Neuropeptide Y and Somatostatin in the Anterior Piriform Cortex Alter Intake of Amino Acid-deficient Diets

Cummings, Sharon L.; Truong, Ban G; Gietzen, Dorothy W.

doi:10.1016/s0196-9781(97)00468-3

Cited by 21 publications

(19 citation statements)

References 55 publications

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“…Ghrelin injections into the third ventricle (intracerebroventricular, icv), but not ip, increase valine-deficient diet intake by about 1 g in 2 h, but this is below the level of control intake. Similar icv injections of NPY increase intake of the deficient diet fully to control levels in 2 h. When we [40] used smaller doses of NPY, injected into the APC, we found the reverse: significant dose-dependent decreases in intake of our threonine-deficient diet are seen with NPY after 3 h. The use of threonine vs valine-deficient diets should not explain the differences, so opposite results with NPY are more likely due to experimental differences such as injection sites and doses. Thus, it is not clear that peptides in the APC take part in the sensory response to IAA depletion, although they may be involved in “appetitive” responses, see below.…”

Section: Protein and Iaa Deficiencymentioning

confidence: 99%

“…This positive feedback loop is kept under control by inhibitory interneurons, many of which are gamma amino butyric acid (GABA)-ergic [39]. Along with the glutamatergic pyramidal cells, axons of other cell types (possibly including neuropeptide Y (NPY) [40]), provide the output of the APC [37], but glutamatergic axons predominate [41]. …”

Section: Protein and Iaa Deficiencymentioning

confidence: 99%

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The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

Gietzen

Aja

2012

Mol Neurobiol

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The essential (indispensable) amino acids (IAA) are neither synthesized nor stored in metazoans, yet they are the building blocks of protein. Survival depends on availability of these protein precursors, which must be obtained in the diet; it follows that food selection is critical for IAA homeostasis. If even one of the IAA is depleted, its tRNA becomes quickly deacylated and the levels of charged tRNA fall, leading to disruption of global protein synthesis. As they have priority in the diet, second only to energy, the missing IAA must be restored promptly or protein catabolism ensues. Animals detect and reject an IAA-deficient meal in 20 min, but how? Here, we review the molecular basis for sensing IAA depletion and repletion in the brain’s IAA chemosensor, the anterior piriform cortex (APC). As animals stop eating an IAA-deficient meal, they display foraging and altered choice behaviors, to improve their chances of encountering a better food. Within 2 h, sensory cues are associated with IAA depletion or repletion, leading to learned aversions and preferences that support better food selection. We show neural projections from the APC to appetitive and consummatory motor control centers, and to hedonic, motivational brain areas that reinforce these adaptive behaviors.

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Section: Protein and Iaa Deficiencymentioning

confidence: 99%

Section: Protein and Iaa Deficiencymentioning

confidence: 99%

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

Gietzen

Aja

2012

Mol Neurobiol

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“…Indeed, high densities of 26RFa receptors have been observed in the olfactory system and notably the granular cell layer of the main olfactory bulb, the piriform cortex, the amygdaloid complex, and the hippocampal formation. In particular, the piriform cortex, which exhibits one of the highest density of 26RFa receptors in the rat brain, plays a key role in the neuroperception of deficiencies in essential amino acids that are always associated with decreased food intake (for review see Gietzen, 1993), and it has been reported that injection of NPY in the piriform cortex results in an alteration of the intake of amino-aciddeficient diets (Cummings et al, 1998). The presence of high densities of 26RFa receptors in the piriform cortex suggests that 26RFa may be involved in the perception of imbalances in essential amino acids and/or in the response to such a deprivation in essential amino acids.…”

Section: Functional Considerationsmentioning

confidence: 99%

Distribution of 26RFa binding sites and GPR103 mRNA in the central nervous system of the rat

