Postnatal Remodeling of Dendritic Structure and Spine Density in Gonadotropin-Releasing Hormone Neurons

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Abstract
The GnRH neurons represent the output cells of the neuronal network controlling gonadal function. Their activation initiates the onset of puberty, but the underlying mechanisms remain unclear. Using a GnRH-green fluorescent protein mouse model, we have been able to fill individual GnRH neurons with biocytin in the acute brain slice preparation to examine their morphological characteristics across puberty. GnRH neurons in prepubertal male mice [postnatal d 10–15 (PND10–15)] exhibited half as many dendritic and somal spines as adult male mice (>PND60; P < 0.05) but, surprisingly, a much more complex dendritic tree with 5-fold greater branch points (P < 0.05). Experiments examining somal and proximal dendritic spine numbers in vivo, in perfusion-fixed tissue from GnRH-green fluorescent protein mice, revealed the same pattern of approximately twice as many spines on adult GnRH neurons compared with PND10 male mice (P < 0.01). In contrast to the spine density alterations, reflecting changing excitatory input, confocal immunofluorescence studies revealed no differences in the numbers of vesicular γ-aminobutyric acid transporter-immunoreactive elements adjacent to GnRH soma or proximal dendrites in prepubertal and adult male mice. Experiments evaluating dendritic tree structure in vivo (PND3, -10, and -35 and adult) revealed that GnRH neurons located in the rostral preoptic area, but not the medial septum, exhibited a more complex branching pattern at PND10, but that this was adult-like by PND35. These studies demonstrate unexpected dendritic tree remodeling in the GnRH neurons and provide evidence for an increase in direct excitatory inputs to GnRH neurons across the time of puberty.

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