Nicotine addiction: More than just dopamine

Kim, Kristen; Picciotto, Marina R.

doi:10.1016/j.conb.2023.102797

Cited by 12 publications

(6 citation statements)

References 59 publications

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“…The small size of the VTA and the habenula and the fact that their main action appears to consist in an early and short-lived (but critical) influence on other areas, particularly the ACC, might be the reason why they are not implicated as frequently in related functional neuroimaging studies in spite of their involvement in multiple neurotransmitter systems. Nevertheless, they appear to play an important role in nicotine use disorder (Kim and Picciotto 2023 ), reward processing and cognitive control (Baker et al 2016 ), emotion and motivation (Ables et al 2023 ) but also major depressive disorder (Browne et al 2018 ). Their inclusion in Fig.…”

Section: Discussionmentioning

confidence: 99%

Changes in distinct brain systems identified with fMRI during smoking cessation treatment with varenicline: a review

Panagopoulos,

Bailey,

Kostopoulos

et al. 2024

Psychopharmacology

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Background Varenicline is considered one of the most effective treatment options for smoking cessation. Nonetheless, it is only modestly effective. A deeper comprehension of the effects of varenicline by means of the in-depth review of relevant fMRI studies may assist in paving the development of more targeted and effective treatments. Methodology A search of PubMed and Google Scholar databases was conducted with the keywords “functional magnetic resonance imaging” or “fMRI”, and “varenicline”. All peer-reviewed articles regarding the assessment of smokers with fMRI while undergoing treatment with varenicline and meeting the predefined criteria were included. Results Several studies utilizing different methodologies and targeting different aspects of brain function were identified. During nicotine withdrawal, decreased mesocorticolimbic activity and increased amygdala activity, as well as elevated amygdala-insula and insula-default-mode-network functional connectivity are alleviated by varenicline under specific testing conditions. However, other nicotine withdrawal-induced changes, including the decreased reward responsivity of the ventral striatum, the bilateral dorsal striatum and the anterior cingulate cortex are not influenced by varenicline suggesting a task-dependent divergence in neurocircuitry activation. Under satiety, varenicline treatment is associated with diminished cue-induced activation of the ventral striatum and medial orbitofrontal cortex concomitant with reduced cravings; during the resting state, varenicline induces activation of the lateral orbitofrontal cortex and suppression of the right amygdala. Conclusions The current review provides important clues with regard to the neurobiological mechanism of action of varenicline and highlights promising research opportunities regarding the development of more selective and effective treatments and predictive biomarkers for treatment efficacy.

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Section: Discussionmentioning

confidence: 99%

Changes in distinct brain systems identified with fMRI during smoking cessation treatment with varenicline: a review

Panagopoulos,

Bailey,

Kostopoulos

et al. 2024

Psychopharmacology

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“…It is now evident that nAChRs not only play an important role in neuronal function and the addiction to nicotine [ 151 , 152 ] but may also serve as targets for therapeutic intervention in various neuropsychiatric/neurodegenerative disorders, including PD [ 25 , 153 , 154 ], depression [ 153 , 155 , 156 ], obsessive–compulsive disorder [ 157 , 158 ], ADHD [ 159 ], Tourette syndrome [ 160 , 161 , 162 ], mild cognitive impairment or Alzheimer’s disease [ 163 , 164 , 165 , 166 ], ischemia [ 167 ], catalepsy [ 168 ], schizophrenia [ 4 , 166 , 169 ], pain [ 147 , 170 ], energy balance [ 171 , 172 ], autoimmune disorders [ 173 ], and even sleep–wake cycle dysregulation [ 174 ]. These receptors are also expressed abundantly in a variety of immune cells, including B cells, T cells, macrophages, and microglia, and are believed to contribute to the anti-inflammatory effects of nicotine [ 175 , 176 , 177 , 178 ].…”

Section: Nachrsmentioning

confidence: 99%

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Soares,

Costa,

Ferrolho

et al. 2024

Cells

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies identified nAChRs in nonneuronal cell types, including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in the prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and, specifically, their nAChRs in PD pathology and/or treatment.

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“…It is now evident that nAChRs not only play an important role in neuronal function and addiction to nicotine [151,152], but may also serve as targets for therapeutic intervention in various neuropsychiatric/neurodegenerative disorders including PD [25,153,154], depression [153,155,156], obsessive-compulsive disorder [157,158] , ADHD [159], Tourette syndrome [160][161][162], mild cognitive impairment or Alzheimer's disease [163][164][165][166], ischemia [167], catalepsy [168], schizophrenia [4,166,169], pain [147,170], energy balance [171,172], autoimmune disorders [173], and even in sleepwake cycle dysregulation [174]. These receptors are also expressed abundantly in a variety of immune cells including B cells, T cells, macrophages, and microglia, and are believed to contribute to the antiinflammatory effects of nicotine [175][176][177][178].…”

Section: Nachrsmentioning

confidence: 99%

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Soares,

Costa,

Ferrolho

et al. 2024

Preprint

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, postural instability, that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address the neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies have identified nAChRs in nonneuronal cell types including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration, and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and specifically their nAChRs in PD pathology and/or treatment.

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Nicotine addiction: More than just dopamine

Cited by 12 publications

References 59 publications

Changes in distinct brain systems identified with fMRI during smoking cessation treatment with varenicline: a review

Changes in distinct brain systems identified with fMRI during smoking cessation treatment with varenicline: a review

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

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