Evidence is presented indicating that the initiation of mammalian puberty requires an array of transsynaptic and glial-neuronal interactions, brought about by neurons using excitatory and inhibitory amino acids as transmitters and astroglial cells producing cell-cell signaling molecules able to regulate neuronal function. Although a glutamate-to-GABA hierarchical arrangement appears prominent in the brain, it is still unclear which of these two neurotransmitter systems is primarily responsible for initiating the transsynaptic cascade of events that unleashes the pubertal increase in LHRH release. In contrast, there is now considerable evidence demonstrating that members of the TGF-β and EGF families of trophic factors are key components of the gila-to-neuron communication pathways used by glial cells to facilitate LHRH release. Progress has also been made toward the identification of genes belonging to the hierarchy of upstream molecules that presumably control the initiation of puberty.
|Original language||English (US)|
|Number of pages||7|
|Journal||Current Opinion in Endocrinology and Diabetes|
|State||Published - 2001|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism