scholarly journals Enhanced aversive memory retrieval by chemogenetic activation of locus coeruleus norepinephrine neurons

2019 ◽  
Author(s):  
Ryoji Fukabori ◽  
Yoshio Iguchi ◽  
Shigeki Kato ◽  
Kazumi Takahashi ◽  
Satoshi Eifuku ◽  
...  

AbstractThe ability to retrieve memory store in response to the environment is essential for animal behavioral adaptation. Norepinephrine (NE)-containing neurons in the brain play a key role in the modulation of synaptic plasticity underlying various processes of memory formation. However, the role of the central NE system in memory retrieval remains unclear. In this study, we developed a neural chemogenetic activation strategy using insect olfactory Ionotropic Receptors (IRs), and used it for selective stimulation of NE neurons in the locus coeruleus (LC) in transgenic mice. Ligand-induced activation of LC NE neurons resulted in enhancement of the retrieval process of conditioned taste aversion, which was mediated through at least partly adrenergic receptors in the amygdala. Pharmacological blockade of LC activity confirmed the facilitative role of these neurons in memory retrieval. Our findings indicate that the LC-amygdalar pathway is required and sufficient for enhancing the recall of taste associative memory.

Endocrinology ◽  
1986 ◽  
Vol 118 (5) ◽  
pp. 1829-1834 ◽  
Author(s):  
KATHLEEN H. BERECEK ◽  
TERRI N. MITCHUM

Development ◽  
2002 ◽  
Vol 129 (4) ◽  
pp. 983-991 ◽  
Author(s):  
Astrid Vogel-Höpker ◽  
Hermann Rohrer

The role of BMPs in the development of the major noradrenergic centre of the brain, the locus coeruleus (LC), was investigated. LC generation is reflected by initial expression of the transcription factors Phox2a and Phox2b in dorsal rhombomere1 (r1), followed by expression of dopamine-β-hydroxylase and tyrosine hydroxylase. Bmp5 is expressed in the dorsal neuroepithelium in proximity to Phox2-expressing cells. BMP inhibition in stage 10 chick embryos resulted in the lack of LC neurones or in their generation at the dorsal midline, and loss of roof plate and rhombic lip, but it did not affect neural crest development. These results reveal late essential BMP functions in the specification of dorsal neuronal phenotypes in r1, including LC neurones, and in the development of dorsal midline structures.


1987 ◽  
Vol 252 (6) ◽  
pp. H1183-H1191
Author(s):  
C. Iadecola ◽  
P. M. Lacombe ◽  
M. D. Underwood ◽  
T. Ishitsuka ◽  
D. J. Reis

We studied whether adrenal medullary catecholamines (CAs) contribute to the metabolically linked increase in regional cerebral blood flow (rCBF) elicited by electrical stimulation of the dorsal medullary reticular formation (DMRF). Rats were anesthetized (alpha-chloralose, 30 mg/kg), paralyzed, and artificially ventilated. The DMRF was electrically stimulated with intermittent trains of pulses through microelectrodes stereotaxically implanted. Blood gases were controlled and, during stimulation, arterial pressure was maintained within the autoregulated range for rCBF. rCBF and blood-brain barrier (BBB) permeability were determined in homogenates of brain regions by using [14C]iodoantipyrine and alpha-aminoisobutyric acid (AIB), respectively, as tracers. Plasma CAs (epinephrine and norepinephrine) were measured radioenzymatically. DMRF stimulation increased rCBF throughout the brain (n = 5; P less than 0.01, analysis of variance) and elevated plasma CAs substantially (n = 4). Acute bilateral adrenalectomy abolished the increase in plasma epinephrine (n = 4), reduced the increases in flow (n = 6) in cerebral cortex (P less than 0.05), and abolished them elsewhere in brain (P greater than 0.05). Comparable effects on rCBF were obtained by selective adrenal demedullation (n = 7) or pretreatment with propranolol (1.5 mg/kg iv) (n = 5). DMRF stimulation did not increase the permeability of the BBB to AIB (n = 5). We conclude that the increases in rCBF elicited from the DMRF has two components, one dependent on, and the other independent of CAs. Since the BBB is impermeable to CAs and DMRF stimulation fails to open the BBB, the results suggest that DMRF stimulation allows, through a mechanism not yet determined, circulating CAs to act on brain and affect brain function.


1991 ◽  
Vol 5 (4) ◽  
pp. 147-153 ◽  
Author(s):  
Kathleen A Fraser ◽  
Samuel S Lee

The role of the autonomic nervous system in circulatory regulation of the splanchnic organs (stomach, small intestine, colon, liver, pancreas and spleen) is reviewed. In general, the sympathetic nervous system is primarily involved in vasoconstriction, while the parasympathetic contributes to vasodilation. Vasoconstriction in the splanchnic circulation appears to be mediated by alpha-2 receptors and vasodilation by activation of primary afferent nerves with subsequent release of vasodilatory peptides, or by stimulation of beta-adrenergic receptors. As well, an important function of the autonomic nervous system is to provide a mechanism by which splanchnic vascular reserve can be mobilized during stress to maintain overall cardiovascular homeostasis.


1988 ◽  
Vol 438 (1-2) ◽  
pp. 299-303 ◽  
Author(s):  
Susan J. Sara ◽  
Valerie Devauges

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.


1993 ◽  
Vol 264 (2) ◽  
pp. G231-G236 ◽  
Author(s):  
M. Yoneda ◽  
Y. Tache

The central action of the stable thyrotropin-releasing hormone (TRH) analogue, RX 77368, to induce vagal release of gastric prostaglandin E2 (PGE2) was investigated in urethan-anesthetized rats. Intracisternal RX 77368 (1.5-1,000 ng) dose dependently increased gastric PGE2 levels measured for 3 h in the perfusate of dialysis fibers implanted into the corpus submucosa. RX 77368 injected intravenously (1,000 ng) had no effect. The stimulatory action of RX 77368 (1.5 ng) on gastric PGE2 release was blocked by indomethacin and bilateral cervical vagotomy. Omeprazole did not alter the PGE2 response to 3 ng of RX 77368 and reduced by 39% PGE2 release induced by the 1,000-ng dose. RX 77368 (1.5 ng) by itself did not influence acid secretion but increased acid output to 117 +/- 18 mumol/2 h in indomethacin-pretreated rats. Indomethacin also increased by 97% the acid response to the 3-ng dose of RX 77368, but the effect of a maximal effective dose of RX 77368 was not modified. These results indicate that RX 77368 acts in the brain to induce a vagal-dependent stimulation of gastric PGE2 secretion which is biologically active to reduce the acid response to submaximal doses of TRH analogue. These data suggest a possible role of medullary TRH in the central vagal regulation of gastric PGE2 release.


Endocrinology ◽  
2012 ◽  
Vol 153 (10) ◽  
pp. 4766-4774 ◽  
Author(s):  
Amandine M. Minni ◽  
Rodolphe Dorey ◽  
Christophe Piérard ◽  
Gaëlle Dominguez ◽  
Jean-Christophe Helbling ◽  
...  

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