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Neural pathway for gut feelings: vagal interoceptive feedback from the gastrointestinal tract is a critical modulator of anxiety-like behavior
Krieger JP, Asker M, Van der Velden P, Börchers S, Richard JE, Maric I, Longo F, Singh A, De Larigue G, Skibicka KP (2022) Neural pathway for gut feelings: vagal interoceptive feedback from the gastrointestinal tract is a critical modulator of anxiety-like behavior. Biological Psychiatry in press. doi: 10.1016/j.biopsych.2022.04.020
Objective: To determine how the sensing of gastrointestinal state affects anxiety.
Summary: Vagal sensory signals from the gastrointestinal tract are critical for baseline and feeding-induced tuning of anxiety via the central amygdala in rats. The article results suggest vagal gut-brain signaling as a target to normalize interoception in anxiety.
Usage: 1.5 ul of CCK-SAP or Blank-SAP were delivered into each nodose ganglion at 250 ng/ul.
Related Products: CCK-SAP (Cat. #IT-31), Blank-SAP (Cat. #IT-21)
Vagal afferent cholecystokinin receptor activation is required for glucagon-like peptide-1-induced satiation
Vana V, Laerke MK, Rehfeld JF, Arnold M, Dmytriyeva O, Langhans W, Schwartz TW, Hansen HS (2022) Vagal afferent cholecystokinin receptor activation is required for glucagon-like peptide-1-induced satiation. Diabetes Obes Metab 24(2):268-280. doi: 10.1111/dom.14575
Objective: To investigate the effect of peripheral GLP-1 on food-intake control.
Summary: Endogenous CCK interacts with GLP-1 to promote satiation and that activation of the FFA1 receptor can initiate this interaction by stimulating the release of CCK.
Usage: Utilized CCK-SAP to selectively ablate the CCK receptor-expressing gastrointestinal vagal afferent neurones (VANs).
Related Products: CCK-SAP (Cat. #IT-31)
Learning of food preferences: mechanisms and implications for obesity & metabolic diseases
Berthoud HR, Morrison CD, Ackroff K, Sclafani A (2021) Learning of food preferences: mechanisms and implications for obesity & metabolic diseases. Int J Obes (Lond) 45(10):2156-2168. doi: 10.1038/s41366-021-00894-3
Objective: This review focuses on postoral nutrient sensing and signaling as an essential part of the reward system that shapes preferences for the associated flavors of foods.
Summary: There is a critical role for the vagal gut-to-brain axis in motivation and reward. An implication for obesity treatment is that bariatric surgery may alter vagal function.
Usage: Han et al. injected 0.5 µl of CCK-SAP (250 ng/µl) into the R-NG of VGlut2-ires-Cre mice.
See: Han W et al. A Neural Circuit for Gut-Induced Reward. Cell 175:665-678, 2018.
Related Products: CCK-SAP (Cat. #IT-31)
Dissection and surgical approaches to the mouse jugular-nodose ganglia
Han W, de Araujo IE (2021) Dissection and surgical approaches to the mouse jugular-nodose ganglia. STAR Protocols 2(2):100474. doi: 10.1016/j.xpro.2021.100474
Usage: Injected 0.5 µl of CCK-SAP (250 ng/µl) into the R-NG of VGlut2-ires-Cre mice.
Related Products: CCK-SAP (Cat. #IT-31)
For complete details on the use and execution of this protocol, please refer to Han et al.
See Also: Han W et al. A neural circuit for gut-induced reward. Cell 175:665-678, 2018.
Vagotomy and insights into the microbiota-gut-brain axis
Liu Y, Forsythe P (2021) Vagotomy and insights into the microbiota-gut-brain axis. Neurosci Res 168:20-27. doi: 10.1016/j.neures.2021.04.001
Objective: To review the use of vagotomy as a tool to explore the role of the vagus nerve in gut to brain signaling.
Summary: This review article is a summary of the knowledge gained from vagotomy, a surgical procedure that involves removing part of the vagus nerve. The article discusses using CCK-SAP to specifically ablate afferent vagal nerves in the gastrointestinal tract.
Usage: The article references a study by Diepenbroek et al. that used CCK-SAP in the following dosages: In vitro: each well was treated with a different dose of saporin conjugates (0, 2.4, 24, or 240 ng) for 24 h. In vivo: An equal volume (rat: 1 µl; mouse: 0.5 µl) of CCK-SAP (250 ng/µl) or Saporin (250 ng/µl) was injected at two sites rostral and caudal to the laryngeal nerve branch.
Related Products: CCK-SAP (Cat. #IT-31), Saporin (Cat. #PR-01)
See Also:
Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet.
