ABSTRACT
The local surgical manipulation of sympathetic and parasympathetic nerves innervating the thyroid-parathyroid territory was employed to search for the existence of a peripheral neuroendocrine link controlling parathyroid hormone (PTH) and calcitonin (CT) release. From 8 to 24 h after superior cervical ganglionectomy (SCGx), at the time of wallerian degeneration of thyroid-parathyroid sympathetic nerve terminals, an alpha-adrenergic inhibition, together with a minor beta-adrenergic stimulation, of hypercalcemia-induced CT release, and an alpha-adrenoceptor inhibition of hypocalcemia-induced PTH release were found. In chronically SCGx rats PTH response to EDTA was slower, and after CaCl2 injection, serum calcium attained higher levels in face of normal CT levels. SCGx blocked the PTH increase found in sham-operated rats stressed by a subcutaneous injection of turpentine oil, but did not affect the greater response to EDTA. The higher hypocalcemia seen after turpentine oil was no longer observed in SCGx rats. The effects of turpentine oil stress on calcium and CT responses to a bolus injection of CaCl2 persisted in rats subjected to SCGx 14 days earlier. Interruption of thyroid-parathyroid parasympathetic input conveyed by the thyroid nerves (TN) and the inferior laryngeal nerves (ILN) caused a fall in total serum calcium, an increase of PTH levels and a decrease of CT levels, when measured 10 days after surgery. Greater responses of serum CT and PTH were detected in TN-sectioned, and in TN- or ILN-sectioned rats, respectively. Physiological concentrations of CT decreased, and those of PTH increased, in vitro cholinergic activity in rat SCG, measured as specific choline uptake, and acetylcholine synthesis and release. The results indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis.
Subject(s)
Autonomic Nervous System/physiology , Calcium/metabolism , Animals , Calcitonin/physiology , Ganglia, Sympathetic/physiology , Homeostasis , Parathyroid Glands/innervation , Parathyroid Hormone/physiology , Rats , Stress, Physiological/metabolism , Turpentine/toxicityABSTRACT
Cerebellar morphogenesis as well as somatometric parameters of progenies from mothers exposed to ethyl-ether, chloroform, turpentine or thinner were registered a 24, 48 and 7 hours of age. 1. Mortality rate of 20 and 59% was observed in progenies of thinner or turpentine exposed mothers, correspondingly. 2. Delay of intrauterine growth manifested by body weight, size and cephalic diameter was evident in chloroform exposed groups (P < 0.01). 3. Cerebellar maturation delay was found in thinner or turpentine prenatally exposed litters. 4. The number of Purkinje cells was significantly reduced in ethyl-ether and chloroform exposed groups (P < 0.01). These cells were found less affected by thinner or turpentine exposure (P < 0.01).
Subject(s)
Abnormalities, Drug-Induced/etiology , Cerebellar Diseases/chemically induced , Fetal Growth Retardation/chemically induced , Pregnancy, Animal/drug effects , Solvents/toxicity , Administration, Inhalation , Animals , Animals, Newborn , Cephalometry , Cerebellar Diseases/embryology , Cerebellar Diseases/pathology , Chloroform/administration & dosage , Chloroform/toxicity , Ether/administration & dosage , Ether/toxicity , Female , Male , Maternal-Fetal Exchange , Pharmaceutical Vehicles/administration & dosage , Pharmaceutical Vehicles/toxicity , Pregnancy , Purkinje Cells/drug effects , Purkinje Cells/pathology , Rats , Rats, Sprague-Dawley/embryology , Solvents/administration & dosage , Turpentine/administration & dosage , Turpentine/toxicityABSTRACT
1. Turpentine and thinner exposed rats, during the last stage of pregnancy, delivered 59% and 20% of dead newborn, respectively. 2. Turpentine and thinner delayed foetal growth and caused no effects on neonates body size. 3. Cerebral cortex of newborn rats, prenatally exposed to organic solvents showed to histological alterations.