The effects of sympathetic and parasympathetic stimulation on the heart rate in frogs were tested after hearts were reinnervated with a somatic motor nerve. When frogs were vagotomized and hypoglossal axons were redirected to the heart for 8 or more weeks, stimulating the redirected hypoglossus nerve produced a parasympathetic-like inhibition of the heart. Stimulating sympathetic rami of the anastomosed hypoglossus nerve produced cardiac acceleration. Individual parasympathetic neurones received synaptic input from hypoglossal terminals. The excitatory post-synaptic potentials evoked by hypoglossal stimulation were much smaller than those evoked by vagal stimulation in control or vagal-reinnervated ganglia. However, hypoglossal axons innervated most (71%) of the ganglion cells and this level of innervation persisted for at least 60 weeks. Hypoglossal axons formed networks of varicose terminals within cardiac ganglia and established axo-axonic synapses with parasympathetic neurones. Hypoglossal terminals did not reinnervate the neuronal perikarya, in contrast to vagal axons in control or vagal-reinnervated ganglia. Axo-axonic synapses from redirected hypoglossal axons were identified in cardiac ganglia by bathing isolated hearts in horseradish peroxidase (HRP) and stimulating the redirected nerve. Electron micrographs showed that axo-axonic synapses contained HRP-labelled presynaptic vesicles. The source of foreign innervation in experimental cardiac ganglia was confirmed to be hypoglossal motoneurones (a), by comparing the conduction velocity of the redirected presynaptic axons (1.32 m/sec) with regenerating vagal preganglionic fibres ( < 0.3 m/sec), and (b), by retrograde HRP-labelling of large motoneurones in the hypoglossal nucleus after applying peroxidase to the axons which had grown into the heart.
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