An electrophysiological characterization of ventral tegmental area dopaminergic neurons during differential pavlovian fear conditioning in the awake rabbit

Guarraci, Fay A.; Kapp, Bruce S.

doi:10.1016/s0166-4328(98)00102-8

Cited by 178 publications

(125 citation statements)

References 42 publications

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“…However, in terms of absolute magnitude, the increase was relatively week (~12 imp/s). This response pattern well agrees with preferential excitations of presumed DA neurons induced by arousing somato-sensory stimuli in awake animals, as shown both in the SNc (Freeman et al, 1985;Freeman and Bunney, 1987;Steinfels et al, 1983;Strecker et al, 1985;Schultz, 1986;Trulson, 1985) and VTA (Guarraci and Kapp, 1999;Freeman and Bunney, 1987;Kiyatkin, 1988;Horvitz et al, 1997;Schultz, 1986). These data are also consistent with large body of neurochemical data (DA metabolism, [DA] evaluated by microdialysis or electrochemistry) suggesting increased DA release, especially in cortical projections, associated with arousing and aversive stimulation (Abercrombie et al, 1989;Deutch et al, 1985;Fadda et al, 1978;Feenstra et al, 2000Feenstra et al, , 2001Kiyatkin, 1995;Le Moal and Simon, 1991;Thierry et al, 1976).…”

Section: Sensory Responses Of Ls and Ss Vta Neuronssupporting

confidence: 86%

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Brown

Kiyatkin

2008

Brain Research

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Intravenous (iv) cocaine mimics salient somato-sensory stimuli in their ability to induce rapid physiological effects, which appear to involve its action on peripherally located neural elements and fast neural transmission via somato-sensory pathways. To further clarify this mechanism, single-unit recording with fine glass electrodes was used in awake rats to examine responses of ventral tegmental area (VTA) neurons, both presumed dopamine (DA) and non-DA, to iv cocaine and tail-press, a typical somato-sensory stimulus. To exclude the contribution of DA mechanisms to the observed neuronal responses to sensory stimuli and cocaine, recordings were conducted during full DA receptor blockade (SCH23390+eticloptide).Iv cocaine (0.25 mg/kg delivered over 10 s) induces significant excitations of ~63% of long-spike (presumed DA) and ~70% of short-spike (presumed non-DA) VTA neurons. In both subgroups, neuronal excitations occurred with short latencies (4-8 s), peaked at 10-20 s (30-40% increase over baseline) and disappeared at 30-40 s after the injection onset. Most long-(67%) and short-spike (89%) VTA neurons also showed phasic responses to tail-press (5-s). All responsive long-spike cells were excited by tail-press; excitations were very rapid (peak at 1 s) and strong (100% rate increase over baseline) but brief (2-3 s). In contrast, both excitations (60%) and inhibitions (29%) were seen in short-spike cells. These responses were also rapid and transient, but excitations of short-spike units were more prolonged and sustained (10-15 s) than in long-spike cells.These data suggest that in awake animals iv cocaine, like somato-sensory stimuli, rapidly and transiently excites VTA neurons of different subtypes. Therefore, along with direct action on specific brain substrates, central effects of cocaine may occur via indirect mechanism, involving peripheral neural elements, visceral sensory nerves and rapid neural transmission. Via this mechanism, cocaine, like somato-sensory stimuli, can rapidly activate DA neurons and induce phasic DA release, creating the conditions for DA accumulation by a later occurring and prolonged direct inhibiting action on DA uptake. By providing a rapid neural signal and triggering transient neural activation, such a peripherally driven action might play a crucial role in the sensory effects of COC, thus contributing to learning and development of drug-taking behavior.

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Section: Sensory Responses Of Ls and Ss Vta Neuronssupporting

confidence: 86%

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Brown

Kiyatkin

2008

Brain Research

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“…Dopaminergic activity also falls below baseline when the monkey is presented with a stimulus that predicts punishment (Mirenowicz & Schultz, 1996; but see Guarraci & Kapp, 1999).…”

Section: The Mesencephalic Dopamine Systemmentioning

confidence: 99%

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

Holroyd¹,

Coles²

2002

Psychological Review

3,439

357

3,712

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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.Human beings learn from the consequences of their actions. Thorndike (1911Thorndike ( /1970 originally described this phenomenon with his law of effect, which made explicit the commonsense notion that actions that are followed by feelings of satisfaction are more likely to be generated again in the future, whereas actions that are followed by negative outcomes are less likely to reoccur. This fundamental reinforcement learning principle has been developed by the artificial intelligence community into a body of algorithms used to train autonomous systems to operate independently in complex and uncertain environments (Barto & Sutton, 1997;Sutton & Barto, 1998). Research has also evaluated the neural mechanisms underlying reinforcement learning in biological systems, but these mechanisms are still poorly understood.In this article, we provide a framework for understanding the neural basis of reinforcement learning in humans. Our proposal links together two areas of research that have, until now, been considered separately. On the one hand, we have previously inferred the existence of a generic, high-level error-processing system in humans from the error-related negativity (ERN), a negative deflection in the ongoing electroencephalogram (EEG) seen when human participants commit errors in a wide variety of psychological tasks. The ERN appears to be generated in the anterior cingulate cortex. On the other hand, other researchers have argued that the mesencephalic dopamine system conveys reinforcement learning signals to the basal ganglia and frontal cortex, where they are used to facilitate the development of adaptive motor programs. Although the reinforcement learning function attributed to the mesencephalic dopamine system and the error-processing function associated with the ERN appear to be concerned with the same problem-namely, evaluating the appropriateness of ongoing events, and using that information to facilitate the development and expression of adaptive behaviors-a possible relationship between these two systems remains to be explored.In this article, we propose a hypothesis that unifies the two accounts by explicitly linking the gen...

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“…those that give rise to mesolimbocortical DA pathways, respond to each of these types of salient events [57]. Single-unit recordings have demonstrated that VTA DA neurons show phasic elevations in activity in response to novel events [72], unexpected rewards [72,79], conditioned predictors of reward [72,79], primary and conditioned aversive stimuli [46,66] but see [80], and high intensity auditory and visual events with neither conditioned reward nor aversive properties [59].…”

Section: Da Neurons Respond To Salient Unexpected Eventsmentioning

confidence: 99%

“…If DA neurons are similarly activated by the onset of aversive events, the scenario becomes less plausible, for it would lead to the strengthening of behavioral responses that lead to the onset of aversive consequences. While there is evidence to suggest that the DA response to reward events may be in some way distinct from the DA response to aversive events [14,74,80,102], other evidence suggests that the DA response to reward and aversive event onset is likely to be similar, given that the events are of comparable intensity or significance [46,57,66,99]. If DA neurons respond to surprising/arousing events, regardless of appetitive or aversive value, one would postulate that DA activation does not serve to increase the likelihood that a given behavioral response is repeated under similar input conditions; that is to say, the primary function of DA in striatal plasticity is unlikely to involve a strengthening of stimulus Á/response (SÁ/R) connections.…”

Section: Da Activity Gates the Throughput Of Sensorimotor And Incentimentioning

confidence: 99%

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

Horvitz

2002

Behavioural Brain Research

186

148

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An electrophysiological characterization of ventral tegmental area dopaminergic neurons during differential pavlovian fear conditioning in the awake rabbit

Cited by 178 publications

References 42 publications

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

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

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

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