Organization of peptidergic and catecholaminergic efferents from the nucleus of the solitary tract to the rat amygdala

We recently reported that brief, remotely controlled intrameal hepatic‐portal vein infusions of glucagon‐like peptide‐1 (GLP‐1) reduced spontaneous meal size in rats. To investigate the neurobehavioural correlates of this effect, we equipped male Sprague‐Dawley rats with hepatic‐portal vein catheters and assessed (i) the effect on eating of remotely triggered infusions of GLP‐1 (1 nmol/kg, 5 min) or vehicle during the first nocturnal meal after 3 h of food deprivation and (ii) the effect of identical infusions performed at dark onset on c‐Fos expression in several brain areas involved in the control of eating. GLP‐1 reduced (P < 0.05) the size of the first nocturnal meal and increased its satiety ratio. Also, GLP‐1 increased (P < 0.05) the number of c‐Fos‐expressing cells in the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala, but not in the arcuate or paraventricular hypothalamic nuclei. These data suggest that the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala play a role in the eating‐inhibitory actions of GLP‐1 infused into the hepatic‐portal vein; it remains to be established whether activation of these brain nuclei reflect satiation, aversion, or both.

Area postrema

Solitary nucleus

10.1111/j.1365-2826.2010.01995.x

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Citations (56)

Fos expression in non-catecholaminergic neurons in medullary and pontine nuclei after volume depletion induced by polyethylene glycol

Brain Research (2002)

Kathleen S. Curtis Eric G. Krause Robert J. Contreras

Pons

Area postrema

Catecholaminergic cell groups

Locus coeruleus

Solitary tract

Medulla

Rostral ventrolateral medulla

Immunolabeling

Adrenergic Neurons

Phenylethanolamine N-methyltransferase

10.1016/s0006-8993(02)03051-2

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Citations (13)

Transcriptional Activation of Nucleus tractus solitarii/Area postrema Catecholaminergic Neurons by Pharmacological Inhibition of Caudal Hindbrain Monocarboxylate Transporter Function

Neuroendocrinology (2005)

Gopal D. Patil Karen P. Briski

Evidence that intracerebral lactate administration alters electrophysiological sensitivity of metabolic-signaling neurons and hypoglycemic counterregulation suggests that this substrate fuel is a monitored indicator of in central nervous system energy balance. Catecholaminergic (CA) neurons in the caudal hindbrain nucleus tractus solitarii (NTS)/area postrema (AP) complex participate in the origin and/or relay of stimuli that signal deficient glucose provision to the brain. The present studies evaluated the responsiveness of this neurochemical phenotype to lactate insufficiency by investigating the effects of pharmacological inhibition of local monocarboxylate transporter activity on the transcriptional status of these cells. Adult female rats were sacrificed by transcardial perfusion 2 h after infusion of graded doses of the monocarboxylate transporter inhibitor, α-cyano-4-hydroxycinnamic acid (4-CIN), or vehicle into the caudal fourth ventricle, and tissue sections through the NTS/AP were processed by dual-label immunofluorescence histochemistry for demonstration of cytoplasmic tyrosine hydroxylase (TH) and the inducible nuclear AP-1 regulatory factor, Fos. While vehicle administration resulted in negligible Fos immunostaining within the NTS, 4-CIN-treated animals exhibited dose-dependent increases in mean numbers of Fos-ir- and TH-/Fos-ir-positive neurons in this structure. These data show that pharmacological suppression of lactate trafficking in the caudal hindbrain elicits the genomic activation of NTS/AP CA neurons. In light of evidence implicating this neurochemical phenotype in signaling of cellular energy imbalance, the current results support the view that diminished uptake and/or catabolism of lactate may underlie CA neuronal activation of neural pathways governing compensatory behavioral and physiological responses to metabolic substrate deficiency.

Area postrema

Monocarboxylate transporter

Solitary nucleus

Catecholaminergic cell groups

Hindbrain

10.1159/000085522

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Citations (15)

C-terminal tail of β-adrenergic receptors: immunocytochemical localization within astrocytes and their relation to catecholaminergic neurons in N. tractus solitarii and area postrema

Brain Research (1992)

Chiye Aoki Virginia M. Pickel

Area postrema

Catecholaminergic cell groups

Adrenergic Neurons

Solitary nucleus

Phenylethanolamine N-methyltransferase

10.1016/0006-8993(92)90507-6

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Citations (63)

PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

Peptides (2007)

