The authors present a unified account of 2 neural systems concerned with the development and expression of adaptive behaviors: a mesencephalic dopamine system for reinforcement learning and a “generic” error-processing system associated with the anterior cingulate cortex The existence of the error-processing system has been inferred from the error-related negativity (ERN), a component of the event-related brain potential elicited when human participants commit errors in reaction-time tasks The authors propose that the ERN is generated when a negative reinforcement learning signal is conveyed to the anterior cingulate cortex via the mesencephalic dopamine system and that this signal is used by the anterior cingulate cortex to modify performance on the task at hand They provide support for this proposal using both computational modeling and psychophysiological experimentation

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The neural basis of human error processing: Reinforcement learning, dopamine, and the error-related negativity.

A review of central 5-HT receptors and their function

Dopamine transmission in the initiation and expression of drug- and stress-induced sensitization of motor activity

Extraversion has two central characteristics: (1) interpersonal engagement, which consists of affiliation (enjoying and valuing close interpersonal bonds, being warm and affectionate) and agency (being socially dominant, enjoying leadership roles, being assertive, being exhibitionistic, and having a sense of potency in accomplishing goals) and (2) impulsivity, which emerges from the interaction of extraversion and a second, independent trait (constraint). Agency is a more general motivational disposition that includes dominance, ambition, mastery, efficacy, and achievement. Positive affect (a combination of positive feelings and motivation) is closely associated with extraversion. Extraversion is accordingly based on positive incentive motivation. Parallels between extraversion (particularly its agency component) and a mammalian behavioral approach system based on positive incentive motivation implicate a neuroanatomical network and modulatory neurotransmitters in the processing of incentive motivation. A corticolimbic-striatal-thalamic network (1) integrates the salient incentive context in the medial orbital cortex, amygdala, and hippocampus; (2) encodes the intensity of incentive stimuli in a motive circuit composed of the nucleus accumbens, ventral pallidum, and ventral tegmental area dopamine projection system; and (3) creates an incentive motivational state that can be transmitted to the motor system. Individual differences in the functioning of this network arise from functional variation in the ventral tegmental area dopamine projections, which are directly involved in coding the intensity of incentive motivation. The animal evidence suggests that there are three neurodevelopmental sources of individual differences in dopamine: genetic, "experience-expectant," and "experience-dependent." Individual differences in dopamine promote variation in the heterosynaptic plasticity that enhances the connection between incentive context and incentive motivation and behavior. Our psychobiological threshold model explains the effects of individual differences in dopamine transmission on behavior, and their relation to personality traits is discussed.

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Neurobiology of the structure of personality: Dopamine, facilitation of incentive motivation, and extraversion.

Dopamine in Motivational Control: Rewarding, Aversive, and Alerting

Inhibitory effects of ventral tegmental area stimulation on the activity of prefrontal cortical neurons: evidence for the involvement of both dopaminergic and GABAergic components.

Effect of noxious tail pinch on the discharge rate of mesocortical and mesolimbic dopamine neurons: selective activation of the mesocortical system.

Differential effects of ascending neurons containing dopamine and noradrenaline in the control of spontaneous activity and of evoked responses in the rat prefrontal cortex

BACKGROUND Astrocytes represent a major nonneuronal cell population in the central nervous system (CNS) and are actively involved in several brain functions. These cells are coupled by gap junctions (GJ) into a syncytial-like network resulting in cellular communication through ionic and metabolic exchange between adjacent astrocytes. Whether anesthetics affect astrocyte function is not known. In the present study, the effects of general anesthetics on GJ permeability were investigated in primary cultures of mouse striatal astrocytes. METHODS Junctional permeability was determined by using the fluorescent probe Lucifer yellow and the scrape loading/dye transfer technique. Confluent cells were preincubated 5 min with various concentrations of anesthetic agents and GJ permeability was estimated by measuring the area occupied by the dye from digitalized images taken 8 min after cell loading. RESULTS Of the intravenous anesthetics tested, only propofol (P: 10(-4) M, P < 0.01 and 10(-5) M, P < 0.05) and etomidate (ET: 10(-4) M, P < 0.05, but not 10(-5) M) induced a significant reduction of GJ permeability. In contrast, diazepam (10(-5) M), morphine (10(-4) M), ketamine (10(-4) M), thiopental (10(-4) M), and clonidine (10(-7) M) did not affect junctional permeability. In addition, the halogenated anesthetics halothane, enflurane, and isoflurane induced a dose-dependent closure of GJ. For halothane, enflurane, and isoflurane, the maximum effect was achieved with a 10(-4) M, 1.6 x 10(-3) M, and 10(-3) M anesthetic concentration, respectively. Removal of volatile anesthetics resulted in the restoration of the control fluorescence area between 15 and 45 min. The time course of recovery of GJ permeability was examined more precisely for shorter periods of halothane administration (5 min, 1 mM). Under these conditions, the rate of dye spread returned to control values following anesthetic washout, while, during the same period of time, complete uncoupling of GJ was still observed in the presence of a 1 mM halothane concentration. CONCLUSIONS These results indicate that general anesthetics differentially affect GJ permeability in cultured astrocytes. This uncoupling effect (closure of gap junctions) may contribute to the mechanisms of action of some anesthetic agents (primarily volatile anesthetics) at the level of the CNS by altering astrocyte communication.

Effects of General Anesthetics on Intercellular Communications Mediated by Gap Junctions between Astrocytes in Primary Culture

Publisher Summary This chapter focuses on the influence of the ascending monoaminergic systems on the activity of the rat prefrontal cortex (PFC). The analysis of the influence of the aminergic ascending systems on cerebral functions has generated considerable interest because several psychoactive drugs are known to interfere with dopaminergic (DA), noradrenergic (NA), or serotoninergic (5HT) neurotransmission. The PFC has a determining influence in the regulation of emotional states, in the control of motor activity, and in cognitive processes, such as representational memory. The inhibition of the spontaneous firing is the most common effect reported in the cerebral cortex. Ascending DA, 5HT, and NA neurons, which originate respectively from the ventral tegmental area (VTA), the raphe nuclei, and the locus coeruleus markedly modulate neuronal activity in the PFC. The main differences in the influence of DA and 5HT as compared to NA afferents on the spontaneous activity or evoked responses of PFC cells are reviewed in the chapter. The influence of the three aminergic systems— DA, NA, and 5HT—is observed on efferent PFC neurons. A characteristic of the output PFC neurons in the rat is the extensive collateralization of their axons.

J. Mantz

Papers

Inhibitory effects of ventral tegmental area stimulation on the activity of prefrontal cortical neurons: evidence for the involvement of both dopaminergic and GABAergic components.

Effect of noxious tail pinch on the discharge rate of mesocortical and mesolimbic dopamine neurons: selective activation of the mesocortical system.

Differential effects of ascending neurons containing dopamine and noradrenaline in the control of spontaneous activity and of evoked responses in the rat prefrontal cortex

Effects of General Anesthetics on Intercellular Communications Mediated by Gap Junctions between Astrocytes in Primary Culture

Influence of the ascending monoaminergic systems on the activity of the rat prefrontal cortex.