Fos induction in rat brain neurons after stimulation of the hepatoportal Na-sensitive mechanism

1997 ◽  
Vol 272 (3) ◽  
pp. R913-R923 ◽  
Author(s):  
H. Morita ◽  
Y. Yamashita ◽  
Y. Nishida ◽  
M. Tokuda ◽  
O. Hatase ◽  
...  

Responses of hepatic afferent nerves to intraportal bolus injection of hypertonic solutions were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to an intraportal injection of 0.75 M NaCl or NaHCO3 but did not respond to a similar injection of 1.5 M mannitol, 0.75 M LiCl, or 0.15 M NaCl, implying that nerves in the hepatoportal area are sensitive to increases in Na concentrations and that this leads to stimulation of hepatic afferent nerve activity. To study central activation in response to stimulation of the hepatic Na-sensitive mechanism, c-fos induction was monitored. After electrical stimulation of hepatic afferent nerves, neurons containing Fos-like immunoreactivity (Fos-li) were found in the area postrema, nucleus of the solitary tract, paraventricular hypothalamic nucleus, and supraoptic nucleus at 90 min after stimulation. Induction of Fos-li was also studied after simultaneous infusion of 0.45 M NaCl into the portal vein and distilled water into the inferior vena cava in conscious rats so as to keep the total amount of solution introduced into the systemic circulation isotonic, thus avoiding changes in mean arterial pressure, plasma osmolality, and plasma NaCl concentrations. Fos-li-containing neurons were found in the same regions in which they were found after electrical stimulation. However, few, if any, Fos-li-containing cells were found if the rats were hepatically denervated or if they received an intraportal infusion of hypertonic LiCl or mannitol. These data provide evidence for involvement of the brain stem and forebrain structures in NaCl regulatory functions induced by stimulation of the hepatoportal Na-sensitive mechanism. However, stimulation of the hepatoportal osmosensitive mechanism does not activate these central structures.

1988 ◽  
Vol 118 (3) ◽  
pp. 471-483 ◽  
Author(s):  
L. M. Voloschin ◽  
E. Décima ◽  
J. H. Tramezzani

ABSTRACT Electrical stimulation of the XIII thoracic nerve (the 'mammary nerve') causes milk ejection and the release of prolactin and other hormones. We have analysed the route of the suckling stimulus at the level of different subgroups of fibres of the teat branch of the XIII thoracic nerve (TBTN), which innervates the nipple and surrounding skin, and assessed the micromorphology of the TBTN in relation to lactation. There were 844 ± 63 and 868 ± 141 (s.e.m.) nerve fibres in the TBTN (85% non-myelinated) in virgin and lactating rats respectively. Non-myelinated fibres were enlarged in lactating rats; the modal value being 0·3–0·4 μm2 for virgin and 0·4–0·5 μm2 for lactating rats (P > 0·001; Kolmogorov–Smirnov test). The modal value for myelinated fibres was 3–6 μm2 in both groups. The compound action potential of the TBTN in response to electrical stimulation showed two early volleys produced by the Aα- and Aδ-subgroups of myelinated fibres (conduction velocity rate of 60 and 14 m/s respectively), and a late third volley originated in non-myelinated fibres ('C') group; conduction velocity rate 1·4 m/s). Before milk ejection the suckling pups caused 'double bursts' of fibre activity in the Aδ fibres of the TBTN. Each 'double burst' consisted of low amplitude action potentials and comprised two multiple discharges (33–37 ms each) separated by a silent period of around 35 ms. The 'double bursts' occurred at a frequency of 3–4/s, were triggered by the stimulation of the nipple and were related to fast cheek movements visible only by watching the pups closely. In contrast, the Aα fibres of the TBTN showed brief bursts of high amplitude potentials before milk ejection. These were triggered by the stimulation of cutaneous receptors during gross slow sucking motions of the pup (jaw movements). Immediately before the triggering of milk ejection the mother was always asleep and a low nerve activity was recorded in the TBTN at this time. When reflex milk ejection occurred, the mother woke and a brisk increase in nerve activity was detected; this decreased when milk ejection was accomplished. In conscious rats the double-burst type of discharges in Aδ fibres was not observed, possibly because this activity cannot be detected by the recording methods currently employed in conscious animals. During milk ejection, action potentials of high amplitude were conveyed in the Aα fibres of the TBTN. During the treading time of the stretch reaction (SR), a brisk increase in activity occurred in larger fibres; during the stretching periods of the SR a burst-type discharge was again observed in slow-conducting afferents; when the pups changed nipple an abrupt increase in activity occurred in larger fibres. In summary, the non-myelinated fibres of the TBTN are increased in diameter during lactation, and the pattern of suckling-evoked nerve activity in myelinated fibres showed that (a) the double burst of Aδ fibres, produced by individual sucks before milk ejection, could be one of the conditions required for the triggering of the reflex, and (b) the nerve activity displayed during milk-ejection action may result, at least in part, from 'non-specific' stimulation of cutaneous receptors. J. Endocr. (1988) 118, 471–483


1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.


1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.


The observations with which the present communication deals were met with in experiments continuing those on reciprocal innervation of symmetrical muscles. In my previous paper on that subject it had been reported that in regard to symmetrical extensors of the knee the ratio borne by intensity of the ipsilateral inhibition to the contralateral excitation is such that with equal stimuli to right and left symmetrical afferent nerves there is inhibitory suppression of contraction in both the muscles. In other words, under double reciprocal innervation the ipsilateral inhibition by each nerve completely overcomes the contralateral excitation of the other. It was shown that this mutual suppression holds over a wide range of the scale of intensities of stimulation. It was also shown that with quite weak stimuli a simultaneous stimulation of both nerves, stimuli being equal in intensity, often results in concurrent contraction of both muscles. Indeed, with quite weak stimuli, the effect of stimulation of each afferent nerve by itself is, in the decerebrate preparation, usually contraction of the ipsilateral as well as of the contralateral muscle. This being so, it is evident that at some point in the scale of intensities of stimulation there should be a place below which contralateral excitation is stronger than ipsilateral inhibition, whereas above it ipsilateral inhibition is stronger than contralateral excitation.


1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.


1978 ◽  
Vol 234 (3) ◽  
pp. H223-H229
Author(s):  
S. M. Barman ◽  
R. D. Wurster

With the use of computer-aided techniques, the interaction of descending spinal sympathetic pathways and afferent nerve fibers (cervical dorsal roots and tibial nerve) in regulation of thoracic (T2) preganglionic nerve activity was investigated in anesthetized, vagotomized, and paralyzed cats. High-frequency activation of a sympathoinhibitory pathway (ventrolateral funiculus) depressed the evoked discharges in the T2 preganglionic nerve elicited by stimulation of a sympathoexcitatory pathway (dorsolateral funiculus) and the spinal component of the somatosympathetic reflex. Submaximal evoked responses were also inhibited through baroreceptor reflex activation (blood pressure elevations up to 225 mmHg). Facilitation of the spinal component of the somatosympathetic reflex occurred during stimulation of the excitatory pathway. Carotid occlusion (baroreceptor inactivation) facilitated the submaximal evoked discharges from stimulation of the descending excitatory pathway. These data support the contention that sympathetic nerve activity can be modified by the integration of excitatory and inhibitory impulses at the spinal level.


1993 ◽  
Vol 264 (4) ◽  
pp. H1087-H1092
Author(s):  
F. W. Leung

The hypothesis that intravenous nicotine modulates gastric spinal afferent nerve function by its ganglionic-blocking property is tested. Stimulation of the gastric spinal afferent nerves in anesthetized rats is accomplished by intragastric capsaicin irrigation. Gastric blood flow is monitored by laser-Doppler flowmetry. The increase in gastric blood flow during intragastric capsaicin irrigation is significantly reduced by 4 and 40 micrograms.kg-1.min-1 of intravenous nicotine. The inhibition appears to be specific for the spinal afferent nerves as the increase in gastric blood flow induced by electrical stimulation of the vagal afferent nerves is unaltered by these doses of intravenous nicotine. A ganglionic-blocking dose (10 mg/kg) of intraperitoneal hexamethonium also significantly attenuates the gastric vasodilatory effect of intragastric capsaicin. Intravenous nicotine (40 micrograms.kg-1.min-1) combined with intraperitoneal hexamethonium (10 mg/kg) completely abolishes the gastric vasodilatory effect of intragastric capsaicin. These data suggest that intravenous nicotine offers a specific inhibition of the gastric spinal afferent nerve-mediated hyperemia, possibly as a consequence of its ganglionic-blocking property.


1987 ◽  
Vol 253 (1) ◽  
pp. H91-H99 ◽  
Author(s):  
E. M. Hasser ◽  
D. O. Nelson ◽  
J. R. Haywood ◽  
V. S. Bishop

This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.


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