scholarly journals The Neurophysiological Bases of the Impact of Neonicotinoid Pesticides on the Behaviour of Honeybees

Insects ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 344 ◽  
Author(s):  
Amélie Cabirol ◽  
Albrecht Haase
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Sublethal Effects ◽  
Excitatory Neurotransmitter ◽  
Functional Changes ◽  
Wide Range ◽  
Neonicotinoid Pesticides ◽  
State Of The Science ◽  
The Impact ◽  
Honeybee Brain

Acetylcholine is the main excitatory neurotransmitter in the honeybee brain and controls a wide range of behaviours that ensure the survival of the individuals and of the entire colony. Neonicotinoid pesticides target this neurotransmission pathway and can thereby affect the behaviours under its control, even at doses far below the toxicity limit. These sublethal effects of neonicotinoids on honeybee behaviours were suggested to be partly responsible for the decline in honeybee populations. However, the neural mechanisms by which neonicotinoids influence single behaviours are still unclear. This is mainly due to the heterogeneity of the exposure pathways, doses and durations between studies. Here, we provide a review of the state of the science in this field and highlight knowledge gaps that need to be closed. We describe the agonistic effects of neonicotinoids on neurons expressing the different nicotinic acetylcholine receptors and the resulting brain structural and functional changes, which are likely responsible for the behavioural alterations reported in bees exposed to neonicotinoids.

Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures

2004 ◽  
Vol 17 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Merav Kedmi ◽  
Arthur L. Beaudet ◽  
Avi Orr-Urtreger
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Mutant Mice ◽  
Wild Type ◽  
Nicotinic Acetylcholine ◽  
Nocturnal Frontal Lobe Epilepsy ◽  
Wide Range ◽  
High Doses ◽  
Dose Dependent ◽  
Rate Of Response

Nicotine, the main addictive component of tobacco, evokes a wide range of dose-dependent behaviors in rodents, and when administrated in high doses, it can induce clonic-tonic seizures. Nicotine acts through the nicotinic acetylcholine receptors (nAChRs). Mutations in the human α4- and the β2-nAChR subunit genes cause autosomal dominant nocturnal frontal lobe epilepsy. Using transgenic mice with mutations in nAChR subunits, it was demonstrated previously that the α4-, α5-, and α7-subunits are involved in nicotine-induced seizures. To examine the possibility that the β4-subunit is also involved in this phenotype, we tested mice with homozygous β4-subunit deficiency. The β4 null mice were remarkably resistant to nicotine-induced seizures compared with wild-type and α5 null mice. We also generated mice with double deficiency of both α5- and β4-nAChR subunits and demonstrated that they were more resistant to nicotine’s convulsant effect than either the α5 or the β4 single mutant mice. In addition, the single α5 mutants and the double α5β4-deficient mice exhibited a significantly shorter latency time to seizure than that of the wild-type mice. Our results thus show that β4-containing nAChRs have a crucial role in the pathogenesis of nicotine-induced seizures. Furthermore, by comparing multiple mutant mice with single and double subunit deficiency, we suggest that nicotinic receptors containing either α5- or β4-subunits are involved in nicotine-induced seizures and that receptors containing both subunits are likely to contribute to this phenomena as well. However, the α5-subunit, but not the β4-subunit, regulates the rate of response to high doses of nicotine.

Expression patterns of nicotinic subunits α2, α7, α8, and β1 affect the kinetics and pharmacology of ACh-induced currents in adult bee olfactory neuropiles

2011 ◽  
Vol 106 (4) ◽  
pp. 1604-1613 ◽  
Author(s):  
Julien Pierre Dupuis ◽  
Monique Gauthier ◽  
Valérie Raymond-Delpech
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Expression Patterns ◽  
Insect Brain ◽  
Olfactory Pathway ◽  
Excitatory Neurotransmitter ◽  
Kenyon Cells ◽  
Inward Currents ◽  
Induced Currents ◽  
The Brain

