Structure of the neurons of the sympathetic ganglia in guanethidine chemical sympathectomy

As demonstrated the investigation of cell composition of the cranial cervical, cervico-thoracic and the 3d thoracic ganglia of the sympathetic trunk in mature Wistar rats under guanethidine chemical sympathectomy, there are intraganglionic reconstructions and changes in the value of the subpopulations of neurocytes in the preserved cell population. Ratio of the neuronal subpopulations studied with various character of changes revealed adaptive-compensatory processes, developing in the course of sympathectomy at the level of population. The ways of realization of the populational and cellular levels of compensation are considered. The wavy character of sympathectomy is thought to reflect integral behavior of the nervous cells subpopulation in the course of development of homeostatic reactions.     

Histochemical evidence of chemical sympathectomy by guanethidine in newborn rats

Synopsis Guanethidine is known to cause a loss of catecholamines from sympathetically innervated tissues and sympathetic ganglia in adult animals but its effect on newborn animals has not been examined.Newborn rats were injected daily with guanethidine (20 mg/kg body weight) for 8 days. They were killed when 1 month-old along with untreated litter mate controls. Catecholamines were demonstrated in the iris, in the pineal body and in sympathetic ganglia, using the formaldehyde-induced fluorescence method.In the guanethidine-treated rats there was a complete loss of fluorescent nerve fibres from the pineal body and an almost complete loss of similar fibres from the iris. The sympathetic ganglia were reduced to less than 10% of the control ganglia, and the number of nerve cell bodies per unit area was decreased in the ganglion remnants.It is concluded that guanethidine causes, in newborn rats, an irreversible destruction of most sympathetic neurons, i.e. a chemical sympathectomy closely resembling that obtainable in newborn animals by injections of 6-hydroxydopamine or antiserum to nerve growth factor.     

Morphometric and biochemical evaluation of rat prostate and seminal vesicle following chemical sympathectomy with guanethidine.

Selective chemical sympathectomy of the internal genital organs of adult male rats was undertaken by chronic treatment with low doses of guanethidine. Biochemical and morphometric methods revealed that removal of sympathetic innervation prevents fructose secretion in the prostate and seminal vesicle, in addition to promoting reduced efficiency of delivery by the latter.     

Effect of guanethidine sympathectomy on cardiac functions in rat pups

Catecholamine level in the blood, heart and adrenal tissues, and heart sensitivity to catecholamines were determined in 3-week-old rats after chemical sympathectomy. It was shown that tachycardia in sympathectomy rats was caused by increased heart sensitivity to catecholamines due to the reduction in their concentration.     

Age changes in rat vasomotor reflexes and sympathetic neuron ultrastructure following chemical sympathectomy]

Prolonged administration of guanethidine (20 mg/kg) to newborn rats caused a marked reduction in the number of cells in stellate ganglia. The administration of guanethidine for 14 days decreased the amount of cells to 30% of the normal (partial sympathectomy), and for 28 days--to 0.5% (complete sympathectomy). At the age of two months the blood pressure pressor reflexes to asphyxia and femoral nerve stimulation were absent in both groups of the sympathectomized animals. These responses, however, were restored in the partially sympathectomized animals at the age of four months. No restoration took place in the completely sympathectomized animals. The electron microscopic studies of neurons in the partially sympathectomized animals showed the presence of a great number of neurofibrils. According to literature data this fact was typical of cells in which an active growth of axon fibers took place.     

Effect of chemical carcinogens on the synaptic transmission of excitation in the sympathetic ganglia of rats

Acute experiments on rats were performed to study the influence of water-soluble chemical carcinogens on synaptic transmission via the inferior mesenteric sympathetic ganglion. Synaptic transmission was studied before and after intravenous injection of the enterotropic carcinogen 1,2-dimethylhydrazine (DMH) and N-nitrosomethylurea (NMU) which induces the development of mammary gland tumors. Despite the different chemical structure and specificity of the action of the carcinogens used on one or another target tissue, their influence on synaptic transmission via the sympathetic ganglia was of identical character, manifested by the blocking action on transmission of nerve impulses. Comparison of the action of DMH and NMU on synaptic transmission with the influence of some other pharmacological substances suggests that the mechanism of the inhibitory action of the carcinogens on synaptic transmission via the sympathetic ganglia may be linked both with cholinolytic and adrenomimetic influences of the carcinogens.     

Effects of infantile/prepubertal chronic estrogen treatment and chemical sympathectomy with guanethidine on developing cholinergic nerves of the rat uterus.

The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic chemical sympathectomy with guanethidine, and combined sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistochemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.