Postnatal Development of Central Feeding Circuits

Rinaman, Linda

doi:10.1007/0-306-48643-1_8

Cited by 12 publications

(14 citation statements)

References 201 publications

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“…Vagal neurocircuits continue to develop postnatally, and are not fully patterned until approximately P21–28 (Rinaman et al . ; Rinaman, ; Dufour et al . ) which may render them especially vulnerable to developmental alterations in response to dietary manipulations.…”

Section: Discussionmentioning

confidence: 99%

“…Consequently, less attention has been paid to the role of vagal neurocircuits in the longer term regulation of energy balance, satiation and the development of obesity. Vagal neurocircuits continue to develop postnatally, and are not fully patterned until approximately P21-28 (Rinaman et al 2000;Rinaman, 2004;Dufour et al 2010) which may render them especially vulnerable to developmental alterations in response to dietary manipulations. In both humans and rodents, exposure to a perinatal HFD can result in long-term adverse effects in offspring, including alterations in the regulation of energy balance and a tendency to develop metabolic syndrome, diabetes and obesity (Levin, 2006(Levin, , 2010b.…”

Section: Discussionmentioning

confidence: 99%

“…The behaviour and activity of vagal afferents is known to be remarkably labile; pathophysiological conditions such as insult or injury modulate afferent activity (Moore et al 2000;Bielefeldt et al 2002a,b;Gebhart et al 2002;Kollarik & Undem, 2002, 2004Myers et al 2002;Dang et al 2004;Tolstykh et al 2004;Hermes et al 2008). Similarly, the behaviour of vagal afferents is impacted adversely by diet-induced obesity (Covasa et al 2000a,b;Donovan et al 2007;Paulino et al 2009;Daly et al 2011;de Lartigue et al 2011;Kentish et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Sensory information from the GI tract is transduced and relayed to the CNS via the afferent vagus nerve; the central terminals of these vagal afferents enter the brainstem via the tractus solitarius and terminate within the nucleus of the tractus solitarius (NTS) using predominately glutamate as a neurotransmitter (Andresen & Yang, 1990;Andresen & Kunze, 1994;Alywin et al 1997;Baptista et al 2005a). NTS neurones integrate this visceral sensory information with hormonal, metabolic and neural inputs from other brainstem and higher CNS centres involved in the regulation of autonomic homeostatic reflexes (Loewy, 1991;Rinaman, 2004;Berthoud & Morrison, 2008). The resulting neural signal is transmitted to the adjacent dorsal motor nucleus of the vagus (DMV) which contains the preganglionic parasympathetic motoneurones that supply vagal motor output back to the upper GI tract .…”

Section: Introductionmentioning

confidence: 99%

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Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity

Bhagat

Fortna

Browning

2014

The Journal of Physiology

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Key pointsr Obesity is recognized as being multifactorial in origin, involving both genetic and environmental factors. The perinatal period is known to be critically important in the development of neural circuits responsible for energy homeostasis and the integration of autonomic reflexes.r Diet-induced obesity alters the biophysical, pharmacological and morphological properties of vagal neurocircuits regulating upper gastrointestinal tract functions, including satiety. Less information is available, however, regarding the effects of a high fat diet (HFD) itself on the properties of vagal neurocircuits.r The present study was designed to test the hypothesis that exposure to a HFD during the perinatal period alters the electrophysiological, pharmacological and morphological properties of vagal efferent motoneurones innervating the stomach.r Our data indicate that perinatal HFD decreases the excitability of gastric-projecting dorsal motor nucleus neurones and dysregulates neurotransmitter release from synaptic inputs and that these alterations occur prior to the development of obesity. These findings represent the first direct evidence that exposure to a HFD modulates the processing of central vagal neurocircuits even in the absence of obesity.Abstract The perinatal period is critically important to the development of autonomic neural circuits responsible for energy homeostasis. Vagal neurocircuits are vital to the regulation of upper gastrointestinal functions, including satiety. Diet-induced obesity modulates the excitability and responsiveness of both peripheral vagal afferents and central vagal efferents but less information is available regarding the effects of diet per se on vagal neurocircuit functions. The aims of this study were to investigate whether perinatal exposure to a high fat diet (HFD) dysregulated dorsal motor nucleus of the vagus (DMV) neurones, prior to the development of obesity. Whole cell patch clamp recordings were made from gastric-projecting DMV neurones in thin brainstem slices from rats that were exposed to either a control diet or HFD from pregnancy day 13. Our data demonstrate that following perinatal HFD: (i) DMV neurones had decreased excitability and input resistance with a reduced ability to fire action potentials; (ii) the proportion of DMV neurones excited by cholecystokinin (CCK) was unaltered but the proportion of neurones in which CCK increased excitatory glutamatergic synaptic inputs was reduced; (iii) the tonic activation of presynaptic group II metabotropic glutamate receptors on inhibitory nerve terminals was attenuated, allowing modulation of GABAergic synaptic transmission; and (iv) the size and dendritic arborization of gastric-projecting DMV neurones was increased. These results suggest that perinatal HFD exposure compromises the excitability and responsiveness of gastric-projecting DMV neurones, even in the absence of obesity, suggesting that attenuation of vago-vagal reflex signalling may precede the development of obesity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity

