Oxytocin activation of neurons in ventral tegmental area and interfascicular nucleus of mouse midbrain

Tang, Yamei; Chen, Zhiheng; Tao, Huai; Li, Cunyan; Zhang, Xianghui; Tang, Anliu; Liu, Yong

doi:10.1016/j.neuropharm.2013.10.004

Cited by 46 publications

(40 citation statements)

References 49 publications

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“…The plasma [OXT] for mice injected with vehicle only was ∼0.1 nM, with a range of 0.01 to 0.49 nM, similar to the 0.02 to 0.1 nM value reported in other rodent studies [38, 40, 41]. On the other hand, the EC 50 for central OXT-responsive neurons is ∼22 nM and ∼33 nM for OXT-responsive taste cells [26, 41]. Thus, we selected an i.p.…”

Section: Resultssupporting

confidence: 83%

Oxytocin decreases sweet taste sensitivity in mice

Sinclair

Perea-Martinez

Abouyared

et al. 2015

Physiology & Behavior

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Oxytocin (OXT) suppresses food intake and lack of OXT leads to overconsumption of sucrose. Taste bud cells were recently discovered to express OXT-receptor. In the present study we tested whether administering OXT to wild-type mice affects their licking behavior for tastants in a paradigm designed to be sensitive to taste perception. We injected C57BL/6J mice intraperitoneally (i.p.) with 10 mg/kg OXT and assayed their brief-access lick responses, motivated by water deprivation, to NaCl (300 mM), citric acid (20 mM), quinine (0.3 mM), saccharin (10 mM), and a mix of MSG and IMP (100 mM and 0.5 mM respectively). OXT had no effect on licking for NaCl, citric acid, or quinine. A possible effect of OXT on saccharin and MSG+IMP was difficult to interpret due to unexpectedly low lick rates to water (the vehicle for all taste solutions), likely caused by the use of a high OXT dose that suppressed licking and other behaviors. A subsequent experiment focused on another preferred tastant, sucrose, and employed a much lower OXT dose (0.1 mg/kg). This modification, based on our measurements of plasma OXT following i.p. injection, permitted us to elevate plasma [OXT] sufficiently to preferentially activate taste bud cells. OXT at this low dose significantly reduced licking responses to 0.3 M sucrose, and overall shifted the sucrose concentration – behavioral response curves rightward (mean EC50saline = 0.362 M vs. EC50OXT = 0.466 M). Males did not differ from females under any condition in this study. We propose that circulating oxytocin is another factor that modulates taste-based behavior.

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Section: Resultssupporting

confidence: 83%

Oxytocin decreases sweet taste sensitivity in mice

Sinclair

Perea-Martinez

Abouyared

et al. 2015

Physiology & Behavior

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“…In addition, oxytocin-expressing neurons in the PVN project to the VTA (Melis et al, 2007). Oxytocin activates VTA neurons in both mice and humans, influencing the processing of socially relevant cues (Groppe et al, 2013; Tang et al, 2014) and oxytocin receptor blockade in the VTA prevents social attachment in rodents (Pedersen et al, 1994). Given that social stimulation can be particularly rewarding and triggers synaptic potentiation in VTA DA neurons of birds (Huang and Hessler, 2008), we examined whether direct social interaction evokes long-term potentiation (LTP) of synaptic inputs to VTA DA neurons (Figure S7A–S7C).…”

Section: Resultsmentioning

confidence: 99%

Microbial Reconstitution Reverses Maternal Diet-Induced Social and Synaptic Deficits in Offspring

Buffington

Prisco

Auchtung

et al. 2016

Cell

860

845

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SUMMARY Maternal obesity during pregnancy has been associated with increased risk of neurodevelopmental disorders, including autism spectrum disorder (ASD), in offspring. Here we report that maternal high fat diet (MHFD) induces a shift in microbial ecology that negatively impacts offspring social behavior. Social deficits and gut microbiota dysbiosis in MHFD offspring are prevented by co-housing with offspring of mothers on a regular diet (MRD) and transferable to germ-free mice. In addition, social interaction induces synaptic potentiation (LTP) in the ventral tegmental area (VTA) of MRD, but not MHFD offspring. Moreover, MHFD offspring had fewer oxytocin immunoreactive neurons in the hypothalamus. Using metagenomics and precision microbiota reconstitution, we identified a single commensal strain that corrects oxytocin levels, LTP, and social deficits in MHFD offspring. Our findings causally link maternal diet, gut microbial imbalance, VTA plasticity and behavior, and suggest that probiotic treatment may relieve specific behavioral abnormalities associated with neurodevelopmental disorders.

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“…If we apply this interpretation to our findings, our data support a model in which oxytocin administration increases tonic activation of midbrain neurons without affecting phasic responses. In support of this possibility, recent experiments in mice have shown that oxytocin directly activates a subset of neurons in the VTA (Tang et al 2014); how oxytocin influences dopamine dynamics in the midbrain remains unclear. Another possibility is that oxytocin affects vascular responses or neurovascular coupling, prolonging the temporal evolution of the BOLD signal.…”

Section: Discussionmentioning

confidence: 99%

Oxytocin modulates hemodynamic responses to monetary incentives in humans

et al. 2016

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Oxytocin is a neuropeptide widely recognized for its role in regulating social and reproductive behavior. Increasing evidence from animal models suggests that oxytocin also modulates reward circuitry in non-social contexts, but evidence in humans is lacking. Here we examined the effects of oxytocin administration on reward circuit function in 18 healthy men as they performed a monetary incentive task. The blood oxygenation level dependent (BOLD) signal was measured using functional magnetic resonance imaging in the context of a randomized, double-blind, placebo-controlled, crossover trial of intranasal oxytocin. We found that oxytocin increases the BOLD signal in the midbrain (substantia nigra and ventral tegmental area) during the late phase of the hemodynamic response to incentive stimuli. Oxytocin’s effects on midbrain responses correlated positively with its effects on positive emotional state. We did not detect an effect of oxytocin on responses in the nucleus accumbens. Whole-brain analyses revealed that oxytocin attenuated medial prefrontal cortical deactivation specifically during anticipation of loss. Our findings demonstrate that intranasal administration of oxytocin modulates human midbrain and medial prefrontal function during motivated behavior. These findings suggest that endogenous oxytocin is a neurochemical mediator of reward behaviors in humans – even in a non-social context – and that the oxytocinergic system is a potential target of pharmacotherapy for psychiatric disorders that involve dysfunction of reward circuitry.

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Oxytocin activation of neurons in ventral tegmental area and interfascicular nucleus of mouse midbrain

Cited by 46 publications

References 49 publications

Oxytocin decreases sweet taste sensitivity in mice

Oxytocin decreases sweet taste sensitivity in mice

Microbial Reconstitution Reverses Maternal Diet-Induced Social and Synaptic Deficits in Offspring

Oxytocin modulates hemodynamic responses to monetary incentives in humans

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