Decreased Vesicular Somatodendritic Dopamine Stores in Leptin-Deficient Mice

Roseberry, Aaron G.; Painter, Tammie; Mark, Gregory P.; Williams, John T.

doi:10.1523/jneurosci.1235-07.2007

Cited by 54 publications

(48 citation statements)

References 41 publications

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“…6). Forskolin is thought to increase synaptic transmission by increasing the probability of neurotransmitter release, and I have shown previously that forskolin increases the D2R IPSC solely via a presynaptic mechanism, as it does not affect the postsynaptic response to iontophoretically applied dopamine (Roseberry et al 2007). Thus, if dopamine neurons from fasted mice indeed do have a higher probability for dopamine release, the effects of forskolin should be reduced in fasted mice, which is what was observed in these studies.…”

Section: Discussionmentioning

confidence: 99%

Acute fasting increases somatodendritic dopamine release in the ventral tegmental area

Roseberry

2015

Journal of Neurophysiology

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Section: Discussionmentioning

confidence: 99%

Acute fasting increases somatodendritic dopamine release in the ventral tegmental area

Roseberry

2015

Journal of Neurophysiology

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“…Acute brain slices were prepared as previously described (Roseberry et al 2007). Briefly, adult male mice were anesthetized with isofluorane and decapitated.…”

Section: Methodsmentioning

confidence: 99%

“…Putative DA neurons were identified by their location relative to the medial terminal nucleus of the accessory optic tract, the presence of hyperpolarization-activated cation currents (H current), the presence of spontaneous pacemaker firing, and the sensitivity to DA (Johnson and North 1992). Although recent studies have raised questions on the utility of using these measures to identify VTA DA neurons (Margolis et al 2006), the characteristics described above have been widely used in electrophysiology studies to identify DA neurons within the VTA (Beckstead et al 2004;Nimitvilai et al 2012;Nimitvilai et al 2013;Perra et al 2011;Roseberry et al 2007).…”

Section: Methodsmentioning

confidence: 99%

Neurotensin inhibits both dopamine- and GABA-mediated inhibition of ventral tegmental area dopamine neurons

Stuhrman

Roseberry

2015

Journal of Neurophysiology

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Stuhrman K, Roseberry AG. Neurotensin inhibits both dopamine-and GABA-mediated inhibition of ventral tegmental area dopamine neurons. J Neurophysiol 114: 1734 -1745, 2015. First published July 15, 2015 doi:10.1152/jn.00279.2015-Dopamine is an essential neurotransmitter that plays an important role in a number of different physiological processes and disorders. There is substantial evidence that the neuropeptide neurotensin interacts with the mesolimbic dopamine system and can regulate dopamine neuron activity. In these studies we have used whole cell patch-clamp electrophysiology in brain slices from mice to examine how neurotensin regulates dopamine neuron activity by examining the effect of neurotensin on the inhibitory postsynaptic current generated by somatodendritic dopamine release (D2R IPSC) in ventral tegmental area (VTA) dopamine neurons. Neurotensin inhibited the D2R IPSC and activated an inward current in VTA dopamine neurons that appeared to be at least partially mediated by activation of a transient receptor potential C-type channel. Neither the inward current nor the inhibition of the D2R IPSC was affected by blocking PKC or calcium release from intracellular stores, and the inhibition of the D2R IPSC was greater with neurotensin compared with activation of other G q -coupled receptors. Interestingly, the effects of neurotensin were not specific to D2R signaling as neurotensin also inhibited GABA B inhibitory postsynaptic currents in VTA dopamine neurons. Finally, the effects of neurotensin were significantly larger when intracellular Ca 2ϩ was strongly buffered, suggesting that reduced intracellular calcium facilitates these effects. Overall these results suggest that neurotensin may inhibit the D2R and GABA B IPSCs downstream of receptor activation, potentially through regulation of G protein-coupled inwardly rectifying potassium channels. These studies provide an important advance in our understanding of dopamine neuron activity and how it is controlled by neurotensin.

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“…A close interrelation between the signaling pathways controlled by leptin and the dopaminergic and peptidergic signaling systems is supported by the following data obtained with experimental DM and obesity. The leptin deficiency in the obese mice lacking leptin (Lep ob/ob mice) led to a decrease in the content of somatodendritic vesicular DA and the amount of DA to be released (Roseberry et al, 2007). One possible cause is related to a decrease of the number of functionally active DA transporters controlling the synaptic level of DA.…”

Section: Leptinmentioning

confidence: 99%