Bruzzone

Lectez

Dionne‐Laporte

et al. 2007

J of Comparative Neurology

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The novel RFamide peptide 26RFa, the endogenous ligand of the orphan receptor GPR103, affects food intake, locomotion, and activity of the gonadotropic axis. However, little is known regarding the localization of 26RFa receptors. The present report provides the first detailed mapping of 26RFa binding sites and GPR103 mRNA in the rat central nervous system (CNS). 26RFa binding sites were widely distributed in the brain and spinal cord, whereas the expression of GPR103 mRNA was more discrete, notably in the midbrain, the pons, and the medulla oblongata, suggesting that 26RFa can bind to a receptor(s) other than GPR103. Competition experiments confirmed that 26RFa interacts with an RFamide peptide receptor distinct from GPR103 that may be NPFF2. High densities of 26RFa binding sites were observed in olfactory, hypothalamic, and brainstem nuclei involved in the control of feeding behavior, including the piriform cortex, the ventromedial and dorsomedial hypothalamic nuclei, the paraventricular nucleus, the arcuate nucleus, the lateral hypothalamic area, and the nucleus of the solitary tract. The preoptic and anterior hypothalamic areas were also enriched with 26RFa recognition sites, supporting a physiological role of the neuropeptide in the regulation of the gonadotropic axis. A high density of 26RFa binding sites was detected in regions of the CNS involved in the processing of pain, such as the dorsal horn of the spinal cord and the parafascicular thalamic nucleus. The wide distribution of 26RFa binding sites suggests that 26RFa has multiple functions in the CNS that are mediated by at least two distinct receptors.

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“…Some showed an increase in food intake (6 -10), others a decrease (7,11,12) or a biphasic effect (13). These discrepant findings may be explained by different doses used as SST increases food intake when injected intracerebroventricularly (icv) or into the anterior piriform cortex at low doses (0.7-65 ng per rat ϭ 0.4 -40 pmol), whereas higher (3.3-4.9 g per rat ϭ 2-3 nmol) doses decrease chow ingestion (7,12,14).…”

mentioning

confidence: 99%

Central Injection of the Stable Somatostatin Analog ODT8-SST Induces a Somatostatin2 Receptor-Mediated Orexigenic Effect: Role of Neuropeptide Y and Opioid Signaling Pathways in Rats

et al. 2010

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Somatostatin and octreotide injected into the brain have been reported to modulate food intake. However, little is known regarding the underlying mechanisms. The stable oligosomatostatin analog, des-AA 1,2,4,5,12, ]-somatostatin (ODT8-SST), like somatostatin, binds to all five somatostatin receptors (sst 1-5 ). We characterized the effects of ODT8-SST injected intracerebroventricularly (icv) on food consumption and related mechanisms of action in freely fed rats. ODT8-SST (0.3 and 1 g per rat, icv) injected during the light or dark phase induced an early onset (within 1 h) and long-lasting (4 h) increase in food intake in nonfasted rats. By contrast, ip injection (0.3-3 mg/kg) or icv injection of selective sst 1 or sst 4 agonists (1 g per rat) had no effect. The 2 h food intake response during the light phase was blocked by icv injection of a sst 2 antagonist, the neuropeptide Y (NPY) Y 1 receptor antagonist, BIBP-3226, and ip injection of the -opioid receptor antagonist, naloxone, and not associated with changes in plasma ghrelin levels. ODT8-SST (1 g per rat, icv) stimulated gastric emptying of a solid meal which was also blocked by naloxone. The increased food intake was accompanied by a sustained increase in respiratory quotient, energy expenditure, and drinking as well as -opioid receptor-independent grooming behavior and hyperthermia, while ambulatory movements were not altered after ODT8-SST (1 g per rat, icv). These data show that ODT8-SST acts primarily through brain sst 2 receptors to induce a long-lasting orexigenic effect that involves the activation of Y 1 and opiate-receptors, accompanied by enhanced gastric transit and energy expenditure suggesting a modulation of NPYergic and opioidergic orexigenic systems by brain sst 2 receptors. (Endocrinology 151: 4224 -4235, 2010)

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Neuropeptide Y and Somatostatin in the Anterior Piriform Cortex Alter Intake of Amino Acid-deficient Diets

Cited by 21 publications

References 55 publications

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

Distribution of 26RFa binding sites and GPR103 mRNA in the central nervous system of the rat

Central Injection of the Stable Somatostatin Analog ODT8-SST Induces a Somatostatin2 Receptor-Mediated Orexigenic Effect: Role of Neuropeptide Y and Opioid Signaling Pathways in Rats

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