Environment- and activity-dependent dopamine neurotransmitter plasticity in the adult substantia nigra

Aumann, Tim D.

doi:10.1016/j.jchemneu.2015.12.009

Cited by 22 publications

(13 citation statements)

References 89 publications

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“…BPA and phthalates, particularly MEHP, have effects on midbrain dopaminergic neurons, which are implicated in ADHD. 26,39 In our study, we found no differences between serum DEHP levels in the ADHD group when compared to healthy controls. But, in one study, exposures to DEHP metabolites were associated with ADHD in children between the ages of 8 and 11.…”

Section: ____________________________________________________________contrasting

confidence: 56%

May BPA and phthalates have a role in etiopathogenesis of ADHD?

Öztop¹,

Demirci²,

Özmen³

et al. 2017

Anadolu Psikiyatri Derg

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Section: ____________________________________________________________contrasting

confidence: 56%

May BPA and phthalates have a role in etiopathogenesis of ADHD?

Öztop¹,

Demirci²,

Özmen³

et al. 2017

Anadolu Psikiyatri Derg

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“…Because changes in calcium signaling (23)(24)(25) and sustained circuit activation (26,27) have been shown to induce a novel form of DA plasticity referred to as a neurotransmitter (NT) switching, we hypothesized that neonatal nicotine (NN) exposure enhances drug preference in the adult through a mechanism related to DA switching. Consistent with this, recent studies have shown that the number of neurons expressing tyrosine hydroxylase (TH), the DAsynthesizing enzyme, increases in the adult mouse substantia nigra compacta in response to photoperiod (28) and in the VTA following deep brain stimulation (29), social defeat (30), and chronic exposure to methamphetamine (31). Given that the transcription factor Nurr1 (32) is involved in the acquisition (33) and maintenance (34) of the DAergic phenotype (35), and that its expression is activity dependent (36,37), we investigated whether Nurr1 and TH expression are affected by nicotine-mediated circuit activation during development.…”

mentioning

confidence: 67%

Neonatal Nicotine Exposure Primes Midbrain Neurons to a Dopaminergic Phenotype and Increases Adult Drug Consumption

Romoli

Lozada

Sandoval

et al. 2019

Biological Psychiatry

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BACKGROUND: Nicotine intake induces addiction through neuroplasticity of the reward circuitry, altering the activity of dopaminergic neurons of the ventral tegmental area. Prior work demonstrated that altered circuit activity can change neurotransmitter expression in the developing and adult brain. Here we investigated the effects of neonatal nicotine exposure on the dopaminergic system and nicotine consumption in adulthood. METHODS: Male and female mice were used for two-bottle-choice test, progressive ratio breakpoint test, immunohistochemistry, RNAscope, quantitative polymerase chain reaction, calcium imaging, and DREADD (designer receptor exclusively activated by designer drugs)-mediated chemogenic activation/inhibition experiments. RESULTS: Neonatal nicotine exposure potentiates drug preference in adult mice, induces alterations in calcium spike activity of midbrain neurons, and increases the number of dopamine-expressing neurons in the ventral tegmental area. Specifically, glutamatergic neurons are first primed to express transcription factor Nurr1, then acquire the dopaminergic phenotype following nicotine re-exposure in adulthood. Enhanced neuronal activity combined with Nurr1 expression is both necessary and sufficient for the nicotine-mediated neurotransmitter plasticity to occur. CONCLUSIONS: Our findings illuminate a new mechanism of neuroplasticity by which early nicotine exposure primes the reward system to display increased susceptibility to drug consumption in adulthood.

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“…Additionally, the notion of dopaminergic neurons as a plastic population has been shown before in the context of research on activity-dependent neurotransmitter specification. Several studies have reported changes in the numbers of dopaminergic neurons that are activity-dependent [ 70 – 72 ].…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence that dopaminergic neurons can up or downregulate TH expression within specific dopaminergic clusters after chronic activation [ 72 ]. It has also been shown that dopaminergic neurons co-express other neurotransmitters, such as NPY and GABA [ 70 , 71 ]. Activity-dependent neurotransmitter switching is a well- documented phenomenon [ 83 , 84 ].…”

Section: Discussionmentioning

confidence: 99%

Developmental nicotine exposure affects larval brain size and the adult dopaminergic system of Drosophila melanogaster

et al. 2018

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BackgroundPregnant women may be exposed to nicotine if they smoke or use tobacco products, nicotine replacement therapy, or via e-cigarettes. Prenatal nicotine exposure has been shown to have deleterious effects on the nervous system in mammals including changes in brain size and in the dopaminergic system. The genetic and molecular mechanisms for these changes are not well understood. A Drosophila melanogaster model for these effects of nicotine exposure could contribute to faster identification of genes and molecular pathways underlying these effects. The purpose of this study was to determine if developmental nicotine exposure affects the nervous system of Drosophila melanogaster, focusing on changes to brain size and the dopaminergic system at two developmental stages.ResultsWe reared flies on control or nicotine food from egg to 3rd instar larvae or from egg to adult and determined effectiveness of the nicotine treatment. We used immunohistochemistry to visualize the whole brain and dopaminergic neurons, using tyrosine hydroxylase as the marker. We measured brain area, tyrosine hydroxylase fluorescence, and counted the number of dopaminergic neurons in brain clusters.We detected an increase in larval brain hemisphere area, a decrease in tyrosine hydroxylase fluorescence in adult central brains, and a decrease in the number of neurons in the PPM3 adult dopaminergic cluster. We tested involvement of Dα7, one of the nicotinic acetylcholine receptor subunits, and found it was involved in eclosion, as previously described, but not involved in brain size.ConclusionsWe conclude that developmental nicotine exposure in Drosophila melanogaster affects brain size and the dopaminergic system. Prenatal nicotine exposure in mammals has also been shown to have effects on brain size and in the dopaminergic system. This study further establishes Drosophila melanogaster as model organism to study the effects of developmental nicotine exposure. The genetic and molecular tools available for Drosophila research will allow elucidation of the mechanisms underlying the effects of nicotine exposure during development.

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Environment- and activity-dependent dopamine neurotransmitter plasticity in the adult substantia nigra

Cited by 22 publications

References 89 publications

May BPA and phthalates have a role in etiopathogenesis of ADHD?

May BPA and phthalates have a role in etiopathogenesis of ADHD?

Neonatal Nicotine Exposure Primes Midbrain Neurons to a Dopaminergic Phenotype and Increases Adult Drug Consumption

Developmental nicotine exposure affects larval brain size and the adult dopaminergic system of Drosophila melanogaster

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