Acetylcholine (ACh) is the main excitatory neurotransmitter of the insect brain, where nicotinic acetylcholine receptors (nAChRs) mediate fast cholinergic synaptic transmission. In the honeybee Apis mellifera, nAChRs are expressed in diverse structures including the primary olfactory centers of the brain, the antennal lobes (ALs) and the mushroom bodies (MBs), where they participate in olfactory information processing. To understand the nature and properties of the nAChRs involved in these processes, we performed a pharmacological and molecular characterization of nAChRs on cultured Kenyon cells of the MBs, using whole cell patch-clamp recordings combined with single-cell RT-PCR. In all cells, applications of ACh as well as nicotinic agonists such as nicotine and imidacloprid induced inward currents with fast desensitization. These currents were fully blocked by saturating doses of the antagonists α-bungarotoxin (α-BGT), dihydroxy-β-erythroidine (DHE), and methyllycaconitine (MLA) (MLA ≥ α-BGT ≥ DHE). Molecular analysis of ACh-responding cells revealed that of the 11 nicotinic receptor subunits encoded within the honeybee genome, α2, α8, and β1 subunits were expressed in adult Kenyon cells. Comparison with the expression pattern of adult AL cells revealed the supplementary presence of subunit α7, which could be responsible for the kinetic and pharmacological differences observed when comparing ACh-induced currents from AL and Kenyon cells. Together, our data demonstrate the existence of functional nAChRs on adult MB Kenyon cells that differ from nAChRs on AL cells in both their molecular composition and pharmacological properties, suggesting that changing receptor subsets could mediate different processing functions depending on the brain structure within the olfactory pathway.

scholarly journals Acetylcholine-producing NK cells attenuate CNS inflammation via modulation of infiltrating monocytes/macrophages

2017 ◽  
Vol 114 (30) ◽  
pp. E6202-E6211 ◽  
Author(s):  
Wei Jiang ◽  
Daojing Li ◽  
Ranran Han ◽  
Chao Zhang ◽  
Wei-Na Jin ◽  
...  
Keyword(s):  
Nk Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Cholinergic System ◽  
Acetylcholine Receptors ◽  
Nk Cell ◽  
Autoimmune Encephalomyelitis ◽  
Cns Inflammation ◽  
Inflammatory Conditions ◽  
Immunological Homeostasis ◽  
The Impact

The nonneural cholinergic system of immune cells is pivotal for the maintenance of immunological homeostasis. Here we demonstrate the expression of choline acetyltransferase (ChAT) and cholinergic enzymes in murine natural killer (NK) cells. The capacity for acetylcholine synthesis by NK cells increased markedly under inflammatory conditions such as experimental autoimmune encephalomyelitis (EAE), in which ChAT expression escalated along with the maturation of NK cells. ChAT+and ChAT−NK cells displayed distinctive features in terms of cytotoxicity and chemokine/cytokine production. Transfer of ChAT+NK cells into the cerebral ventricles of CX3CR1−/−mice reduced brain and spinal cord damage after EAE induction, and decreased the numbers of CNS-infiltrating CCR2+Ly6Chimonocytes. ChAT+NK cells killed CCR2+Ly6Chimonocytes directly via the disruption of tolerance and inhibited the production of proinflammatory cytokines. Interestingly, ChAT+NK cells and CCR2+Ly6Chimonocytes formed immune synapses; moreover, the impact of ChAT+NK cells was mediated by α7-nicotinic acetylcholine receptors. Finally, the NK cell cholinergic system up-regulated in response to autoimmune activation in multiple sclerosis, perhaps reflecting the severity of disease. Therefore, this study extends our understanding of the nonneural cholinergic system and the protective immune effect of acetylcholine-producing NK cells in autoimmune diseases.

α7 Nicotinic Acetylcholine Receptors on GABAergic Interneurons Evoke Dendritic and Somatic Inhibition of Hippocampal Neurons

2002 ◽  
Vol 87 (1) ◽  
pp. 548-557 ◽  
Author(s):  
A. V. Buhler ◽  
T. V. Dunwiddie
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Gabaergic Interneurons ◽  
Nicotinic Acetylcholine ◽  
Α7 Nicotinic Acetylcholine Receptors ◽  
The Impact ◽  
Two Populations

