DAncing past the DAT at a DA synapse

Cragg, Stephanie J.; Rice, Margaret E.

doi:10.1016/j.tins.2004.03.011

Cited by 339 publications

(381 citation statements)

References 56 publications

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“…In particular, the potentiation of the DA-induced neuronal responses, caused by the blocking effects of MDMA on DAT, could facilitate the activation of DA receptors principally localized at the amine release sites (Cragg and Rice 2004). Interestingly, the same facilitation of DA responses is not observed with drugs that have transportermediated releasing actions (Mercuri et al 1989) and instead release DA at either the synaptic or the extrasynaptic sites.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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Section: Discussionmentioning

confidence: 99%

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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“…Overflow is indeed measured as extracellular transients in dopaminergic concentrations in many cyclic voltammetry experiments (Garris et al, 1997;Phillips et al, 2003;Sombers et al, 2009). However, regarding filtering this signal by slow reuptake, the large transients from DA bursting are relatively rare and are cleared quickly (Cragg and Rice, 2004); thus, it may be that tonic DA is more influenced by other variables, for example, background levels of dopaminergic spiking or the number of active versus silent DA neurons (Floresco et al, 2003;Arbuthnott and Wickens, 2007). This is consistent with the concept of tonic DA as an at least partly independently regulated channel from phasic DA (Grace, 1991), and, in terms of the average reward hypothesis, with a more complex mechanism for computing an average reward signal, drawing on additional sources of information other than the phasic signal (Niv et al, 2007).…”

Section: Modeling the Dual Function Of Damentioning

confidence: 99%

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Cools

Nakamura²,

Daw³

2010

Neuropsychopharmacol

408

369

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Serotonin, like dopamine (DA), has long been implicated in adaptive behavior, including decision making and reinforcement learning. However, although the two neuromodulators are tightly related and have a similar degree of functional importance, compared with DA, we have a much less specific understanding about the mechanisms by which serotonin affects behavior. Here, we draw on recent work on computational models of dopaminergic function to suggest a framework by which many of the seemingly diverse functions associated with both DA and serotoninFcomprising both affective and activational ones, as well as a number of other functions not overtly related to eitherFcan be seen as consequences of a single root mechanism.

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“…The concentration of exogenous DA required to activate comparable D2-IPSCs to those seen with endogenously evoked somatodendritic DA release is at the micromolar level, rather than the nanomolar levels expected for low-affinity-state receptors. Given that [DA] o falls rapidly with distance from a release site [53,69,120], the site of receptor activation would need to be synaptic or at least peri-synaptic. The relatively constant time course of D2-IPSPs would also be consistent with diffusion across a constant distance [23], e.g.…”

Section: What Is the Role Of Volume Transmissionmentioning

confidence: 99%

Somatodendritic dopamine release: recent mechanistic insights

Rice

Patel

2015

Phil. Trans. R. Soc. B

Self Cite

102

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. Dopamine (DA) is a key transmitter in motor, reward and cogitative pathways, with DA dysfunction implicated in disorders including Parkinson's disease and addiction. Located in midbrain, DA neurons of the substantia nigra pars compacta project via the medial forebrain bundle to the dorsal striatum (caudate putamen), and DA neurons in the adjacent ventral tegmental area project to the ventral striatum (nucleus accumbens) and prefrontal cortex. In addition to classical vesicular release from axons, midbrain DA neurons exhibit DA release from their cell bodies and dendrites. Somatodendritic DA release leads to activation of D2 DA autoreceptors on DA neurons that inhibit their firing via G-protein-coupled inwardly rectifying K þ channels. This helps determine patterns of DA signalling at distant axonal release sites. Somatodendritically released DA also acts via volume transmission to extrasynaptic receptors that modulate local transmitter release and neuronal activity in the midbrain. Thus, somatodendritic release is a pivotal intrinsic feature of DA neurons that must be well defined in order to fully understand the physiology and pathophysiology of DA pathways. Here, we review recent mechanistic aspects of somatodendritic DA release, with particular emphasis on the Ca 2þ dependence of release and the potential role of exocytotic proteins.

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DAncing past the DAT at a DA synapse

Cited by 339 publications

References 56 publications

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Somatodendritic dopamine release: recent mechanistic insights

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