scholarly journals Palisade Endings Have an Exocytotic Machinery But Lack Acetylcholine Receptors and Distinct Acetylcholinesterase Activity

2020 ◽  
Vol 61 (14) ◽  
pp. 31
Author(s):  
Roland Blumer ◽  
Johannes Streicher ◽  
Génova Carrero-Rojas ◽  
Paula M. Calvo ◽  
Rosa R. de la Cruz ◽  
...  
Keyword(s):  
Acetylcholine Receptors ◽  
Acetylcholinesterase Activity

Effect of limb immobilization on skeletal muscle

1982 ◽  
Vol 52 (5) ◽  
pp. 1113-1118 ◽  
Author(s):  
F. W. Booth
Keyword(s):  
Acetylcholine Receptors ◽  
Neuromuscular Junctions ◽  
Muscular Atrophy ◽  
Acetylcholinesterase Activity ◽  
Resting Membrane Potential ◽  
Synthesis Rate ◽  
Emg Activity ◽  
Protein Synthesis Rate ◽  
Insulin Responsiveness ◽  
Limb Immobilization

The immobilization of limbs resulted in atrophy of those muscles that are fixed either at or less than resting length. The loss in protein in these muscles can be described by a first-order equation. Decreases in protein synthesis rate in muscles of immobilized limbs occur during the first 6 h of immobilization, and this decrease probably played a role in initiating muscular atrophy. After weeks of immobilization, muscles composed predominately of slow-twitch fibers took on properties characteristic of fast twitch muscles. The EMG activity of muscles in immobilized limbs was reduced to 5--15% of control levels. Insulin responsiveness for 2-deoxyglucose uptake into the soleus muscle of a limb is decreased at the 24th h of limb immobilization. Muscles of immobilized limbs have either no change or a decrease in resting membrane potential, an increase in extrajunctional acetylcholine receptors of lesser magnitude than the increase that occurred in denervated muscle, and no change in acetylcholinesterase activity in neuromuscular junctions. Immobilizing muscles at stretched lengths prevented the decrease in nerve afterhyperpolarization that was seen in muscles immobilized at shortened positions. These observations suggested that metabolic changes in muscles have a retrograde trophic influence on motor nerves. The model of limb immobilization permits the study of many fundamental problems concerned with mechanisms by which a muscle adapts so that it can meet the requirements of the external environment.

scholarly journals Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?—A Systematic Review

2021 ◽  
Vol 22 (16) ◽  
pp. 8413
Author(s):  
Carmen Costas-Ferreira ◽  
Lilian R. F. Faro
Keyword(s):  
Systematic Review ◽  
Nicotinic Acetylcholine Receptors ◽  
Intracellular Signaling ◽  
Acetylcholine Receptors ◽  
Neuronal Development ◽  
Acetylcholinesterase Activity ◽  
Target Species ◽  
Nicotinic Acetylcholine ◽  
Toxic Risk ◽  
Induced Changes

Neonicotinoids are a class of insecticides that exert their effect through a specific action on neuronal nicotinic acetylcholine receptors (nAChRs). The success of these insecticides is due to this mechanism of action, since they act as potent agonists of insect nAChRs, presenting low affinity for vertebrate nAChRs, which reduces potential toxic risk and increases safety for non-target species. However, although neonicotinoids are considered safe, their presence in the environment could increase the risk of exposure and toxicity. On the other hand, although neonicotinoids have low affinity for mammalian nAChRs, the large quantity, variety, and ubiquity of these receptors, combined with its diversity of functions, raises the question of what effects these insecticides can produce in non-target species. In the present systematic review, we investigate the available evidence on the biochemical and behavioral effects of neonicotinoids on the mammalian nervous system. In general, exposure to neonicotinoids at an early age alters the correct neuronal development, with decreases in neurogenesis and alterations in migration, and induces neuroinflammation. In adulthood, neonicotinoids induce neurobehavioral toxicity, these effects being associated with their modulating action on nAChRs, with consequent neurochemical alterations. These alterations include decreased expression of nAChRs, modifications in acetylcholinesterase activity, and significant changes in the function of the nigrostriatal dopaminergic system. All these effects can lead to the activation of a series of intracellular signaling pathways that generate oxidative stress, neuroinflammation and, finally, neuronal death. Neonicotinoid-induced changes in nAChR function could be responsible for most of the effects observed in the different studies.

