Medial prefrontal cortical alpha1 adrenoreceptor modulation of the nucleus accumbens dopamine response to stress in Long–Evans rats

NicNiocaill, Brid; Gratton, Alain

doi:10.1007/s00213-007-0723-1

Cited by 24 publications

(24 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Depletion of noradrenergic and dopaminergic fibres in the PFC produced comparable dopamine efflux in depleted and control animals following exposure to stress, while sparing noradrenergic fibres and depleting dopaminergic fibres in the PFC resulted in decreased prefrontal cortical dopamine efflux in lesioned rats compared to controls following exposure to stress (Venator et al 1999). In addition, both dopamine and noradrenaline neurotransmission in the PFC has been shown to modulate subcortical dopaminergic activity (Darracq et al 1998 ;McKittrick & Abercrombie, 2007 ;Nicniocaill & Gratton, 2007 ;Pascucci et al 2007 ;Tassin, 1998 ;Ventura et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Prefrontal cortical D1 dopamine receptors modulate subcortical D2 dopamine receptor-mediated stress responsiveness

Scornaiencki

Cantrup

Rushlow

et al. 2009

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

Increased responsiveness to stress plays an important role in the manifestation of schizophrenia symptoms. Evidence indicates that the prefrontal cortex (PFC), and dopamine neurotransmission in the PFC in particular, is involved in the modulation of stress responsiveness. Decreased dopaminergic activity and loss of dopamine fibres have been reported in PFC in schizophrenia patients. Consequently, it was hypothesized that depletion of dopamine in PFC may facilitate increased stress responsiveness. Adult Sprague-Dawley rats received injections of 6-hydroxydopamine or saline bilaterally into the medial PFC (mPFC) following desipramine pretreatment to selectively deplete dopaminergic fibres. Following a 3-wk recovery period, the lesioned and control rats received injections of a D1 or D2 dopamine receptor agonist or vehicle into the mPFC and were immediately subjected to forced swimming as a stressor. Results showed that frequency of locomotion and rearing, behavioural measures indicative of increased dopaminergic activity in the nucleus accumbens (NAc), were significantly increased following stress in prefrontal cortical dopamine-depleted rats. This effect was significantly ameliorated by infusions of a D1 dopamine receptor agonist directly into the mPFC in a dose-dependent manner but not by infusion of a D2 dopamine receptor agonist. In addition, stress-induced behavioural changes in prefrontal cortical dopamine-depleted rats were significantly reduced following selective discrete infusions of a D2 dopamine receptor antagonist into the NAc shell. The results suggest that dopaminergic transmission via D1 receptors in the mPFC modulates D2 dopamine receptor-mediated stress responsiveness in the NAc, a feature that may be disrupted in schizophrenia patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Prefrontal cortical D1 dopamine receptors modulate subcortical D2 dopamine receptor-mediated stress responsiveness

Scornaiencki

Cantrup

Rushlow

et al. 2009

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

show abstract

“…found that the novel and unescapable/uncontrollable stressor initially induced an increase in tonic levels of DA in NAc and then led to a decrease in DA level in NAc even below prestress levels which lasted as long as the stressful situation (Nicniocaill & Gratton, 2007; Pascucci, Ventura, Latagliata, Cabib, & Puglisi‐Allegra,2007; Ventura, Cabib, & Puglisi‐Allegra, 2002). This different response corresponds with the process of the primary and secondary appraisal of a stressor which cannot be removed, escaped, or predicted by the organism, and NAc DA fluctuations are modulated by the medial prefrontal cortex, which is also involved in stress appraisal (Pascucci et al.,2007).…”

Section: Discussionmentioning

confidence: 99%

Divergent anomaly in mesocorticolimbic dopaminergic circuits might be associated with different depressive behaviors, an animal study