GABAergic interneurons in the hippocampus express high levels of α7 nicotinic acetylcholine receptors, but because of the diverse roles played by hippocampal interneurons, the impact of activation of these receptors on hippocampal output neurons (i.e., CA1 pyramidal cells) is unclear. Activation of hippocampal interneurons could directly inhibit pyramidal neuron activity but could also produce inhibition of other GABAergic cells leading to disinhibition of pyramidal cells. To characterize the inhibitory circuits activated by these receptors, exogenous acetylcholine was applied directly to CA1 interneurons in hippocampal slices, and the resulting postsynaptic responses were recorded from pyramidal neurons or interneurons. Inhibitory currents mediated by GABAA receptors were observed in 27/131 interneuron/pyramidal cell pairs, but no instances of disinhibition of spontaneous inhibitory events or GABAB receptor-mediated responses were observed. Two populations of bicuculline-sensitive GABAAreceptor-mediated currents could be distinguished based on their kinetics and amplitude. Anatomical reconstructions of the interneurons in a subset of connected pairs support the hypothesis that these two populations correspond to inhibitory synapses located either on the somata or dendrites of pyramidal cells. In 11 interneuron/interneuron cell pairs, one presynaptic neuron was observed that produced strong inhibitory currents in several nearby interneurons, suggesting that disinhibition of pyramidal neurons may also occur. All three types of inhibitory responses (somatic-pyramidal, dendritic-pyramidal, and interneuronal) were blocked by the α7 receptor-selective antagonist methyllycaconitine. These data suggest activation of these functionally distinct circuits by α7 receptors results in significant inhibition of both hippocampal pyramidal neurons as well as interneurons.

scholarly journals Smoking Enigma in Coronavirus Disease 2019: A Tug of War between Predisposition and Possible Way Out

2021 ◽  
Vol 14 ◽  
pp. 1179173X2098867
Author(s):  
Nadira Naznin Rakhi ◽  
Ritu Biswas
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotine Patch ◽  
Respiratory Pathogen ◽  
Respiratory Pathogens ◽  
Angiotensin Converting Enzyme 2 ◽  
Scientific World ◽  
Gender Dependence ◽  
Respiratory Coronavirus ◽  
The Impact

Background: The recent global inclination for smoking during the Coronavirus Disease 2019 (COVID-19) pandemic has drawn attention to the impact of smoking on COVID-19. While smoking increases susceptibility to common respiratory pathogens including the closely related coronaviruses, COVID-19 causing Severe Acute Respiratory Coronavirus 2 (SARS-CoV-2) being a respiratory pathogen intrigues the possible association between smoking and viral pathogenicity. Smoking and COVID-19: The gender dependence of COVID-19 infection rates and a higher prevalence of smokers among males made the scientific world assume smoking to be a confounding variable in sex predisposition to COVID-19. Conversely, the controversial findings of discrepant morbidity and mortality rates of COVID-19 among smokers questioned the credibility of this hypothesis. More importantly, nicotine in smoking has been hypothesized to downregulate Interleukin-6 (IL-6) which plays a role in COVID-19 severity and to interfere with the Angiotensin-Converting Enzyme 2 (ACE2), the receptor of SARS-CoV-2 led the scientists to experiment nicotine patch prophylactically against COVID-19. Besides, interaction between spike protein and nicotinic acetylcholine receptors (nAChRs) supports the nicotinic cholinergic system dysregulation hypothesis in COVID-19 pathophysiology leading to its therapeutic use. However, despite the contradictions in the direct impact of smoking, it surely acts as fomites for viral transmission. Conclusion: Irrespective of the role nicotine in COVID-management, compassionate use of smoking against SARS-CoV-2 cannot be recommended until the therapeutic value gets proved and therapeutic form becomes available.

scholarly journals Activity-dependent Golgi satellite formation in dendrites reshapes the neuronal surface glycoproteome

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Anitha P Govind ◽  
Okunola Jeyifous ◽  
Theron A Russell ◽  
Zola Yi ◽  
Aubrey V Weigel ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Secretory Pathway ◽  
Synapse Formation ◽  
Close Association ◽  
Endocytic Pathway ◽  
Structural Protein ◽  
Functional Changes ◽  
Early Endosomes ◽  
Surface Glycoproteins

