scholarly journals Cardiovascular and respiratory effects of stimulation of cell bodies of the parabrachial nuclei in the anaesthetized rat.

1994 ◽  
Vol 477 (2) ◽  
pp. 321-329 ◽  
Author(s):  
J P Lara ◽  
M J Parkes ◽  
L Silva-Carvhalo ◽  
P Izzo ◽  
M S Dawid-Milner ◽  
...  
1983 ◽  
Vol 245 (6) ◽  
pp. R811-R819 ◽  
Author(s):  
D. F. Cechetto ◽  
F. R. Calaresu

Spontaneously firing units in the region of parabrachial nuclei (PB) and Kolliker-Fuse nuclei (KF) of 19 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves, of central nucleus of the amygdala (ACE), and of paraventricular nuclei of the hypothalamus (PVH). In the ipsilateral PB 64 of 189 and in the contralateral PB 9 of 103 units responded to CSN stimulation; 18 of 185 ipsilaterally and 7 of 97 contralaterally responded to ADN stimulation. Responses were primarily excitatory, and units were located primarily in the ventrolateral portion of the PB. Only 9 of 267 units responded to stimulation of both CSN and ADN. Stimulation of the ACE and PVH antidromically activated 9 and 7 units, respectively, in PB and approximately half of these also responded to buffer nerve stimulation. In the ipsilateral PB 56 of 207 and in the contralateral PB 11 of 103 units responded orthodromically to ACE stimulation, and 23 of 177 ipsilaterally and 2 of 103 contralaterally responded orthodromically to PVH stimulation with primarily excitatory responses and were located primarily in the ventrolateral portion of the PB and KF. Of these units approximately half also responded to buffer nerve stimulation. These results suggest an important role for PB-KF in mediating ascending and descending cardiovascular and respiratory control signals.


1993 ◽  
Vol 43 ◽  
pp. 104
Author(s):  
G. Raimondi ◽  
J.M. Legramante ◽  
S. Cassarino ◽  
S. Forlani ◽  
F. Bellegrandi ◽  
...  

1982 ◽  
Vol 53 (4) ◽  
pp. 805-814 ◽  
Author(s):  
S. F. Al-Shway ◽  
J. P. Mortola

Kittens, puppies, cats, and dogs were anesthetized with pentobarbital sodium and tracheotomized. The ventilatory pattern was recorded before, during, and after the delivery of steady flows of room air of 20 or 50 ml X s-1 X kg-1 in the expiratory direction through a cannula inserted just below the larynx. In the newborn, a reduction in breathing frequency, mainly due to a prolongation of the expiratory time, and a decrease in tidal volume contributed to a reduction in minute ventilation particularly with the higher flows; in some instances apnea resulted. Small or no effects were observed in the adult. The ventilatory inhibition was still present when humidified 37 degrees C warmed airstreams were delivered, and it was unchanged when airflows of 4.9% CO21.5% O2–82.6% N2 were applied. After local anesthesia of the laryngeal region or after bypassing the larynx, the ventilatory inhibition disappeared. By closure of a nostril at any given airflow, the upper airway pressure was substantially increased; however, this maneuver did not enhance the respiratory depression. We conclude that airflow through the upper airways can inhibit ventilation in newborn kittens and puppies presumably through the stimulation of airflow-sensitive laryngeal receptors.


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.


2015 ◽  
Vol 113 (10) ◽  
pp. 3778-3786 ◽  
Author(s):  
Cheng-Shu Li ◽  
Da-Peng Lu ◽  
Young K. Cho

The nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN) are the first and second relays in the rodent central taste pathway. A series of electrophysiological experiments revealed that spontaneous and taste-evoked activities of brain stem gustatory neurons are altered by descending input from multiple forebrain nuclei in the central taste pathway. The nucleus accumbens shell (NAcSh) is a key neural substrate of reward circuitry, but it has not been verified as a classical gustatory nucleus. A recent in vivo electrophysiological study demonstrated that the NAcSh modulates the spontaneous and gustatory activities of hamster pontine taste neurons. In the present study, we investigated whether activation of the NAcSh modulates gustatory responses of the NST neurons. Extracellular single-unit activity was recorded from medullary neurons in urethane-anesthetized hamsters. After taste response was confirmed by delivery of sucrose, NaCl, citric acid, and quinine hydrochloride to the anterior tongue, the NAcSh was stimulated bilaterally with concentric bipolar stimulating electrodes. Stimulation of the ipsilateral and contralateral NAcSh induced firings from 54 and 37 of 90 medullary taste neurons, respectively. Thirty cells were affected bilaterally. No inhibitory responses or antidromic invasion was observed after NAcSh activation. In the subset of taste cells tested, high-frequency electrical stimulation of the NAcSh during taste delivery enhanced taste-evoked neuronal firing. These results demonstrate that two-thirds of the medullary gustatory neurons are under excitatory descending influence from the NAcSh, which is a strong indication of communication between the gustatory pathway and the mesolimbic reward pathway.


2012 ◽  
Vol 108 (5) ◽  
pp. 1288-1298 ◽  
Author(s):  
Cheng-Shu Li ◽  
Sooyoung Chung ◽  
Da-Peng Lu ◽  
Young K. Cho

The parabrachial nuclei (PbN), the second central relay for the gustatory pathway, transfers taste information to various forebrain gustatory nuclei and to the gustatory cortex. The nucleus accumbens is one of the critical neural substrates of the reward system, and the nucleus accumbens shell region (NAcSh) is associated with feeding behavior. Taste-evoked neuronal responses of PbN neurons are modulated by descending projections from the gustatory nuclei in the forebrain. In the present study, we investigated whether taste-responsive neurons in the PbN project to the NAcSh and whether pontine gustatory neurons are subject to modulatory influence from the NAcSh in urethane-anesthetized hamsters. Extracellular single-unit activity was recorded in the PbN, and taste responses were confirmed by the delivery of 32 mM sucrose, NaCl, quinine hydrochloride, and 3.2 mM citric acid to the anterior tongue. The NAcSh was then stimulated (0.5 ms, ≤100 μA) bilaterally using concentric bipolar stimulating electrodes. A total of 98 taste neurons were recorded from the PbN. Eighteen neurons were antidromically invaded from the NAcSh, mostly the ipsilateral NAcSh ( n = 16). Stimulation of the ipsilateral and contralateral NAcSh suppressed the neuronal activity of 88 and 55 neurons, respectively; 52 cells were affected bilaterally. In a subset of pontine neurons tested, electrical stimulation of the NAcSh during taste stimulation also suppressed taste-evoked neuronal firing. These results demonstrated that taste-responsive neurons in the PbN not only project to the NAcSh but also are under substantial descending inhibitory influence from the bilateral NAcSh.


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