scholarly journals Mechanisms of Imidacloprid-Induced Alteration of Hypothalamic-Pituitary-Adrenal (HPA) Axis after Subchronic Exposure in Male Rats

2015 ◽  
Vol 01 ◽  
pp. 51 ◽  
Author(s):  
Alya Annabi ◽  
Ines El-Bini Dhouib ◽  
Houssem Dkhili ◽  
Yassine Bdiri ◽  
Ines Rejeb ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Relative Weight ◽  
Acetylcholinesterase Activity ◽  
Male Rats ◽  
Oral Exposure ◽  
Glutathione S Transferase ◽  
Biochemical Processes ◽  
Mammalian Tissues

Imidacloprid (IMI) is known to target the nicotinic acetylcholine receptors (nAChRs) in insects, and potentially in mammals. However, IMI toxicity on mammalian tissues has not been adequately evaluated. The aim of the present study was to examine whether IMI induced functional impairment in hypthalamic-pituitary-adrenal (HPA) axis tissues. An oral exposure of 40 mg IMI/kg for 28 days in male rats caused a significant increase in malondialdehyde (MDA) level. The antioxidant catalase, superoxide dismutase, and glutathione S-transferase showed various alterations following administration, but a significantly depleted thiol (SH) groups was only recorded in hypothalamic tissues. The increase in the relative weight of adrenal glands and the increased adrenal cholesterol and plasma adrenocorticotropic hormone (ACTH) levels are indicative of general adaptation syndrome. The hypothalamic and pituitary acetylcholinesterase activity and calcium level were significantly increased, highlighting the alteration of cholinergic transmission. In conclusion, the findings obtained show that chronic exposure to IMI may alter biochemical processes of HPA axis.

scholarly journals Acetylcholine Receptors on the Cell Body Membrane of Giant Interneurone 2 in the Cockroach, Periplaneta Americana

1983 ◽  
Vol 105 (1) ◽  
pp. 339-350
Author(s):  
I. D. HARROW ◽  
D. B. SATTELLE
Keyword(s):  
Central Nervous System ◽  
Cell Body ◽  
Acetylcholine Receptors ◽  
Periplaneta Americana ◽  
Acetylcholinesterase Activity ◽  
Resting Potential ◽  
Detectable Effect ◽  
The Central Nervous System ◽  
Giant Interneurone ◽  
Quinuclidinyl Benzilate

1. Ionophoresis of acetylcholine (ACh) onto the cell body membrane of an identified giant interneurone (GI2) in the central nervous system of the cockroach Periplaneta americana induced a depolarizing response at resting potential which was attributed to a population of extrasynaptic ACh receptors. 2. The sensitivity of the cell body membrane of GI 2 to ionophoresis of ACh was determined. 3. Perfusion of 1.0 × 10−6M neostigmine, an inhibitor of acetylcholinesterase, potentiated the ACh sensitivity of the cell body membrane of GI2. This indicated that a high acetylcholinesterase activity was present in the periphery of the sixth abdominal ganglion (A6). 4. The nicotinic antagonist, α-bungarotoxin (at a concentration of 1.0 × 10−7M) was found to block the ACh response of the cell body membrane of GI2. By contrast, the muscarinic antagonist, quinuclidinyl benzilate, (at concentrations up to 1.0 × 10−5 M) had no detectable effect on the ACh response. 5. It is suggested that an extrasynaptic nicotinic type of ACh receptor is present on the cell body membrane of GI2.