Activity-driven changes in the neuronal surface glycoproteome are known to occur with synapse formation, plasticity and related diseases, but their mechanistic basis and significance are unclear. Here, we observed that N-glycans on surface glycoproteins of dendrites shift from immature to mature forms containing sialic acid in response to increased neuronal activation. In exploring the basis of these N-glycosylation alterations, we discovered they result from the growth and proliferation of Golgi satellites scattered throughout the dendrite. Golgi satellites that formed during neuronal excitation were in close association with ER exit sites and early endosomes and contained glycosylation machinery without the Golgi structural protein, GM130. They functioned as distal glycosylation stations in dendrites, terminally modifying sugars either on newly synthesized glycoproteins passing through the secretory pathway, or on surface glycoproteins taken up from the endocytic pathway. These activities led to major changes in the dendritic surface of excited neurons, impacting binding and uptake of lectins, as well as causing functional changes in neurotransmitter receptors such as nicotinic acetylcholine receptors. Neural activity thus boosts the activity of the dendrite’s satellite micro-secretory system by redistributing Golgi enzymes involved in glycan modifications into peripheral Golgi satellites. This remodeling of the neuronal surface has potential significance for synaptic plasticity, addiction and disease.

scholarly journals Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function

2009 ◽  
Vol 89 (1) ◽  
pp. 73-120 ◽  
Author(s):  
Edson X. Albuquerque ◽  
Edna F. R. Pereira ◽  
Manickavasagom Alkondon ◽  
Scott W. Rogers
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Drugs Of Abuse ◽  
Electric Organ ◽  
The Body ◽  
Mammalian Brain ◽  
Comprehensive Overview ◽  
Rich Diversity ◽  
The Rich ◽  
The Impact

The classical studies of nicotine by Langley at the turn of the 20th century introduced the concept of a “receptive substance,” from which the idea of a “receptor” came to light. Subsequent studies aided by the Torpedo electric organ, a rich source of muscle-type nicotinic receptors (nAChRs), and the discovery of α-bungarotoxin, a snake toxin that binds pseudo-irreversibly to the muscle nAChR, resulted in the muscle nAChR being the best characterized ligand-gated ion channel hitherto. With the advancement of functional and genetic studies in the late 1980s, the existence of nAChRs in the mammalian brain was confirmed and the realization that the numerous nAChR subtypes contribute to the psychoactive properties of nicotine and other drugs of abuse and to the neuropathology of various diseases, including Alzheimer's, Parkinson's, and schizophrenia, has since emerged. This review provides a comprehensive overview of these findings and the more recent revelations of the impact that the rich diversity in function and expression of this receptor family has on neuronal and nonneuronal cells throughout the body. Despite these numerous developments, our understanding of the contributions of specific neuronal nAChR subtypes to the many facets of physiology throughout the body remains in its infancy.

scholarly journals Acetylcholine and Its Receptors in Honeybees: Involvement in Development and Impairments by Neonicotinoids

Insects ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 420 ◽  
Author(s):  
Bernd Grünewald ◽  
Paul Siefert
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Royal Jelly ◽  
Crop Protection ◽  
Hypopharyngeal Gland ◽  
Excitatory Neurotransmitter ◽  
Developmental Disturbances ◽  
Pollinating Insects ◽  
Behavioral Impairments ◽  
Insect Central Nervous System

Acetylcholine (ACh) is the major excitatory neurotransmitter in the insect central nervous system (CNS). However, besides the neuronal expression of ACh receptors (AChR), the existence of non-neuronal AChR in honeybees is plausible. The cholinergic system is a popular target of insecticides because the pharmacology of insect nicotinic acetylcholine receptors (nAChRs) differs substantially from their vertebrate counterparts. Neonicotinoids are agonists of the nAChR and are largely used in crop protection. In contrast to their relatively high safety for humans and livestock, neonicotinoids pose a threat to pollinating insects such as bees. In addition to its effects on behavior, it becomes increasingly evident that neonicotinoids affect developmental processes in bees that appear to be independent of neuronal AChRs. Brood food (royal jelly, worker jelly, or drone jelly) produced in the hypopharyngeal glands of nurse bees contains millimolar concentrations of ACh, which is required for proper larval development. Neonicotinoids reduce the secreted ACh-content in brood food, reduce hypopharyngeal gland size, and lead to developmental impairments within the colony. We assume that potential hazards of neonicotinoids on pollinating bees occur neuronally causing behavioral impairments on adult individuals, and non-neuronally causing developmental disturbances as well as destroying gland functioning.

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