McDougle M, Quinn D, Diepenbroek C, Singh A, de la Serre C, de Lartigue G (2021) Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet. Acta Physiol (Oxf) 231(3):e13530. doi: 10.1111/apha.13530
Objective: To assess the function of the vagus nerve lack specificity.
Summary: Intact sensory vagal neurons prevent hyperphagia and exacerbation of weight gain in response to a HFHS diet by promoting lipid-mediated satiation.
Usage: Rat nodose ganglia were injected bilaterally with either CCK-SAP or unconjugated saporin as a control.
Related Products: CCK-SAP (Cat. #IT-31)
From obesity to hippocampal neurodegeneration: Pathogenesis and non-pharmacological interventions
Lee TH, Yau SY (2021) From obesity to hippocampal neurodegeneration: Pathogenesis and non-pharmacological interventions. Int J Mol Sci 22(1):201. doi: 10.3390/ijms22010201
Summary: This review provides insights into how chronic metabolic disorders, like obesity, could impair brain health and cognitive functions in later life. The authors reference the use of CCK-SAP into the nodose ganglia to impair spatial memory and contextual episodic memory.
Related Products: CCK-SAP (Cat. #IT-31)
Intestinal glucagon-like peptide-1 effects on food intake: Physiological relevance and emerging mechanisms
Krieger JP (2020) Intestinal glucagon-like peptide-1 effects on food intake: Physiological relevance and emerging mechanisms. Peptides 131:170342. doi: 10.1016/j.peptides.2020.170342 PMID: 32522585
Objective: Review of findings of GLP-1 involvement in obesity.
Summary: The most selective method of gastrointestinal vagal deafferentation to date used CCK-SAP injected into the nodose ganglia which blunts the anorexigenic effect of IP GLP-1 administration.
Related Products: CCK-SAP (Cat. #IT-31)
See Also:
OP11: Role of spinal cholecystokinin receptor 2 in alloknesis models.
Tominaga M, Kusube F, Honda K, Komiya E, Takahashi N, Naito H, Suga Y, Takamori K (2019) OP11: Role of spinal cholecystokinin receptor 2 in alloknesis models. Itch 4:1-62. doi: 10.1097/itx.0000000000000030
Objective: To determine the detailed molecular and cellular mechanisms that induce alloknesis via the spinal CCK2 receptor.
Summary: Ablation of spinal CCK receptor-expressing cells by i.t. injection of CCK-SAP attenuated CCK8S-induced alloknesis in comparison with Blank-SAP control mice.
Usage: Intrathecal injection
Related Products: CCK-SAP (Cat. #IT-31), Blank-SAP (Cat. #IT-21)
Medial septum cholinergic signaling regulates gastrointestinal-derived vagus sensory nerve communication to the hippocampus
Suarez AN, Liu CM, Cortella AM, Noble EN, Kanoski SE (2019) Medial septum cholinergic signaling regulates gastrointestinal-derived vagus sensory nerve communication to the hippocampus. Neuroscience 2019 Abstracts 601.19. Society for Neuroscience, Chicago, IL.
Summary: The vagus nerve delivers bi-directional communication between feeding-relevant gastrointestinal (GI) signals and the brain. Vagal sensory-mediated GI satiation signals, including gastric distension and intra-gastric nutrient infusion, activate neurons in the hippocampus (HPC). Recent work from our lab revealed that selective GI-derived vagal sensory signaling is required for HPC-dependent episodic and visuospatial memory, effects accompanied by reduced dorsal HPC (dHPC) expression of neurotrophic and neurogenic markers. To investigate the neural pathways mediating gut regulation of hippocampal-dependent memory, here we investigate the hypothesis that GI-derived signals communicate to dHPC neurons via cholinergic input from the medial septum, a memory-promoting pathway that is vulnerable to disruption in various degenerative dementia diseases. To explore this putative gut-to-brain pathway, we administered 192IgG-saporin, a neurotoxin that selectively kills cholinergic neurons via apoptosis, in the medial septum to determine whether septal cholinergic neurons regulate vagally-mediated neuronal activation in dHPC. Results revealed that elimination of cholinergic neurons in the MS reduced peripherally-administered cholecystokinin (CCK)-induced c-Fos expression in the dHPC, suggesting that cholinergic inputs from the MS transmit GI-derived signaling to the dHPC. Consistent with this interpretation, dHPC protein expression of vesicular acetylcholine transporter (VAChT), which promotes memory function and acetylcholine release without disrupting other co- released molecules, was significantly reduced in rats with GI-specific vagal sensory ablation via nodose ganglion injections of CCK conjugated to saporin. Collectively these results suggest that GI-derived vagal sensory signaling infuences memory function via enhancement of MS cholinergic signaling to the dPHC.
Related Products: 192-IgG-SAP (Cat. #IT-01), CCK-SAP (Cat. #IT-31)