Parabrachial Calcitonin Gene-Related Peptide Neurons Mediate Conditioned Taste Aversion

Carter, Matthew E.; Han, Sung; Palmiter, Richard D.

doi:10.1523/jneurosci.3729-14.2015

Cited by 144 publications

(155 citation statements)

References 35 publications

Supporting

Mentioning

146

Contrasting

Order By: Relevance

“…A two-way ANOVA detected a significant interaction of group and treatment ( F (1,14) = 8.077, p = 0.0131). This result is consistent with the direct, excitatory connection between CCK NTS neurons and CGRP neurons within the external lateral PBN found in previous work (Roman et al 2016), because photostimulating CGRP neurons has been shown to induce aversive behaviors such as freezing (Han et al, 2015) and CTA (Carter et al, 2015). Although an aversion was elicited in the RTPP test and Fos was induced in the PBN (Fig.…”

Section: Resultssupporting

confidence: 92%

A tale of two circuits: CCK NTS neuron stimulation controls appetite and induces opposing motivational states by projections to distinct brain regions

2017

View full text Add to dashboard Cite

Cholecystokinin (CCK)-expressing neurons within the nucleus of the solitary tract (CCKNTS) are responsive to satiety signals and their chemogenetic activation suppresses appetite. Optogenetic activation of CCKNTS axon terminals within either the parabrachial nucleus (PBN) or the paraventricular nucleus of the hypothalamus (PVH) is sufficient to suppress feeding. An interesting dichotomy has been revealed when assessing the motivational valence of these two circuits. Activating CCKNTS cell bodies is aversive as demonstrated by conditioned taste aversion and place-preference assays. Activation of the CCKNTS→PBN pathway is also aversive; however, stimulating the CCKNTS→PVH pathway is appetitive when assayed using a real-time, place-preference task. Thus, these two projections from CCKNTS neurons reduce food intake through opposite motivational states; one pathway signals positive valence (CCKNTS→PVH) and the other signals negative valence (CCKNTS→PBN).

show abstract

Section: Resultssupporting

confidence: 92%

A tale of two circuits: CCK NTS neuron stimulation controls appetite and induces opposing motivational states by projections to distinct brain regions

2017

View full text Add to dashboard Cite

show abstract

“…To the best of our knowledge, designer receptors exclusively activated by designer drug has been seldom used to investigate inflammatory anorexia (42). A unique advantage of this technique is that it allows for robust stimulation of feeding without the need for fasting of animals, which can interfere with immunity and the endocrine axis (43)(44)(45).…”

Section: Pharmacogenetics and Brain Surgerymentioning

confidence: 99%

“…In particular, one previous study showed that neuronal activity in the LPBE was required for LPS-induced anorexia (42). Briefly, the LPBE was a major relay for viscerosensory signals originating from the DVC (57,79).…”

Section: Central Viscerosensory Pathways Involved In Inflammatory Anomentioning

confidence: 99%

Lipopolysacharide Rapidly and Completely Suppresses AgRP Neuron-Mediated Food Intake in Male Mice

Liu

Huang

Liu³

et al. 2016

Endocrinology

View full text Add to dashboard Cite

Although Agouti-related peptide (AgRP) neurons play a key role in the regulation of food intake, their contribution to the anorexia caused by proinflammatory insults has yet to be identified. Using a combination of neuroanatomical and pharmacogenetics experiments, this study sought to investigate the importance of AgRP neurons and downstream targets in the anorexia caused by the peripheral administration of a moderate dose of lipopolysaccharide (LPS) (100 μg/kg, ip). First, in the C57/Bl6 mouse, we demonstrated that LPS induced c-fos in select AgRP-innervated brain sites involved in feeding but not in any arcuate proopiomelanocortin neurons. Double immunohistochemistry further showed that LPS selectively induced c-Fos in a large subset of melanocortin 4 receptor-expressing neurons in the lateral parabrachial nucleus. Secondly, we used pharmacogenetics to stimulate the activity of AgRP neurons during the course of LPS-induced anorexia. In AgRP-Cre mice expressing the designer receptor hM3Dq-Gq only in AgRP neurons, the administration of the designer drug clozapine-N-oxide (CNO) induced robust food intake. Strikingly, CNO-mediated food intake was rapidly and completely blunted by the coadministration of LPS. Neuroanatomical experiments further indicated that LPS did not interfere with the ability of CNO to stimulate c-Fos in AgRP neurons. In summary, our findings combined together support the view that the stimulation of select AgRP-innervated brain sites and target neurons, rather than the inhibition of AgRP neurons themselves, is likely to contribute to the rapid suppression of food intake observed during acute bacterial endotoxemia.

show abstract

“…For example, the lateral parabrachial nucleus contains GLP-1 receptors that when activated, suppress food intake (Richard et al, 2014). Neurons in this region have recently been shown to play an essential role in LiCl-induced conditioned taste aversion learning (Carter et al, 2015). These neurons may indirectly influence dopamine signaling through their projection to the central nucleus of the amygdala (Carter et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The Aversive Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central GLP-1 Receptors

Fortin

Chartoff

Roitman

2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent lithium chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiClmediated suppression of NAc dopamine release. Neuropsychopharmacology (2016) 41, 906-915;

show abstract

Parabrachial Calcitonin Gene-Related Peptide Neurons Mediate Conditioned Taste Aversion

Cited by 144 publications

References 35 publications

A tale of two circuits: CCK NTS neuron stimulation controls appetite and induces opposing motivational states by projections to distinct brain regions

A tale of two circuits: CCK NTS neuron stimulation controls appetite and induces opposing motivational states by projections to distinct brain regions

Lipopolysacharide Rapidly and Completely Suppresses AgRP Neuron-Mediated Food Intake in Male Mice

The Aversive Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central GLP-1 Receptors

Contact Info

Product

Resources

About