Nicotine-induced acute hyperactivity is mediated by dopaminergic system in a sexually dimorphic manner

Zhang, Yunpeng; Guo, Jing; Guo, Aike; Li, Yan

doi:10.1016/j.neuroscience.2016.06.043

Cited by 13 publications

(6 citation statements)

References 48 publications

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“…Determining how sexually isomorphic circuits are modified to produce sexually dimorphic behaviors is a complex endeavor. Even shared systems for such basic activities like movement are modified in a sex-specific way in species ranging from C. elegans and Drosophila to humans, and this modification is dependent on the sex of the nervous system, not just differences in body morphology ( Mowrey et al 2014 ; Smith and Mittendorfer 2016 ; Zhang et al 2016 ). However, little is known about the underlying mechanisms driving the sexual dimorphism.…”

Section: Discussionmentioning

confidence: 99%

Caenorhabditis elegansMale Copulation Circuitry Incorporates Sex-Shared Defecation Components To Promote Intromission and Sperm Transfer

LeBoeuf¹,

García

2017

G3 Genes|Genomes|Genetics

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Sexual dimorphism can be achieved using a variety of mechanisms, including sex-specific circuits and sex-specific function of shared circuits, though how these work together to produce sexually dimorphic behaviors requires further investigation. Here, we explore how components of the sex-shared defecation circuitry are incorporated into the sex-specific male mating circuitry in Caenorhabditis elegans to produce successful copulation. Using behavioral studies, calcium imaging, and genetic manipulation, we show that aspects of the defecation system are coopted by the male copulatory circuitry to facilitate intromission and ejaculation. Similar to hermaphrodites, male defecation is initiated by an intestinal calcium wave, but circuit activity is coordinated differently during mating. In hermaphrodites, the tail neuron DVB promotes expulsion of gut contents through the release of the neurotransmitter GABA onto the anal depressor muscle. However, in the male, both neuron and muscle take on modified functions to promote successful copulation. Males require calcium-dependent activator protein for secretion (CAPS)/unc-31, a dense core vesicle exocytosis activator protein, in the DVB to regulate copulatory spicule insertion, while the anal depressor is remodeled to promote release of sperm into the hermaphrodite. This work shows how sex-shared circuitry is modified in multiple ways to contribute to sex-specific mating.

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Section: Discussionmentioning

confidence: 99%

Caenorhabditis elegansMale Copulation Circuitry Incorporates Sex-Shared Defecation Components To Promote Intromission and Sperm Transfer

LeBoeuf¹,

García

2017

G3 Genes|Genomes|Genetics

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“…More recently, Zhang et al showed that dopamine also mediates the chronic nicotine exposure-induced locomotor hyperactivity in adult flies described by Ren et al [42,69]. In mammals and Drosophila , alpha7 receptors have been associated to biogenic amine release [41,63].…”

Section: Discussionmentioning

confidence: 99%

A Drosophila model for developmental nicotine exposure

Velazquez-Ulloa

2017

PLoS ONE

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Despite the known health risks of tobacco smoking, many people including pregnant women continue smoking. The effects of developmental nicotine exposure are known, but the underlying mechanisms are not well understood. Drosophila melanogaster is a model organism that can be used for uncovering genetic and molecular mechanisms for drugs of abuse. Here I show that Drosophila can be a model to elucidate the mechanisms for nicotine’s effects on a developing organism. Drosophila reared on nicotine food display developmental and behavioral effects similar to those in mammals including decreased survival and weight, increased developmental time, and decreased sensitivity to acute nicotine and ethanol. The Drosophila nicotinic acetylcholine receptor subunit alpha 7 (Dα7) mediates some of these effects. A novel role for Dα7 on ethanol sedation in Drosophila is also shown. Future research taking advantage of the genetic and molecular tools for Drosophila will allow additional discovery of the mechanisms behind the effects of nicotine during development.

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“…Drosophila strains with mutations of Dα1, Dα2, or Dβ2 nAChR subunits are highly resistant to the neonicotinoids nitenpyram and imidacloprid (Perry et al, 2008). The behavioral effects of nicotine on Drosophila are regulated by dopamine (Bainton et al, 2000), and Dβ1 subunit in dopaminergic neurons play a role in acute locomotor hyperactivity caused by nicotine in male Drosophila (Zhang et al, 2016). Therefore, understanding how nAChR control dopamine release is critical for understanding the effects of neonicotinoids.…”

Section: Introductionmentioning

confidence: 99%

Nicotinic acetylcholine receptor (nAChR) mediated dopamine release in larval Drosophila melanogaster

Pyakurel

Shin

Venton

2018

Neurochemistry International

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Acetylcholine is an excitatory neurotransmitter in the central nervous system of insects and the nicotinic acetylcholine receptor (nAChR) is a target for neonicotinoid insecticides. Functional insect nAChRs are difficult to express in host cells, and hence difficult to study. In mammals, acetylcholine and nicotine evoke dopamine release, but the extent to which this mechanism is conserved in insects is unknown. In intact larval ventral nerve cords (VNCs), we studied dopamine evoked by acetylcholine, nicotine, or neonicotinoids. Using fast-scan cyclic voltammetry, we confirmed dopamine was measured by its cyclic voltammogram and also by feeding Drosophila the synthesis inhibitor, 3-iodotyrosine, which lowered the evoked dopamine response. Acetylcholine (1.8 pmol) evoked on average 0.43 ± 0.04 μM dopamine. Dopamine release significantly decreased after incubation with α-bungarotoxin, demonstrating the release is mediated by nAChR, but atropine, a muscarinic AChR antagonist, had no effect. Nicotine (t = 71 s) and the neonicotinoids nitenpyram and imidacloprid (t = 86 s, 121 s respectively) also evoked dopamine release, which lasted longer than acetylcholine-stimulated release (t = 19 s). Nicotine-stimulated dopamine was significantly lower in the presence of sodium channel blocker, tetrodotoxin, showing that the release is exocytotic. Drosophila that have mutations in the nAChR subunit α1 or β2 have significantly lower neonicotinoid-stimulated release but no changes in nicotine-stimulated release. This work demonstrates that nAChR agonists mediate dopamine release in Drosophila larval VNC and that mutations in nAChR subunits affect how insecticides stimulate dopamine release.

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Nicotine-induced acute hyperactivity is mediated by dopaminergic system in a sexually dimorphic manner

Cited by 13 publications

References 48 publications

Caenorhabditis elegansMale Copulation Circuitry Incorporates Sex-Shared Defecation Components To Promote Intromission and Sperm Transfer

Caenorhabditis elegansMale Copulation Circuitry Incorporates Sex-Shared Defecation Components To Promote Intromission and Sperm Transfer

A Drosophila model for developmental nicotine exposure

Nicotinic acetylcholine receptor (nAChR) mediated dopamine release in larval Drosophila melanogaster

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