In mice, a small group of brain cells that make growth‑hormone‑releasing hormone also have IGF‑1 receptors. Removing those receptors makes male mice grow slower during puberty and cuts the number of growth‑hormone spikes, but the effect is temporary and disappears later. Deleting both IGF‑1 and growth‑hormone receptors in those cells stops the growth slowdown, showing the IGF‑1 signal in these neurons helps regulate growth‑hormone release.

Growth hormone (GH) secretion is controlled by various mechanisms, including negative feedback loops mediated by either GH or insulin-like growth factor 1 (IGF-1). Previous studies suggest that GH receptor (GHR) signaling in tyrosine hydroxylase (TH)-expressing cells regulates GH secretion. However, it is still unknown whether hypothalamic TH neurons are also responsive to IGF-1 to control GH secretion. Here, we show that a subset of TH neurons in the arcuate nucleus of the hypothalamus (ARH) expresses the GH-releasing hormone (GHRH) and the IGF-1 receptor (IGF1R). Mice with IGF1R deletion in TH cells (TH^ΔIGF1R mice) experienced a decline in growth during the peripubertal period - mainly in males - that was not observed after 8 or 10 weeks of age (female or male, respectively). Male TH^{∆IGF1R} mice also displayed reduced GH pulse frequency. Mice with both IGF1R and GHR ablated in TH-expressing cells were generated. Unlike TH^{∆IGF1R} mice, TH^{∆IGF1R/GHR} mice did not show a peripubertal reduction in body weight, lean mass, or fat mass. In summary, IGF-1 action on TH-expressing cells influences GH pulse frequency in male mice, and the absence of IGF1R signaling in these cells results in a mild, temporary impact on body growth.