The sympathetic superior cervical ganglia (SCG) provide innervation through the internal carotid nerve to the pineal gland and median eminence, and through the external carotid nerve to the thyroid and parathyroid glands. Activation of autonomic fibers during anterograde degeneration of median eminence nerve terminals after superior cervical ganglionectomy (SCGx) was accompanied by depressions in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. Decreases in thyroid-stimulating hormone (TSH) and growth hormone release and increases in stress-induced adrenocorticotropic hormone (ACTH) and prolactin release were also found during nerve degeneration after SCGx. These effects were mediated by alpha-1-adrenoceptors and were, in general, independent of the presence of the pineal. In thyroid and parathyroid tissue, the following were observed during the wallerian degeneration phase after SCGx: (a) alpha-1-adrenoceptor inhibition of thyroxine release; (b) alpha-1-adrenoceptor inhibition, together with beta-adrenoceptor stimulation, of calcitonin release; and (c) alpha-1-adrenoceptor inhibition of parathyroid hormone release. Thyroid sympathetic nerves modulate compensatory thyroid growth. In rats subjected to cholinergic decentralization of the thyroid, an impaired goitrogenic and thyroid compensatory response was detectable. The results presented suggest that peripheral autonomic nerves constitute a parallel pathway through which the brain communicates with the endocrine system.