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The rodent hypothalamic neurosecretory system normally exhibits remarkable functional
and structural plasticity following injury. However, the present study describes a
newly observed phenomenon in which neurohypophysectomized animals receiving chronically
administered exogenous vasopressin during the post-lesion period (a treatment which
insures maximal renal antidiuresis over this time frame) lose all capacity for recovery
of antidiuretic function. Functional deficits are accompanied by a severe reduction
in the number of neurons exhibiting immunohistochemical staining for arginine vasopressin.
These data indicate that the presence of neurological stimulation signaling vasopressin
release may play an important role in promoting neural regeneration of the vasopressinergic
component of the neurosecretory system.