Bhagat

Fortna

Browning

2014

The Journal of Physiology

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“…The early controls of such independent intake are different from those that control suckling, and appear instead to be developmentally continuous with the neural controls of adultlike feeding that emerge later (Hall, 1990;Rinaman, 2004). The early existence of an independent, adultlike ingestive system in neonatal rats presents a unique opportunity to examine the neural underpinnings of this system as it matures during the course of early postnatal life.…”

Section: Introductionmentioning

confidence: 97%

Ontogeny of hypothalamic-hindbrain feeding control circuits

Rinaman

2006

Dev. Psychobiol.

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Ingestive behavior is a complex product of distributed central control systems that respond to a diverse array of internal and external sensory stimuli. Relatively little is known regarding the pathways and mechanisms by which relevant signals are conveyed to the neural circuits that ultimately control ingestive motor output. This report summarizes findings regarding the postnatal development of descending hypothalamic inputs to the hindbrain dorsal vagal complex (DVC). Evidence accumulated primarily in rats indicates that descending neural projections from the hypothalamus to the DVC are both structurally and functionally immature at birth. The progressive postnatal maturation of these projections occurs in parallel with newly emerging physiological and behavioral responsiveness to treatments and stimuli that affect food intake in adults. Thus, the postnatal emergence of new feeding controls may reflect the emerging access of these controls to DVC neural circuits.

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The ontogeny of postingestive inhibitory stimuli: Examining the role of CCK

Weller

2006

Dev. Psychobiol.

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Cholecystokinin (CCK) inhibits food intake in adults. This paper describes research examining the ability of CCK to affect feeding in infant rats and the role of CCK in the developmentally emerging ability of the rat pup to inhibit ingestion in response to sensory characteristics of food. First, data will be described from studies that asked if the CCK system is functional in preweanling rats. Specifically, these studies examined whether exogenous and endogenous CCK can decrease intake of the infant rat during independent ingestion (of a milk diet, away from the dam). In addition, the ability of exogenous CCK to activate central feeding-control areas in the brain stem and hypothalamus in infant rats was examined by C-FOS staining. Next, experiments examining which specific intake-inhibitory sensory aspects of food are mediated by CCK will be described. The volume, hypertonicity, fat, carbohydrate and protein content of a preload were separately manipulated in different studies, followed closely by a 30-min test meal. The selective CCK(1) receptor antagonist devazepide was used to assess CCK mediation of the control of intake produced by particular sensory aspects of food, at the earliest age in which this ability to control intake appears. Finally, the pattern of independent ingestion in infant OLETF rats lacking CCK(1) receptors was examined. The results suggest that the CCK intake-inhibitory mechanism is potentially available to the young, suckling pup even before it starts to feed on its own. However, it appears to mediate only a portion of the controls of intake during nursing and early stages of weaning. Some aspects of the CCK system (e.g., forebrain-hindbrain connections) and CCK's role in mediating the effects of other stimulus aspects of food apparently undergo a post-weaning maturational process.

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Postnatal Development of Central Feeding Circuits

Cited by 12 publications

References 201 publications

Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity

Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity

Ontogeny of hypothalamic-hindbrain feeding control circuits

The ontogeny of postingestive inhibitory stimuli: Examining the role of CCK

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