Wired for eating: how is an active feeding circuitry established in the postnatal brain?

Abstract

From birth, mammals have to find food and maximize caloric intake to ensure growth and survival. Suckling must be initiated quickly after birth and then maintained and controlled until weaning. It is a complex process involving interactions between sensory and motor neuronal pathways. Meanwhile, the control of food intake and energy homeostasis is progressively established via the development of hypothalamic circuits. The development of these circuits is influenced by hormonal and nutritional signals and can be disturbed in a variety of developmental disorders leading to long-term metabolic, behavioral and cognitive dysfunctions. This review summarizes our current knowledge of the neuronal circuits involved in early postnatal feeding processes.

Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development

“…There is a high level of conservation of these genes, as a colinear set, across multiple vertebrates, including the mouse, in which 28 of the 32 minimally critically deleted genes are found adjacent to one another on murine Chromosome 16 (Meechan et al, 2015). There is remarkable homology of the colinear set of 22q11-deleted genes in multiple species, and their cellular, developmental, and homeostatic functions in a broad range of cells, tissues, and organs appear to be similar in most vertebrates -and even some invertebrates -analyzed thus far (Meechan et al, 2015;Motahari et al, 2019). A key aspect of 22q11 gene function across these species may be the apparent relationship to neural crest, and non-axial M/E signaling at midgestation, and its consequences for subsequent morphogenesis and neural circuit development.…”

“…Rather than a few 22q11 deleted genes, we found that 21/28 are expressed selectively at these sites based upon qPCR analysis in micro-dissected samples of each M/E inductive site as well as whole mount in situ or immunolabeling ( Figure 5). None of the 22q11 genes is known to selectively alter neural crest specification or migration (Motahari et al, 2019). Instead, many of these genes, including several candidates for specific 22q11DS phenotypes, seem to modulate either local patterning, differentiation, or signaling.…”

“…Instead, many of these genes, including several candidates for specific 22q11DS phenotypes, seem to modulate either local patterning, differentiation, or signaling. Complete loss of function mutations of some of these genes lead to substantial dysmorphology at several sites of non-axial M/E induction (Scambler, 2010;Paronett et al, 2015;Motahari et al, 2019), while heterozygous deletion, usually in the context of broader 22q11 gene deletion, leads to variable dysmorphology or dysfunction in a variety of organ systems.…”

“…(B) PCR, in situ hybridization, immunoblotting, and immunlocalization identify expression of 22 of the 28 murine 22q11 orthologues in the developing and adult mouse brain. (C) Multiple 22q11 orthologues are expressed uniformly at sites of neural crest-mediated M/E induction as well as in the nascent central nervous system in the midgestation mouse embryo (E10.5).The purple-blue label shows in situ hybridization labeling of mRNA for several 22q11 genes at these sites, and the brown label shows the localization of proteins encoded by three of the deleted genes (panel A, B, adapted fromMeechan et al, 2015; panel C adapted fromMotahari et al, 2019).…”

Increased Hypothalamic Projections to the Lateral Hypothalamus and Responses to Leptin in Rat Neonates From High Fat Fed Mothers

“…In rodents, connections between "homeostatic" hypothalamic nuclei and the LHA are not fully established at birth and mature over the first weeks postnatally, making them susceptible to changes in the perinatal nutritional environment (Muscatelli and Bouret, 2018). Projections from the ARC to the DMH mature by postnatal day (PND) 6, whereas those reaching the PVN and the LHA are observed between PND8-10 and PND12, respectively (Bouret et al, 2004a).…”