Dopamine and noradrenaline efflux in the rat prefrontal cortex after classical aversive conditioning to an auditory cue

Feenstra, Matthijs G.P.; Vogel, Michael W.; Botterblom, M.H.A.; Joosten, R; Bruin, Jan

doi:10.1046/j.0953-816x.2001.01471.x

Cited by 79 publications

(59 citation statements)

References 32 publications

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“…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). It appears that this response is typical to the awake conditions when sensory effects and activation mechanisms are intact and functional; somatosensory-evoked discharges typical to most striatal neurons were greatly eliminated during general anesthesia (see Kiyatkin and Brown, 2007;West, 1996).…”

Section: Sensory Responses Of Ls and Ss Vta Neuronssupporting

confidence: 85%

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: 85%

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

Brown

Kiyatkin

2008

Brain Research

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“…Rats were trained in a fully controlled environment (Skinner box) to associate a neutral auditory stimulus with the receipt of an unconditioned stimulus. Applying this approach, we reported that presentation of aversive conditioned stimuli increased both prefrontal NA and DA in vivo efflux (Feenstra et al, 2001), indicating a role for both catecholamines in coding the significance value of stimuli. Therefore, we tested the hypothesis that presentation of appetitive conditioned stimuli would also lead to activation of both catecholamine afferents to the PFC.…”

Section: Introductionmentioning

confidence: 99%

Noradrenaline and Dopamine Efflux in the Prefrontal Cortex in Relation to Appetitive Classical Conditioning

Mingote¹,

Bruin²,

Feenstra³

2004

J. Neurosci.

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We trained rats to learn that an auditory stimulus predicted delivery of reward pellets in the Skinner box. After 2 d of training, we measured changes in efflux of noradrenaline (NA) and dopamine (DA) in the medial prefrontal cortex using microdialysis on the third day. Animals were subjected to a normal rewarded session and an extinction session, in which the auditory stimulus was presented alone. In the rewarded session, both NA and DA efflux were increased, but in extinction, only NA was activated. The data suggest that NA has a role in the reaction to reward-predicting stimuli, which complements that of DA.

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“…GBR increases extracellular dopamine, which in turn generates reactive oxygen species (ROS) (39,40) in regions richly innervated by dopaminergic terminals, such as the ACC. This pharmacological approach partially mimics the pronounced prefrontal dopamine release during psychosocial stress (41,42).…”

Section: Sixmentioning

confidence: 99%

Perineuronal nets protect fast-spiking interneurons against oxidative stress

Cabungcal

Steullet

Morishita

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

437

391

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A hallmark of schizophrenia pathophysiology is the dysfunction of cortical inhibitory GABA neurons expressing parvalbumin, which are essential for coordinating neuronal synchrony during various sensory and cognitive tasks. The high metabolic requirements of these fast-spiking cells may render them susceptible to redox dysregulation and oxidative stress. Using mice carrying a genetic redox imbalance, we demonstrate that extracellular perineuronal nets, which constitute a specialized polyanionic matrix enwrapping most of these interneurons as they mature, play a critical role in the protection against oxidative stress. These nets limit the effect of genetically impaired antioxidant systems and/or excessive reactive oxygen species produced by severe environmental insults. We observe an inverse relationship between the robustness of the perineuronal nets around parvalbumin cells and the degree of intracellular oxidative stress they display. Enzymatic degradation of the perineuronal nets renders mature parvalbumin cells and fast rhythmic neuronal synchrony more susceptible to oxidative stress. In parallel, parvalbumin cells enwrapped with mature perineuronal nets are better protected than immature parvalbumin cells surrounded by less-condensed perineuronal nets. Although the perineuronal nets act as a protective shield, they are also themselves sensitive to excess oxidative stress. The protection might therefore reflect a balance between the oxidative burden on perineuronal net degradation and the capacity of the system to maintain the nets. Abnormal perineuronal nets, as observed in the postmortem patient brain, may thus underlie the vulnerability and functional impairment of pivotal inhibitory circuits in schizophrenia.critical period | extracellular matrix | glutamate cysteine ligase | glutathione | neuronal synchronization F ast-spiking interneurons expressing parvalbumin (PV) constitute a subpopulation of GABA cells that control the output of principal neurons and are necessary for fast rhythmic neuronal synchrony, facilitating information processing during cognitive tasks (1, 2). To coordinate the activity of neuronal assemblies, PV cells are interconnected by both chemical and electrical synapses, have the capacity to fire at high frequency without adaptation, and selectively position inhibitory synaptic terminals onto the cell body and axon initial segment of their target neurons. Fast-spiking properties consequently impose high metabolic demand and increased mitochondrial density, which renders PV cells, but not other interneurons such as calretinin and calbindin cells, particularly sensitive to oxidative stress (3). For instance, ketamine induces superoxide overproduction that strongly impairs PV cells (i.e., loss of normal phenotype including PV immunoreactivity but without cell death) (4, 5). Moreover, severe environmental stressors produce oxidative stress in the brain and impair PV cells (6)(7)(8). Postmortem studies reveal PV-cell anomalies in individuals with schizophrenia or bipolar disorder (9-11). ...

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Dopamine and noradrenaline efflux in the rat prefrontal cortex after classical aversive conditioning to an auditory cue

Cited by 79 publications

References 32 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

Noradrenaline and Dopamine Efflux in the Prefrontal Cortex in Relation to Appetitive Classical Conditioning

Perineuronal nets protect fast-spiking interneurons against oxidative stress

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