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Department of Psychiatry (N.K.M., J.P.H.) and Cell Biology, Neurobiology, and Anatomy (J.P.H.), University of Cincinnati Medical Center, Cincinnati, Ohio 45237-0506; Department of Cell and Molecular Biology (S.D.), Tulane University, New Orleans, Louisiana 70118; and Department of Cell Biology and Neuroscience (C.M.P.), Montana State University, Bozeman, Montana 59717-3148
Address all correspondence and requests for reprints to: James P. Herman, Ph.D., Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Cincinnati, Ohio 45237-0506. E-mail james.herman{at}uc.edu.
Confocal microscopy was used to assess activity-dependent neuroplasticity in neurotransmitter innervation of vasopressin immunoreactive magnocellular neurons in the supraoptic nucleus (SON). Vesicular glutamate transporter 2, glutamic acid decarboxylase, and dopamine ß-hydroxylase (DBH) synaptic boutons were visualized in apposition to vasopressin neurons in the SON. A decrease in DBH synaptic boutons per cell was seen upon salt loading, indicating diminished noradrenergic/adrenergic innervation. Loss of DBH appositions to vasopressin neurons was associated with a general loss of DBH immunoreactivity in the SON. In contrast, the number of vesicular glutamate transporter 2 synaptic boutons per neuron increased with salt loading, consistent with increased glutamatergic drive of magnocellular SON neurons. Salt loading also caused an increase in the total number of glutamic acid decarboxylase synaptic boutons on vasopressinergic neurons, suggesting enhanced inhibitory innervation as well. These studies indicate that synaptic plasticity compensates for increased secretory demand and may indeed underlie increased secretion, perhaps via neurotransmitter-specific, activity-related changes in synaptic contacts on vasopressinergic magnocellular neurons in the SON.
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