Toward understanding thalamocortical dysfunction in schizophrenia through computational models of neural circuit dynamics

Murray, John D.; Antičević, Alan

doi:10.1016/j.schres.2016.10.021

Cited by 57 publications

(33 citation statements)

References 61 publications

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“…It remains unclear the extent to which structural deficits contribute to the functional abnormalities that we observe, and it may be that both increases and decreases in the volume of different basal ganglia structures can influence its functional properties. Thalamic abnormalities are well established in SCZ (Murray and Anticevic, 2017), and in the present context, thalamic structural abnormalities in SCZ may lead to altered modulatory influences on reward-related function via its connectivity with this striatum.…”

Section: Discussionmentioning

confidence: 81%

Meta‐analytic evidence for altered mesolimbic responses to reward in schizophrenia

Chase

Loriemi

Wensing

et al. 2018

Human Brain Mapping

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Dysfunction of reward-related neural circuitry in schizophrenia (SCZ) has been widely reported, and may provide insight into the motivational and cognitive disturbances that characterize the disorder. Although previous meta-analyses of reward learning paradigms in SCZ have been performed, a meta-analysis of whole-brain coordinate maps in SCZ alone has not been conducted. In this study, we performed an activation likelihood estimate (ALE) meta-analysis, and performed a follow-up analysis of functional connectivity and functional decoding of identified regions. We report several salient findings that extend prior work in this area. First, an alteration in reward-related activation was observed in the right ventral striatum, but this was not solely driven by hypoactivation in the SCZ group compared to healthy controls. Second, the region was characterized by functional connectivity primarily with the lateral prefrontal cortex and pre-supplementary motor area (preSMA), as well as subcortical regions such as the thalamus which show structural deficits in SCZ. Finally, although the meta-analysis showed no regions outside the ventral striatum to be significantly altered, regions with higher functional connectivity with the ventral striatum showed a greater number of subthreshold foci. Together, these findings confirm the alteration of ventral striatal function in SCZ, but suggest that a network-based approach may assist future analysis of the functional underpinnings of the disorder.

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Section: Discussionmentioning

confidence: 81%

Meta‐analytic evidence for altered mesolimbic responses to reward in schizophrenia

Chase

Loriemi

Wensing

et al. 2018

Human Brain Mapping

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“…Notably, patients with schizophrenia and bipolar disorder exhibit reduced MD-PFC functional connectivity relative to healthy controls (Welsh et al, 2010;Woodward et al, 2012;Anticevic et al, 2014). An emerging hypothesis posits that local disinhibition of PFC may destabilize the flow of information through the thalamofrontal loop and contribute to cognitive and negative symptoms in schizophrenia and related disorders (Anticevic et al, 2012;Murray and Anticevic, 2017). Structural alterations within thalamofrontal circuits have also been linked to cognitive deficits associated with aging (Hughes et al, 2012) and epilepsy (Pulsipher et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Parvalbumin Interneuron Dysfunction in a Thalamo-Prefrontal Cortical Circuit inDisc1Locus Impairment Mice

Delevich

Jaaro-Peled

Penzo

et al. 2020

eNeuro

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Altered cortical excitation-inhibition (E-I) balance resulting from abnormal parvalbumin interneuron (PV IN) function is a proposed pathophysiological mechanism of schizophrenia and other major psychiatric disorders. Preclinical studies have indicated that disrupted-in-schizophrenia-1 (Disc1) is a useful molecular lead to address the biology of prefrontal cortex (PFC)-dependent cognition and PV IN function. To date, PFC inhibitory circuit function has not been investigated in depth in Disc1 locus impairment (LI) mouse models. Therefore, we used a Disc1 LI mouse model to investigate E-I balance in medial PFC (mPFC) circuits. We found that inhibition onto layer 2/3 excitatory pyramidal neurons in the mPFC was significantly reduced in Disc1 LI mice. This reduced inhibition was accompanied by decreased GABA release from local PV, but not somatostatin (SOM) INs, and by impaired feedforward inhibition (FFI) in the mediodorsal thalamus (MD) to mPFC circuit. Our mechanistic findings of abnormal PV IN function in a Disc1 LI model provide insight into biology that may be relevant to neuropsychiatric disorders including schizophrenia.

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“…Indeed, based on extensive evidence, an E/I imbalance in favor of excitation is a central neurophysiological impairment in patients with schizophrenia (Foss-Feig et al, 2017;Jardri et al, 2016), a psychiatric disorder that has been linked to CI (Jardri & Denève, 2013;Jardri et al, 2017). At the implementation level, various mechanisms have been suggested, including dysfunctions of local interneurons in cortical microcircuits (Lewis, Pierri, Volk, Melchitzky, & Woo, 1999) or a dysconnectivity within long-range inhibitory loops (Murray & Anticevic, 2016). In both cases, reverberations (and interactions) occur on a fast timescale, within a few tens/hundreds of milliseconds (timescale of a single trial).…”

Section: Discussionmentioning

confidence: 99%

Circular inference in bistable perception

Leptourgos

Notredame²,

Eck³

et al. 2020

Journal of Vision

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When facing ambiguous images, the brain switches between mutually exclusive interpretations, a phenomenon known as bistable perception. Despite years of research, a consensus on whether bistability is driven primarily by bottom-up or top-down mechanisms has not been achieved. Here, we adopted a Bayesian approach to reconcile these two theories. Fifty-five healthy participants were exposed to an adaptation of the Necker cube paradigm, in which we manipulated sensory evidence and prior knowledge. Manipulations of both sensory evidence and priors significantly affected the way participants perceived the Necker cube. However, we observed an interaction between the effect of the cue and the effect of the instructions, a finding that is incompatible with Bayes-optimal integration. In contrast, the data were well predicted by a circular inference model. In this model, ambiguous sensory evidence is systematically biased in the direction of current expectations, ultimately resulting in a bistable percept.

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Toward understanding thalamocortical dysfunction in schizophrenia through computational models of neural circuit dynamics

Cited by 57 publications

References 61 publications

Meta‐analytic evidence for altered mesolimbic responses to reward in schizophrenia

Meta‐analytic evidence for altered mesolimbic responses to reward in schizophrenia

Parvalbumin Interneuron Dysfunction in a Thalamo-Prefrontal Cortical Circuit inDisc1Locus Impairment Mice

Circular inference in bistable perception

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