

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.


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

2003 ◽  
Vol 284 (2) ◽  
pp. R455-R466 ◽  
Author(s):  
Irene C. Solomon

10.1152/ajpregu.00395.2002. We have previously demonstrated that microinjection of dl-homocysteic acid (DLH), a glutamate analog, into the pre-Bötzinger complex (pre-BötC) can produce either phasic or tonic excitation of phrenic nerve discharge during hyperoxic normocapnia. Breathing, however, is influenced by input from both central and peripheral chemoreceptor activation. This influence of increased respiratory network drive on pre-BötC-induced modulation of phrenic motor output is unclear. Therefore, these experiments were designed to examine the effects of chemical stimulation of neurons (DLH; 10 mM; 10–20 nl) in the pre-BötC during hyperoxic modulation of CO2 (i.e., hypercapnia and hypocapnia) and during normocapnic hypoxia in chloralose-anesthetized, vagotomized, mechanically ventilated cats. For these experiments, sites were selected in which unilateral microinjection of DLH into the pre-BötC during baseline conditions of hyperoxic normocapnia [arterial Pco 2 (PaCO2 ) = 37–43 mmHg; n = 22] produced a tonic (nonphasic) excitation of phrenic nerve discharge. During hypercapnia (PaCO2 = 59.7 ± 2.8 mmHg; n= 17), similar microinjection produced excitation in which phasic respiratory bursts were superimposed on varying levels of tonic discharge. These DLH-induced phasic respiratory bursts had an increased frequency compared with the preinjection baseline frequency ( P < 0.01). In contrast, during hypocapnia (PaCO2 = 29.4 ± 1.5 mmHg; n= 11), microinjection of DLH produced nonphasic tonic excitation of phrenic nerve discharge that was less robust than the initial (normocapnic) response (i.e., decreased amplitude). During normocapnic hypoxia (PaCO2 = 38.5 ± 3.7; arterial Po 2 = 38.4 ± 4.4; n= 8) microinjection of DLH produced phrenic excitation similar to that seen during hypercapnia (i.e., increased frequency of phasic respiratory bursts superimposed on tonic discharge). These findings demonstrate that phrenic motor activity evoked by chemical stimulation of the pre-BötC is influenced by and integrates with modulation of respiratory network drive mediated by input from central and peripheral chemoreceptors.


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.


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