The Neuropharmacology of Impulsive Behaviour, an Update

Pattij, Tommy; Vanderschuren, Louk J. M. J.

doi:10.1007/7854_2020_143

Cited by 13 publications

(5 citation statements)

References 112 publications

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“…More specifically, the orbital frontal gyrus was one of the significant brain regions in the frontal-temporal-limbic circuit discovered in previous studies that contribute to apathy using other image modalities ( Godefroy et al, 2022 ; Valotassiou et al, 2022 ). And it is well-acknowledged that orbital frontal gyrus is linked to impulsive and disinhibition behavior ( Migliaccio et al, 2020 ; Pattij and Vanderschuren, 2020 ; Tanguy et al, 2022 ), imbalanced activity in the orbitofrontal cortex and nucleus accumbens was known to disrupt behavior inhibition ( Meyer and Bucci, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Clinical relevance of disrupted topological organization of anatomical connectivity in behavioral variant frontotemporal dementia

Chu

Jiang

liu

et al. 2023

Neurobiology of Aging

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Section: Discussionmentioning

confidence: 99%

Clinical relevance of disrupted topological organization of anatomical connectivity in behavioral variant frontotemporal dementia

Chu

Jiang

liu

et al. 2023

Neurobiology of Aging

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“…Compensatory enhancement of connectivity was found in the sub-insula and prefrontal pole. The prefrontal brain area— especially the orbital frontal gyrus— was shown to be associated with inhibition of impulsive behaviors, which may arise from the limbic connectome including the insula [ 27 ]. The enhanced connectivity might inhibit some behavioral impulses in MAPT P301L mutation carriers, who thus maintain asymptomatic status with normal behavior and cognitive function.…”

Section: Discussionmentioning

confidence: 99%

Altered Anterior Insular Metabolic Connectivity in Asymptomatic MAPT P301L Carriers

Chu

Jiang

Liu

et al. 2023

JAD

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Background: The insula is the predominant brain region impaired in behavior variant frontotemporal dementia (bvFTD). However, structural and functional changes in the sub-insula in the asymptomatic stage of bvFTD are unknown. Objective: To describe structural and functional changes in insula subregions in asymptomatic carriers of the P301L mutation of the microtubule-associated protein tau (MAPT) gene and patients with bvFTD. Methods: Six asymptomatic MAPT P301L mutation carriers and 12 MAPT negative control subjects of the same pedigree were enrolled, along with 30 patients with a clinical diagnosis of bvFTD and 30 matched controls. All subjects underwent hybrid positron emission tomography/magnetic resonance imaging. Atlas-based parcellation using a fine-grained Brainnetome Atlas was conducted to assess gray matter (GM) volume, metabolism, and metabolic connectivity in the sub-insula (region of interest). Results: There was no significant GM atrophy or hypometabolism in insula subregions in asymptomatic MAPT P301L carriers, although decreased metabolic connectivity between vIa-middle temporal gyrus, vIa-temporal poles, dIa-middle temporal gyrus and dIa-temporal poles; and increased connectivity between vIa-orbitofrontal, vIa-dorsal lateral superior frontal gyrus, and dIa-orbitofrontal and dIa-dorsal lateral superior frontal gyrus were observed. Patients with bvFTD had significant atrophy and hypometabolism in all insula subregions and decreased metabolic connectivity in the whole brain, including vIa/dIa-middle temporal and vIa/dIa-temporal poles. The standardized uptake value ratios of vIa and dIa were negatively associated with behavioral disinhibition scale scores. Conclusion: Metabolic connectivity is altered in vIa and dIa subregions of the sub-insula in MAPT P301L mutation carriers before the occurrence of atrophy, hypometabolism, and clinical symptoms.

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“…Since then, many other studies have further elaborated on this and earlier work from Pattij and colleagues demonstrated the critical involvement of DA and, more specifically, of dopamine D1-like and dopamine D2-like receptors in inhibitory response control (Van Gaalen et al, 2006). Subsequent functional neuroanatomical approaches, including intracranial microinfusions of dopamine ligands and sophisticated rodent micro-positron emission tomography (PET) studies with dopamine D2/D3 ligands, have pinpointed the ventral striatum as a main brain region where dopamine D1like and dopamine D2-like receptors modulate impulse control (e.g., Dalley et al, 2007;Pattij et al, 2007;Pezze et al, 2009;Besson et al, 2010;Caprioli et al, 2013;Jupp et al, 2013;Pattij and Vanderschuren, 2020). Importantly, the pre-clinical data are paralleled by clinical observations.…”

Section: Dopaminergic and Cholinergic Modulation Of Impulse Controlmentioning

confidence: 99%

Where Dopaminergic and Cholinergic Systems Interact: A Gateway for Tuning Neurodegenerative Disorders

Amalric

Pattij

Sotiropoulos

et al. 2021

Front. Behav. Neurosci.

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Historically, many investigations into neurodegenerative diseases have focused on alterations in specific neuronal populations such as, for example, the loss of midbrain dopaminergic neurons in Parkinson’s disease (PD) and loss of cholinergic transmission in Alzheimer’s disease (AD). However, it has become increasingly clear that mammalian brain activities, from executive and motor functioning to memory and emotional responses, are strictly regulated by the integrity of multiple interdependent neuronal circuits. Among subcortical structures, the dopaminergic nigrostriatal and mesolimbic pathways as well as cholinergic innervation from basal forebrain and brainstem, play pivotal roles in orchestrating cognitive and non-cognitive symptoms in PD and AD. Understanding the functional interactions of these circuits and the consequent neurological changes that occur during degeneration provides new opportunities to understand the fundamental inter-workings of the human brain as well as develop new potential treatments for patients with dysfunctional neuronal circuits. Here, excerpted from a session of the European Behavioral Pharmacology Society meeting (Braga, Portugal, August 2019), we provide an update on our recent work in behavioral and cellular neuroscience that primarily focuses on interactions between cholinergic and dopaminergic systems in PD models, as well as stress in AD. These brief discussions include descriptions of (1) striatal cholinergic interneurons (CINs) and PD, (2) dopaminergic and cholinergic modulation of impulse control, and (3) the use of an implantable cell-based system for drug delivery directly the into brain and (4) the mechanisms through which day life stress, a risk factor for AD, damage protein and RNA homeostasis leading to AD neuronal malfunction.

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The Neuropharmacology of Impulsive Behaviour, an Update

Cited by 13 publications

References 112 publications

Clinical relevance of disrupted topological organization of anatomical connectivity in behavioral variant frontotemporal dementia

Clinical relevance of disrupted topological organization of anatomical connectivity in behavioral variant frontotemporal dementia

Altered Anterior Insular Metabolic Connectivity in Asymptomatic MAPT P301L Carriers

Where Dopaminergic and Cholinergic Systems Interact: A Gateway for Tuning Neurodegenerative Disorders

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