Effects of gastric distension and electrical stimulation of dorsomedial medulla on neurons in parabrachial nucleus of rats

1994 ◽  
Vol 48 (3) ◽  
pp. 221-229 ◽  
Author(s):  
Kazuhiko Suemori ◽  
Motoi Kobashi ◽  
Akira Adachi
1988 ◽  
Vol 254 (4) ◽  
pp. E468-E475
Author(s):  
T. Fujiwara ◽  
K. Nagai ◽  
S. Takagi ◽  
H. Nakagawa

Electrical stimulation of the lateral part of the dorsal parabrachial nucleus (PBD) induces hyperglycemia by enhancing glucagon secretion and suppressing insulin secretion in rats. The mechanism of this effect in the light period was examined by use of blockers of the autonomic nervous system. Hexamethonium, a ganglion blocker, and propranolol, a beta-adrenergic blocker, markedly inhibited the hyperglycemic response to stimulation of the lateral part of the PBD (LPBD). In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine methylnitrate, a muscarinic blocker, had no effect. Because previous studies showed that bilateral lesions of the suprachiasmatic nucleus (SCN) eliminated hyperglycemia induced by intracranial injection of 2-deoxy-D-glucose and that blinding largely suppressed the hyperglycemia, the effects of these two treatments on hyperglycemia induced by electrical stimulation of the LPBD were examined. SCN lesions abolished the hyperglycemic response but did not affect the hyperglucagonemic response. Results 4 wk after orbital enucleation were similar to those after SCN lesions. These findings suggest that the SCN and a beta-adrenergic mechanism are involved in the hyperglycemic response to LPBD stimulation.


2016 ◽  
Vol 306 ◽  
pp. 20-25 ◽  
Author(s):  
Fanuel Muindi ◽  
Jonathan D. Kenny ◽  
Norman E. Taylor ◽  
Ken Solt ◽  
Matthew A. Wilson ◽  
...  

1987 ◽  
Vol 3 (3) ◽  
pp. 209-216 ◽  
Author(s):  
Hidetoshi INO ◽  
Katsuya NAGAI ◽  
Tsutomu FUJIWARA ◽  
Mariko YAMANO ◽  
Shinobu INAGAKI ◽  
...  

1985 ◽  
Vol 341 (2) ◽  
pp. 283-296 ◽  
Author(s):  
Sima Mraovitch ◽  
Costantino Iadecola ◽  
David A. Ruggiero ◽  
Donald J. Reis

2002 ◽  
Vol 87 (4) ◽  
pp. 1981-1992 ◽  
Author(s):  
Young K. Cho ◽  
Cheng-Shu Li ◽  
David V. Smith

Gustatory responses in the brain stem are modifiable by several physiological factors, including blood insulin and glucose, intraduodenal lipids, gastric distension, and learning, although the neural substrates for these modulatory effects are not known. Stimulation of the lateral hypothalamus (LH) produces increases in food intake and alterations in taste preference behavior, whereas damage to this area has opposite effects. In the present study, we investigated the effects of LH stimulation on the neural activity of taste-responsive cells in the nucleus of the solitary tract (NST) of the hamster. Bipolar stimulating electrodes were bilaterally implanted in the LH, and the responses of 99 neurons in the NST, which were first characterized for their taste sensitivities, were tested for their response to both ipsilateral and contralateral LH stimulation. Half of the taste-responsive cells in the NST (49/99) were modulated by LH stimulation. Contralateral stimulation was more often effective (41 cells) than ipsilateral (13 cells) and always excitatory; 10 cells were excited bilaterally. Six cells were inhibited by ipsilateral stimulation. A subset of these cells ( n = 13) was examined for the effects of microinjection of dl-homocysteic acid (DLH), a glutamate receptor agonist, into the LH. The effects of electrical stimulation were completely mimicked by DLH, indicating that cell somata in and around the LH are responsible for these effects. Other cells ( n = 14) were tested for the effects of electrical stimulation of the LH on the responses to stimulation of the tongue with 0.032 M sucrose, NaCl, and quinine hydrochloride, and 0.0032 M citric acid. Responses to taste stimuli were more than doubled by the excitatory influence of the LH. These data show that the LH, in addition to its role in feeding and metabolism, exerts descending control over the processing of gustatory information through the brain stem.


1985 ◽  
Vol 248 (1) ◽  
pp. R38-R45 ◽  
Author(s):  
D. F. Cechetto ◽  
F. R. Calaresu

It has been suggested that cardiovascular information to the amygdala is relayed through the paraventricular nucleus of the hypothalamus (PVH) and the parabrachial nucleus (PB;7). To test this possibility spontaneously firing units in the amygdala of 12 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of PVH and PB and for their responsiveness to baroreceptor (BA) and chemoreceptor (CA) activation. In the ipsilateral amygdala 27 of 140 units responded to PVH stimulation, 9 of which also responded to CA and none to BA, whereas 46 of 150 units responded to PB stimulation, 11 of which also responded to CA and 2 to BA. To demonstrate the relative contribution of the PVH and PB in relaying cardiovascular information to the amygdala, in an additional six cats, the effect of neuronal block and lesions of these two nuclei on potentials evoked in the amygdala by stimulation of the buffer nerves was tested. Reversible neuronal block with injections of procaine in the PB significantly attenuated these evoked potentials. Electrolytic and chemical (kainic acid) lesions in the same PB sites also were effective in attenuating the responses. The potentials were unaltered by injection of procaine in the PVH. These results indicate that the PB is a site of relay of chemoreceptor and of some baroreceptor information from the medulla to the amygdala.


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