Source comparison
Neurological Biology: Hypothalamic and Hippocampal GHS-R1a vs Absent CNS GHRHR
GHS-R1a is expressed not only in the pituitary but also in hypothalamic nuclei (arcuate, ventromedial, paraventricular), hippocampal CA1-CA3 and dentate gyrus, and cortical and subcortical regions. This peripheral-to-central GHS-R1a distribution gives Hexareli
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- GHS-R1a is expressed not only in the pituitary but also in hypothalamic nuclei (arcuate, ventromedial, paraventricular), hippocampal CA1-CA3 and dentate gyrus, and cortical and subcortical regions. This peripheral-to-central GHS-R1a distribution gives Hexarelin direct CNS access when administered systemically at pharmacologically relevant doses.
- In 6-OHDA unilateral striatal lesion models of dopaminergic degeneration, Hexarelin at 80 µg/kg sc for 21 days increases striatal DA +22–28% on the lesioned side (vs vehicle +8%) — an effect blocked 68–72% by [D-Lys³]-GHRP-6 (GHS-R1a antagonist) and 28–34% by hypophysectomy, indicating a direct central GHS-R1a mechanism (~70%) plus indirect GH-IGF-1 component (~30%). Hippocampal BDNF is increased 28–34% (vs baseline), with TrkB-pY816 +1.4×.
- GHRHR is not expressed in the CNS at pharmacologically relevant levels — it is a pituitary-selective receptor. CJC-1295 therefore produces no direct neurological effects via receptor binding; all CNS effects of CJC-1295 are secondary to elevated circulating GH and IGF-1. IGF-1 crosses the blood-brain barrier via IGF-1R-mediated transcytosis, and in aged hippocampus produces dendritic spine density +18–22% and BDNF +24–28% at steady-state — but with a 48–72-hour lag versus Hexarelin’s acute central GHS-R1a activation.
- For acute neuroprotection studies (TBI, stroke, excitotoxicity), Hexarelin’s direct central GHS-R1a action provides rapid onset. For chronic neurodegenerative disease models requiring sustained IGF-1 support, CJC-1295 DAC may be superior by maintaining continuous IGF-1 elevation without pulsatile variation.