Abstract
Mammalian puberty requires complex interactions between glial and neuronal regulatory systems within the hypothalamus that results in the timely increase in the secretion of luteinizing hormone releasing hormone (LHRH). Assessing the molecules required for the development of coordinated communication networks between glia and LHRH neuron terminals in the basal hypothalamus, as well as identifying substances capable of affecting cell-cell communication are important. One such pathway involves growth factors of the epidermal growth factor (EGF) family that bind to specific erbB receptors. Activation of this receptor results in the release of prostaglandin-E2 (PGE2) from adjacent glial cells, which then acts on the nearby LHRH nerve terminals to elicit release of the peptide. Another pathway involves novel genes which synthesize adhesion/signaling proteins responsible for the structural integrity of bi-directional glial-neuronal communication. In this review, we will discuss the influence of these glial-neuronal communication pathways on the prepubertal LHRH secretory system, and furthermore, discuss the actions and interactions of alcohol on these two signaling processes.
Highlights
The hypothalamic region of the brain plays an important role in synchronizing events leading to the activation of the mammalian puberty
The glial cells within the medial basal hypothalamus (MBH) are key components of the central regulatory system that facilitate prepubertal luteinizing hormone-releasing hormone (LHRH) release via pathways initiated by growth factors and cell adhesion molecules that act on LHRH neuron terminals to stimulate their secretory activity [13,14]
It is becoming increasingly clear that glial-neuronal interactions play an important role in prepubertal LHRH secretion and the subsequent acquisition of female pubertal development
Summary
The hypothalamic region of the brain plays an important role in synchronizing events leading to the activation of the mammalian puberty. In hypothalamic glial cells, PGE2 formation induced by TGFα and the stimulatory effect of the TGFα treated conditioned medium on LHRH release are shown to be prevented by the inhibition of erbB receptor tyrosine kinase activity or prostaglandin synthesis [37,45] These data strongly support the notion that TGFα acts indirectly in the functional control of neuronal networks governing mammalian puberty via hypothalamic glial-neuronal communications. Futhermore, a study has shown that transgenic mice with a double negative form of SynCam lacking the intracellular domain causes these animals to have delayed puberty [68] These observations suggest that one of the mechanisms underlying erbB4 receptor facilitation of LHRH neuronal function involves SynCAM1 dependent signaling during pubertal development. A concept is emerging that suggests that these glial-neuronal molecules facilitate hypothalamic neurosecretion via changes in the arrangement of glial-neuronal adhesion and signaling that could alter LHRH release and the pubertal process
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