Degeneration activity of the pineal gland after sympathetic denervation

Luchelli-Fortis, M. A.; Stefano, F. J. E.; Perec, Carlos J.

doi:10.1007/bf00498517

Cited by 9 publications

(4 citation statements)

References 13 publications

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“…The present results, to gether with prior data indicating that melatonin [II,20,28], FSH [10], LH [10], TSH [6], thyroxine [6,25], oxytocin [19] and parathyroid hormone release [5] can be affected by SCGx, strengthen the concept that cervical sympathetic neurons play a significant role in neuroendocrine regula tion in rodents [7],…”

Section: Discussionsupporting

confidence: 71%

Changes in Calcitonin Release during Sympathetic Nerve Degeneration after Superior Cervical Ganglionectomy of Rats

Cardinali¹,

Sartorio²,

Ladizesky³

et al. 1986

Neuroendocrinology

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To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16–28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter that accompanies anterograde degeneration of nerve varicosities as well as during the neural paralysis that ensues thereafter. At the time intervals examined, SCGx did not result in significant changes of basal serum calcitonin or Ca levels. The intraperitoneal administration of CaCI₂ brought about an impending increase of serum Ca to the same extent in SCGx and sham-operated rats. A significant depression of calcitonin release was observed in rats killed around the time of nerve terminal degeneration (16–21 h post SCGx) but not about 10 h later. Additionally a delay to achieve a maximal calcitonin response was apparent during nerve degeneration. Injection of the α-adrenoceptor blocker phenoxybenzamine significantly increased basal calcitonin levels and restored the depressed calcitonin response to hypercalcemia seen in SCGx rats. Treatment with the β-adrenoceptor blocker propranolol counteracted phenoxybenzamine activity but was unable to modify per se calcitonin release in SCGx or sham-operated rats. Basal Ca levels and their increase after intraperitoneal CaCl₂ were similar in all examined groups regardless of the drug injected. In an additional experiment phenoxybenzamine injected into SCGx rats in doses one-fifth those employed earlier still reversed both the depression in maximal calcitonin response as well as the delay to attain maximal release after CaCl₂, but was unable to affect basal calcitonin levels. These results indicate that at the time of nerve terminal degeneration in the superior cervical ganglion territory there is a depression in C cell response to hypercalcemia. An α-adrenoceptor-mediated inhibitory influence of neropinephrine as well as a less important β-adrenoceptor-mediated stimulatory influence of the sympathetic transmitter may explain the observed results.

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Section: Discussionsupporting

confidence: 71%

Changes in Calcitonin Release during Sympathetic Nerve Degeneration after Superior Cervical Ganglionectomy of Rats

Cardinali¹,

Sartorio²,

Ladizesky³

et al. 1986

Neuroendocrinology

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“…administration of melatonin. Superior cervical ganglionectomy has been shown to deplete the amount of noradrenaline in the pineal gland [16] and to abolish the circadian fluctuation of plasma melatonin [17,18]. In the present experiment, superior cervical ganglionectomy also reduced urinary excretion of 6-sulfatoxymelatonin (a main urinary melatonin metabolite).…”

Section: Discussionsupporting

confidence: 56%

Interleukin-1β-Induced Increases of Plasma Catecholamine Levels in Rats: Enhancement by Superior Cervical Ganglionectomy

Wang¹,

Murakami²,

Okada³

et al. 2002

Pharmacology

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In urethane-anesthetized rats, we examined the effect of bilateral superior cervical ganglionectomy on interleukin-1β (IL-1β)-induced elevation of plasma catecholamines. In sham-operated rats, intracerebroventricularly (i.c.v.) administered IL-1β (100 ng/animal) effectively elevated plasma noradrenaline rather than plasma adrenaline. In superior cervical ganglionectomized rats, however, IL-1β significantly elevated adrenaline to a greater extent than noradrenaline, and they were attenuated by i.c.v. administration of melatonin (100 ng/animal). Superior cervical ganglionectomy effectively reduced the plasma level of melatonin and urinary excretion of 6-sulfatoxymelatonin (a main urinary melatonin metabolite). These results suggest that superior cervical ganglia inhibit central sympatho-adrenomedullary outflow (especially adrenomedullary outflow) by increasing melatonin synthesis in the pineal gland of rats.

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“…So the reduction of CBF could be attributed to many factors after sympathectomy: decrease in the thickness of the turnica media of the cerebral vessels [19], a modification of membrane mechanisms of the smooth muscle fibers [20], depolarization without any possible modification in the threshold of excitability, a hypersensitivity to calcium ion, and possible metabolic changes revealed by a decrease in sodium-potassium-adenosine triphosphatase activity and modification in the level of adenosine triphosphate [18]. Suppression of the whole cervical sympathetic innervation could also result in a reduction in pineal gland activity [21], alterations in the numerous neuroendocrine systems [22], or a modification in the activity of the carotid sinus [23]. Some of these phenomena may modify CBF and CBV in the long term.…”

Section: Discussionmentioning

confidence: 99%

Role of the Peripheral Sympathetic Innervations in Controlling Cerebral Blood Flow after the Transection of Bilateral Superior Cervical Sympathetic Ganglia Two Weeks Later

Hsieh¹,

Shinn-Zong²,

Liu³

2011

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Background: Cerebral blood vessels are mainly supplied by sympathetic nerves arising from the superior cervical ganglia and cerebral blood volume may be influenced by bilateral superior cervical ganglionectomy (SCG). Various stages of cerebral blood volume changes depended on the time following bilateral excision of SCG. In this study, we emphasize the subacute effect (two weeks) on the local cerebral blood flow (LCBF). Material and Methods: Sprague-Dawley rats weighing 250 ~ 400 gm (n = 20) were selected into two groups. Under the ambient temperature 20oC, the first group animals (n = 10) received sham operation and the other group animals (n = 10) underwent bilateral SCG. The LCBF and O2 delivery of 14 brain struc-tures were measured for each animal by the use of 14C-iodoantipyrine technique two weeks after the opera-tion. Results: The average of LCBF was decreased from 150 ml/100 gm/min to 129 ml/100 gm/min after bi-lateral SCG. Only the LCBF at basal ganglia was increased from 108 ml/min/100 g in the sham-operated group to 118 ml/min/100g in the SCG group. A mean of 14% reduction of LCBF was estimated. In 14 brain structures, the delivery amount of O2 was all decreased, except in basal ganglia. However, these changes of LCBF and the delivery amount of O2 at these 14 brain structures did not reach the significant differences. Conclusions: The present results show that chronic effect (two weeks) of bilateral SCG on LCBF was not only in a decrease of the LCBF, but also a decrease of local cerebral O2 delivery. However, the changes didn’t show the significant differences

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Degeneration activity of the pineal gland after sympathetic denervation

Cited by 9 publications

References 13 publications

Changes in Calcitonin Release during Sympathetic Nerve Degeneration after Superior Cervical Ganglionectomy of Rats

Changes in Calcitonin Release during Sympathetic Nerve Degeneration after Superior Cervical Ganglionectomy of Rats

Interleukin-1β-Induced Increases of Plasma Catecholamine Levels in Rats: Enhancement by Superior Cervical Ganglionectomy

Role of the Peripheral Sympathetic Innervations in Controlling Cerebral Blood Flow after the Transection of Bilateral Superior Cervical Sympathetic Ganglia Two Weeks Later

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