James E. Blevins Prasanth K. Chelikani Alvin C. Haver Roger D. Reidelberger

Area postrema

Catecholaminergic cell groups

Solitary nucleus

Peptide YY

Hindbrain

Solitary tract

10.1016/j.peptides.2007.11.003

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Citations (64)

Organization of peptidergic and catecholaminergic efferents from the nucleus of the solitary tract to the rat amygdala

Brain Research Bulletin (1990)

Andrea M. Zardetto‐Smith Thackery S. Gray

Solitary tract

Area postrema

Adrenergic Neurons

Solitary nucleus

Catecholaminergic cell groups

10.1016/0361-9230(90)90183-z

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Citations (130)

Caudal brainstem Fos expression is restricted to periventricular catecholamine neuron-containing loci following intraventricular administration of 2-deoxy- d -glucose

Experimental Brain Research (2000)

Karen P. Briski Edith S. Marshall

Area postrema

Locus coeruleus

Catecholaminergic cell groups

Solitary tract

Immunostaining

Adrenergic Neurons

Solitary nucleus

10.1007/s002210000448

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Citations (27)

Influencia de la hipertensión sobre el contenido de catecolaminas del complejo vagal dorsal de la rata

Majorensis: Revista Electrónica de Ciencia y Tecnología (2008)

Emilia María Carmona Calero Leandro Castañeyra-Ruiz Héctor de Paz Carmona Agustín Ruiz Juan M. González Toledo

The dorsal vagal complex (CVD) is formed by the nucleus tractus solitarii, (NTS), the dorsal motor nucleus of the vagus nerve (NMDV) and the area postrema (AP).The CVD functions has been connected with the cardiovascular regulations and is considered a relay centre for integrating central and peripheral signals related to cardiovascular regulation. The NTS is the primary site for cardiovascular afferent fibres termination and which are innervated by catecholaminergic neurons. The present work quest more evidences on the implication of the CVD catecholaminergic neurons in the development of and arterial hypertension. Control WKY and hypertensive SHR rats were used. Antibodies to the catecholamine synthetic enzymes tyrosine-hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) were used in the immunohistochemical and western blot analysis. The TH and DBH material immunoreactive were located throughout the rostrocaudal and dorsoventral extent of the area postrema, as well as in neurons within the NTS. The distribution and the number of TH neurons were the similar as those DBH, except in the dorsal motor nucleus of the vagus. In the area postrema the number of neurons immunocytochemical labelled for TH was higher than those labelled for DBH. The hypertension produced an increase of the IRM for both of two antibodies TH and DBH in the three nuclei that form the CVD. Thereafter, we could conclude that in the SHR rat is produced an activation of the catecholaminergic central system expressed by an increase of the catecholamines in the dorsal vagal complex.

Area postrema

Dorsal motor nucleus

Catecholaminergic cell groups

Solitary nucleus

Solitary tract

Adrenergic Neurons

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PYY(3-36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats.

Default journal (2008)

James E. Blevins Prasanth K. Chelikani Alvin C. Haver Roger D. Reidelberger

Peptide YY (3-36) [PYY(3-36)] inhibits feeding in rodents, nonhuman primates and humans, yet the neural circuits underlying this action remain to be determined. Here we assessed whether PYY(3-36) inhibits feeding by activating neurons in forebrain and hindbrain sites containing Y2 receptors and linked to control of food intake, or in hindbrain sites immediately downstream of vagal afferent neurons. Rats received an anorexigenic dose of PYY(3-36), and the number of neurons expressing Fos, an indicator of neuronal activation, was determined in anterior hypothalamus (AH), arcuate nucleus (ARC), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), ventromedial hypothalamus (VMH), central nucleus of the amygdala (CeA), area postrema (AP), and caudal medial nucleus tractus solitarius (cmNTS), commissural NTS (cNTS), and gelatinosus NTS (gNTS). Expression of tyrosine hydroxylase (TH), an indicator of catecholamine synthesis, was also measured in the cmNTS. PYY(3-36) increased Fos in ARC, cmNTS, gNTS and AP. Approximately 10% of Fos+ neurons in the cmNTS were TH+. These results suggest that PYY(3-36) inhibits feeding through direct activation of ARC neurons, and direct and/or indirect activation via vagal afferent nerves of cmNTS, gNTS and AP, including some catecholaminergic neurons in the cmNTS.

Area postrema

Catecholaminergic cell groups

Peptide YY

Solitary nucleus

Hindbrain

Solitary tract

Lateral hypothalamus

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Citations (0)