et al. 2017

View full text Add to dashboard Cite

BackgroundThe mesocorticolimbic dopamine system, which originates from the ventral tegmental area (VTA) and projects primarily to the prefrontal cortex (PFC), olfactory tubercle (OT), nucleus accumbens (NAc), dorsal striatum (ST), and the amygdala (AMy), plays a pivotal role in determining individual motivation and sensitivity to rewards, namely, anhedonia. Not all depressive individuals exhibited anhedonia, thus, it is natural to speculate that the heterogenous manifestations of depression might be related to the mesocorticolimbic dopamine system. Maternal deprivation (MD) and chronic unpredictable stress (CUPS) are two well‐established depressogenic stressors, and they were proven to induce different depressive phenotypes.MethodsThe depressive and anxiety‐like behaviors of MD and CUPS‐treated rats were measured by classical behavioral tests including open field, forced swimming, and sucrose preference test. The expression of D1‐5 dopamine receptors and DAT mRNA and protein in the mesocorticolimbic dopamine system of rats exposed to MD and CUPS were measured by real‐time PCR and Western blot, respectively.ResultsSevere anhedonia was observed in MD but not CUPS rats. Divergent expression of D1 and D2 receptors and DAT mRNA and protein in the mesocorticolimbic dopamine system were found between MD and CUPS rats. Significant correlations between different depressive behaviors and D1‐/D2‐like receptors and DAT protein levels in the mesocorticolimbic dopamine system were observed.ConclusionDifferent depressive behaviors of rats such as anhedonia, passive coping behavior, and declined exploratory interest might be related to divergent dopaminergic pathways. Anhedonia is associated with the dysfunction of VTA‐NAc and VTA‐OT dopaminergic pathways, the passive coping behavior is related to the dysregulation of VTA‐PFC and VTA‐AMy pathways, and individual exploratory interest is associated with abnormal activity of VTA‐PFC and VTA‐ST pathways.

show abstract

“…This was done by two independent laboratories and published in 2007. These studies showed that novel stressful experiences enhance DA release in the NAc through activation of prefrontal cortical alpha-1 adrenergic receptors (ARs) by high levels of released NE (Nicniocaill and Gratton, 2007; Pascucci et al, 2007). Indeed, the experience with a novel stressor promotes a rapid, massive, and transient increase in NE release within the mpFC which parallels the enhancement of mesoaccumbens DA release (Pascucci et al, 2007).…”

Section: Prefrontal-accumbal Catecholamine Systemmentioning

confidence: 99%

“…A selective depletion of prefrontal cortical NE prevents both the cortical NE response and the increase in accumbal DA, leaving stress-induced enhancement of prefrontal cortical DA release as well as basal CAs levels unaffected (Pascucci et al, 2007). Moreover, applications of the alpha-1 AR selective antagonist benoxathian into the mpFC inhibits stress-induced DA release in the NAc dose-dependently (Nicniocaill and Gratton, 2007). Pascucci et al (2007) also confirmed that stress-induced enhanced NAc DA release is constrained by activation of mpFC DA.…”

Section: Prefrontal-accumbal Catecholamine Systemmentioning

confidence: 99%

Prefrontal/accumbal catecholamine system processes high motivational salience

Puglisi-Allegra¹,

Ventura²

2012

Front. Behav. Neurosci.

View full text Add to dashboard Cite

Motivational salience regulates the strength of goal seeking, the amount of risk taken, and the energy invested from mild to extreme. Highly motivational experiences promote highly persistent memories. Although this phenomenon is adaptive in normal conditions, experiences with extremely high levels of motivational salience can promote development of memories that can be re-experienced intrusively for long time resulting in maladaptive outcomes. Neural mechanisms mediating motivational salience attribution are, therefore, very important for individual and species survival and for well-being. However, these neural mechanisms could be implicated in attribution of abnormal motivational salience to different stimuli leading to maladaptive compulsive seeking or avoidance. We have offered the first evidence that prefrontal cortical norepinephrine (NE) transmission is a necessary condition for motivational salience attribution to highly salient stimuli, through modulation of dopamine (DA) in the nucleus accumbens (NAc), a brain area involved in all motivated behaviors. Moreover, we have shown that prefrontal-accumbal catecholamine (CA) system determines approach or avoidance responses to both reward- and aversion-related stimuli only when the salience of the unconditioned stimulus (UCS) is high enough to induce sustained CA activation, thus affirming that this system processes motivational salience attribution selectively to highly salient events.

show abstract

Medial prefrontal cortical alpha1 adrenoreceptor modulation of the nucleus accumbens dopamine response to stress in Long–Evans rats

Abstract: These data indicate that stress-induced activation of subcortical DA transmission is modulated by the NE input to PFC acting at alpha(1) receptors. They suggest that, under normal circumstances, this system exerts a facilitatory or enabling influence on the NAcc DA stress response.

Cited by 24 publications

References 41 publications

Prefrontal cortical D1 dopamine receptors modulate subcortical D2 dopamine receptor-mediated stress responsiveness

Prefrontal cortical D1 dopamine receptors modulate subcortical D2 dopamine receptor-mediated stress responsiveness

Divergent anomaly in mesocorticolimbic dopaminergic circuits might be associated with different depressive behaviors, an animal study

Prefrontal/accumbal catecholamine system processes high motivational salience

Contact Info

Product

Resources

About