Hypothalamic Neurogenesis as an Adaptive Metabolic Mechanism

Abstract

In the adult brain, well-characterized neurogenic niches are located in the subventricular zone (SVZ) of the lateral ventricles and in the subgranular zone (SGZ) of the hippocampus. In both regions, neural precursor cells (NPCs) share markers of embryonic radial glia and astroglial cells, and in vitro clonal expansion of these cells leads to neurosphere formation. It has also been more recently demonstrated that neurogenesis occurs in the adult hypothalamus, a brain structure that integrates peripheral signals to control energy balance and dietary intake. The NPCs of this region, termed tanycytes, are ependymal-glial cells, which comprise the walls of the infundibular recess of the third ventricle and contact the median eminence. Thus, tanycytes are in a privileged position to detect hormonal, nutritional and mitogenic signals. Recent studies reveal that in response to nutritional signals, tanycytes are capable of differentiating into orexigenic or anorexigenic neurons, suggesting that these cells are crucial for control of feeding behavior. In this review, we discuss evidence, which suggests that hypothalamic neurogenesis may act as an additional adaptive mechanism in order to respond to changes in diet.

Keywords: feeding behavior; glucosensing; hypothalamus; neurogenesis; tanycytes.

Figure 1

Schematic representation of the basal hypothalamus. Ciliated ependymocytes (Ep) line the dorsal wall of the 3V. The α1d-tanycytes (α1d) and α1v-tanycytes (α1v) have long projections that make contact with the neurons of the VMN. The α2-tancycytes (α2) β1d-tanycytes (β1d) and β1v-tanycytes (β1v) make projections to the AN, making contact with orexigenic and anorexigenic neurons and blood vessels. In the floor of the 3V, the β2 lateral-tanycytes (β2la) and β2 medial-tanycytes (β2me) are joined by tight junctions forming part of the median eminence (ME)-cerebrospinal fluid (CSF) barrier, and their projections make contact with the fenestrated blood vessels of the ME. Redrawn from a previously published (Elizondo-Vega et al., 2015).