Axon/Schwann-cell relationships in the giant nerve fibre of the squid

1981 ◽  
Vol 95 (1) ◽  
pp. 135-151
Author(s):  
J. Villegas
Keyword(s):  
Membrane Potential ◽  
Schwann Cell ◽  
Nerve Fibre ◽  
Acetylcholine Receptors ◽  
Acetylcholinesterase Activity ◽  
Feedback Mechanism ◽  
External Application ◽  
Cell Responses ◽  
Acetylcholinesterase Enzyme ◽  
Acetylcholine Concentration

This communication summarizes the experimental evidence obtained in the giant nerve fibre of the tropical squid Sepioteuthis sepioidea, on the nature of the mechanism responsible for the long-lasting effects of axonal excitation on the membrane potential of the Schwann cell. In these nerve fibres the propagation of a train of nerve impulses by the axon is followed by a prolonged hyperpolarization of the Schwann cell which can be reproduced, or modified, by the external application of cholinergic compounds. The presence and exact localization of the different components of the acetylcholine system directly involved in such Schwann-cell responses was detected by means of pharmacological, histochemical and chemical procedures. Thus, the results of the experiments herein discussed revealed that, under physiological conditions: the Schwann cell is able to synthesize, store and release acetylcholine; and that it has acetylcholine receptors of the nicotinic type, and acetylcholinesterase enzyme activity in its plasma membrane. On the other hand, the axon has low acetyltransferase activity and acetylcholine concentration in its axoplasm, and a high acetylcholinesterase activity in its axolemma. It was also found that acetylcholine hyperpolarizes the Schwann cell by increasing its relative permeability to the potassium ion. The distribution pattern of the acetylcholine system indicates that it operates as a feedback mechanism for the regulation of the Schwann-cell membrane potential and ionic permeability following axonal excitation.

scholarly journals In Vivo Effects of Neonicotinoid-Sulfoximine Insecticide Sulfoxaflor on Acetylcholinesterase Activity in the Tissues of Zebrafish (Danio rerio)

Toxics ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 73
Author(s):  
Petek Piner Benli ◽  
Mehmet Çelik
Keyword(s):  
Enzyme Activity ◽  
Danio Rerio ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Model Organism ◽  
Acetylcholinesterase Activity ◽  
Muscle Tissues ◽  
In Vivo Effects ◽  
The Brain

Sulfoxaflor is the first member of the neonicotinoid-sulfoximine insecticides that acts as an agonist of nicotinic acetylcholine receptors (nAChRs). This study investigated the acute effects of sulfoxaflor on acetylcholinesterase (AChE; EC 3.1.1.7) enzyme activity in the brain and muscle tissues of zebrafish (Danio rerio) as a model organism. The zebrafish were exposed to 0.87 mg/L (2.5% of 96 h 50% lethal concentration (LC50), 1.75 mg/L (5% of 96 h LC50) and 3.51 mg/L (10% of 96 h LC50) of sulfoxaflor for 24 h–48 h and 96 h periods. AChE enzyme activities were analysed by a spectrophotometric method in the brain and muscle tissues. The results of this study showed that in vivo acute sulfoxaflor exposure significantly increased AChE enzyme activity in the brain and muscle tissues of zebrafish. The induction percentages of AChE were between 10 and 83%, and 19 and 79% for brain and muscle tissues, respectively. As a result, it was found that sulfoxaflor had an effect on AChE enzyme activity in the two main tissues containing this enzyme, and it can be considered as a potential neuroactive compound for zebrafish.

Chemically Contaminated Eel Fed to Pregnant and Lactating Mouse Dams Causes Hyperactivity in Their Offspring

2016 ◽  
Vol 86 (1-2) ◽  
pp. 36-47 ◽  
Author(s):  
Imen Dridi ◽  
Nidhal Soualeh ◽  
Torsten Bohn ◽  
Rachid Soulimani ◽  
Jaouad Bouayed
Keyword(s):  
Open Field ◽  
Early Life ◽  
Home Cage ◽  
Anguilla Anguilla ◽  
Acetylcholinesterase Activity ◽  
Female Offspring ◽  
Significant Inhibition ◽  
Standard Diet ◽  
Early Life Exposure ◽  
Cage Test

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.

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