The ability of the mesocortical dopamine system to operate in distinct temporal modes.
BACKGROUND
This review discusses evidence that cells in the mesocortical dopamine (DA) system influence information processing in target areas across three distinct temporal domains.


CONCLUSIONS
Phasic bursting of midbrain DA neurons may provide temporally precise information about the mismatch between expected and actual rewards (prediction errors) that has been hypothesized to serve as a learning signal in efferent regions. However, because DA acts as a relatively slow modulator of cortical neurotransmission, it is unclear whether DA can indeed act to precisely transmit prediction errors to prefrontal cortex (PFC). In light of recent physiological and anatomical evidence, we propose that corelease of glutamate from DA and/or non-DA neurons in the VTA could serve to transmit this temporally precise signal. In contrast, DA acts in a protracted manner to provide spatially and temporally diffuse modulation of PFC pyramidal neurons and interneurons. This modulation occurs first via a relatively rapid depolarization of fast-spiking interneurons that acts on the order of seconds. This is followed by a more protracted modulation of a variety of other ionic currents on timescales of minutes to hours, which may bias the manner in which cortical networks process information. However, the prolonged actions of DA may be curtailed by counteracting influences, which likely include opposing actions at D1 and D2-like receptors that have been shown to be time- and concentration-dependent. In this way, the mesocortical DA system optimizes the characteristics of glutamate, GABA, and DA neurotransmission both within the midbrain and cortex to communicate temporally precise information and to modulate network activity patterns on prolonged timescales.
Lapish
Christopher C
CC
Department of Neurosciences, Medical University of South Carolina, Suite 430 BSB 173 Ashley, Charleston, SC, USA. lapishc@musc.edu
Kroener
Sven
S
Durstewitz
Daniel
D
Lavin
Antonieta
A
Seamans
Jeremy K
JK
D000818:Animals; D003071:Cognition / Q000502:physiology*; D004298:Dopamine / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007395:Interneurons / Q000378:metabolism; D007858:Learning / Q000502:physiology*; D008636:Mesencephalon / Q000166:cytology / Q000378:metabolism*; D009431:Neural Conduction; D009434:Neural Pathways / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism*; D017397:Prefrontal Cortex / Q000166:cytology / Q000378:metabolism*; D017966:Pyramidal Cells / Q000378:metabolism; D011954:Receptors, Dopamine / Q000378:metabolism*; D012201:Reward; D009435:Synaptic Transmission; D013997:Time Factors; D017557:Ventral Tegmental Area / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018377:Neurotransmitter Agents; D011954:Receptors, Dopamine; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D004298:Dopamine