Representations of Distinct Salience Signals in the Nucleus Accumbens

Murty, Vishnu P.; Stanek, Jessica; Heusser, Andrew C.

doi:10.1523/jneurosci.3002-13.2013

Cited by 3 publications

(1 citation statement)

References 8 publications

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“…This circuit underpins another crucial component of behavioural learning 28 , i.e. regulating the switch between rest and effortful cognitive activity based on the salience of external stimuli with respect to behavioural goals.…”

Section: Discussionmentioning

confidence: 99%

Salience network structural integrity predicts executive impairment in alcohol use disorders

Galandra

Basso

Manera

et al. 2018

Sci Rep

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The neural bases of cognitive impairment(s) in alcohol use disorders (AUDs) might reflect either a global brain damage underlying different neuro-cognitive alterations, or the involvement of specific regions mostly affected by alcohol neuro-toxic effects. While voxel-based-morphometry (VBM) studies have shown a distributed atrophic pattern in fronto-limbic and cerebellar structures, the lack of comprehensive neuro-cognitive assessments prevents previous studies from drawing robust inferences on the specificity of the association between neuro-structural and cognitive impairments in AUDs. To fill this gap, we addressed the neuro-structural bases of cognitive impairment in AUDs, by coupling VBM with an in-depth neuropsychological assessment. VBM results highlighted a diffuse pattern of grey matter reduction in patients, involving the key-nodes of the meso-cortico-limbic (striatum, hippocampus, medial prefrontal cortex), salience (insular and dorsal anterior cingulate cortex) and executive (inferior frontal cortex) networks. Grey matter density in the insular and anterior cingulate sectors of the salience network, significantly decreased in patients, explained almost half of variability in their defective attentional and working-memory performance. The multiple cognitive and neurological impairments observed in AUDs might thus reflect a specific executive deficit associated with the selective damage of a salience-based neural mechanism enhancing access to cognitive resources required for controlled cognition and behaviour.

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Section: Discussionmentioning

confidence: 99%

Salience network structural integrity predicts executive impairment in alcohol use disorders

Galandra

Basso

Manera

et al. 2018

Sci Rep

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Persistent pain alters AMPA receptor subunit levels in the nucleus accumbens

D'Amour

Lee

et al. 2015

Mol Brain

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BackgroundA variety of pain conditions have been found to be associated with depressed mood in clinical studies. Depression-like behaviors have also been described in animal models of persistent or chronic pain. In rodent chronic neuropathic pain models, elevated levels of GluA1 subunits of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the nucleus accumbens (NAc) have been found to inhibit depressive symptoms. However, the effect of reversible post-surgical pain or inflammatory pain on affective behaviors such as depression has not been well characterized in animal models. Neither is it known what time frame is required to elicit AMPA receptor subunit changes in the NAc in various pain conditions.ResultsIn this study, we compared behavioral and biochemical changes in three pain models: the paw incision (PI) model for post-incisional pain, the Complete Freund’s Adjuvant (CFA) model for persistent but reversible inflammatory pain, and the spared nerve injury (SNI) model for chronic postoperative neuropathic pain. In all three models, rats developed depressive symptoms that were concurrent with the presentation of sensory allodynia. GluA1 levels at the synapses of the NAc, however, differed in these three models. The level of GluA1 subunits of AMPA-type receptors at NAc synapses was not altered in the PI model. GluA1 levels were elevated in the CFA model after a period (7 d) of persistent pain, leading to the formation of GluA2-lacking AMPA receptors. As pain symptoms began to resolve, however, GluA1 levels returned to baseline. Meanwhile, in the SNI model, in which pain persisted beyond 14 days, GluA1 levels began to rise after pain became persistent and remained elevated. In addition, we found that blocking GluA2-lacking AMPA receptors in the NAc further decreased the depressive symptoms only in persistent pain models.ConclusionOur study shows that while both short-term and persistent pain can trigger depression-like behaviors, GluA1 upregulation in the NAc likely represents a unique adaptive response to minimize depressive symptoms in persistent pain states.

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