No abstract

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.

No abstract

1. During normoxia, heart rate was governed by a vagal tone which increased at higher acclimation temperatures. This tonic influence was exerted predominantly via the branchial cardiac nerves. The increase in heart rate following atropinization or cardiac vagotomy was associated with a reduction in stroke flow in the ventral aorta in accordance with Starling's Law of the heart. 2. During slowly induced hypoxia there was a reflex bradycardia, the onset and extent of which varied with acclimation temperature, and which was mediated predominantly via the pair of branchial cardiac vagi. The branchial cardiac vagi were also wholely responsible for the transient marked bradycardia at the onset of rapidly induced hypoxia. 3. Direct measurement of blood flow to the anterior two pairs of branchial arteries demonstrated that they received approximately 37% of total cardiac output in normoxia and that this proportion was unchanged during hypoxia. 4. The bradycardia during hypoxia in control animals was partially offset by a rise in cardiac stroke volume so that cardiac output decreased slightly. Injection of the adrenergic -receptor blocker, Propranolol, abolished the increase in stroke flow during hypoxia, but did not effect the bradycardia, and the total blood flow was therefore reduced. 5. The values of PO2 during hypoxia from fish acclimated to 17 °C were significantly reduced from the control values following atropinization and either branchial cardiac vagotomy or total cardiac vagotomy. 6. The apparent power output of the heart was reduced during hypoxia at high acclimation temperatures due to the marked bradycardia.

Experiments involving supra-maximal electrical stimulation of the vagus have indicated that the stimulation of the peripheral cut ends of the branchial cardiac branches produces a more intense cardio-inhibition than the stimulation of visceral cardiac branches. It is suggested that the visceral cardiac branches may have a mainly sensory function. In no case could cardioacceleration be obtained during vagal stimulation either before or after injection of atropine, and any increases in stroke volume that occurred accompanied reductions in heart rate. This relationship was considered to be a manifestation of Starling's Law of the heart and it has been concluded that there is no augmentary sympathetic innervation to the dogfish heart. Evidence also indicates that the Starling relationship is responsible for the increase in stroke volume which accompanies the bradycardia during hypoxia. Circulating catecholamines do not appear to be of importance in this response although they are concerned in cardio-vascular regulation during normoxia.