scholarly journals Common Pesticide Rotenone Interference with Neuronal Transmission in Hippocampus

2013 ◽  
Vol 2 (6) ◽  
pp. 212-217
Author(s):  
Fatih Akkentli ◽  
Yusuf P. Tan ◽  
Hale Saybasili
Keyword(s):  
Neuronal Transmission

scholarly journals Physiological and Pathological Ageing of Astrocytes in the Human Brain

2021 ◽  
Author(s):  
Marloes Verkerke ◽  
Elly M. Hol ◽  
Jinte Middeldorp
Keyword(s):  
Risk Factor ◽  
Morphological Changes ◽  
Ion Homeostasis ◽  
Brain Functioning ◽  
Physiological Ageing ◽  
Human Astrocytes ◽  
Age Related ◽  
Technical Issues ◽  
Neuronal Transmission ◽  
Ageing Brain

AbstractAgeing is the greatest risk factor for dementia, although physiological ageing by itself does not lead to cognitive decline. In addition to ageing, APOE ε4 is genetically the strongest risk factor for Alzheimer’s disease and is highly expressed in astrocytes. There are indications that human astrocytes change with age and upon expression of APOE4. As these glial cells maintain water and ion homeostasis in the brain and regulate neuronal transmission, it is likely that age- and APOE4-related changes in astrocytes have a major impact on brain functioning and play a role in age-related diseases. In this review, we will discuss the molecular and morphological changes of human astrocytes in ageing and the contribution of APOE4. We conclude this review with a discussion on technical issues, innovations, and future perspectives on how to gain more knowledge on astrocytes in the human ageing brain.

Motor and learning dysfunction during postnatal development in mice defective in dopamine neuronal transmission

1998 ◽  
Vol 54 (4) ◽  
pp. 450-464 ◽  
Author(s):  
Kazuhiro Nishii ◽  
Natsuki Matsushita ◽  
Hirohide Sawada ◽  
Hiromi Sano ◽  
Yukihiro Noda ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Neuronal Transmission ◽  
Learning Dysfunction

scholarly journals 17Α-METHYLTESTOSTERONE (ANABOLIC ANDROGENIC STEROIDS) ALTERS ACETYLCHOLINESTERASE ENZYME ACTIVITY IN DIFFERENT PARTS OF THE BRAIN IN FEMALE MICE, MUS MUSCULUS

2018 ◽  
Vol 11 (5) ◽  
pp. 410
Author(s):  
Sachin B Patil ◽  
Laxmi S Inamdar
Keyword(s):  
Enzyme Activity ◽  
Ache Activity ◽  
Negative Impact ◽  
Memory Loss ◽  
Anabolic Androgenic Steroids ◽  
Female Mice ◽  
Neuronal Transmission ◽  
Androgenic Steroids ◽  
The Impact ◽  
Different Parts

Aim: Anabolic androgenic steroids (AAS) are synthetic derivatives of the male sex hormone testosterone. Androgens and anabolic steroids have been used for therapeutic purpose with few exceptions. However, the abuse of AAS is a remarkably prevalent problem, particularly among athletes and adolescents. Supraphysiological doses of AAS exert profound effects on mental state and behaviors such as depression, anxiety, aggressiveness, and cognitive deterioration.Objective: In the present investigation, we studied the impact of one of the AAS compounds, i.e., 17α-methyltestosterone on acetylcholinesterase (AChE) enzyme activity in different brain parts of mice, namely, forebrain, hippocampus, midbrain, and hindbrain.Methods: The adult female mice were assigned to four experimental groups to which different doses of 17α-MT (0.5, 5.0 and 7.5 mg/kg bwt, respectively) were administrated s.c. for 30 days. A significant increase in AChE activity in forebrain and midbrain (low and medium dose treatment) suggests a reduction of cholinergic neurotransmission efficiency due to decrease in acetylcholine levels in trans-synaptic cleft. Further, concurrent reduction in AChE activity was observed in whole brain, hippocampus, and hindbrain of 17α-MT-treated mice suggests the impairment in neuronal transmission. Since the regulation of cholinergic system through acetylcholine hydrolysis has been largely attributed to AChE activity, a significant reduction in its activity may lead to stress-related anxiety, memory loss with some cognitive and behavioral aspects in the mice.Conclusion: Based on the observed results, we propose that 17α-MT, an alkylated steroid compound, has a negative impact on AChE enzyme activity in different parts of mice brain, leading to impairment in neuronal transmission.

Effect of calcium channel noise in astrocytes on neuronal transmission

2016 ◽  
Vol 32 ◽  
pp. 262-272 ◽  
Author(s):  
Jun Tang ◽  
Tong-Bo Liu ◽  
Jun Ma ◽  
Jin-Ming Luo ◽  
Xian-Qing Yang
Keyword(s):  
Calcium Channel ◽  
Channel Noise ◽  
Neuronal Transmission

Brain lactic acidosis and synaptic function

1990 ◽  
Vol 68 (2) ◽  
pp. 164-169 ◽  
Author(s):  
Wolfgang Walz ◽  
Diane E. Harold
Keyword(s):  
Lactic Acid ◽  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Sodium Lactate ◽  
Extracellular Ph ◽  
Synaptic Function ◽  
Excitatory Postsynaptic Potential ◽  
Irreversible Damage ◽  
Acid Release ◽  
Neuronal Transmission

Measurements of the presynaptic fiber volley (PSFV), the population excitatory postsynaptic potential (EPSP), and the extracellular pH in the dendritic CA1 layer of rat hippocampal slices were used to evaluate the effects of lactacidosis on central synaptic transmission. Replacement of NaCl with sodium lactate (up to 30 mM) was found not to affect the PSFV; however, the EPSP was reversibly suppressed. Sodium citrate, with added CaCl2 to adjust for Ca2+ chelation, had the same effect as sodium lactate. Addition of lactic acid influenced the PSFV only when, at a concentration of 30 mM, the extracellular pH dropped to 6.6 or lower. With lactic acid concentrations of up to 20 mM, which produced pH levels of 6.8 in the slice, effects on the EPSP were reversible. However, 30 mM lactic acid suppressed both the PSFV and EPSP irreversibly. These results show that synaptic transmission is much more susceptible to lactacidosis than presynaptic axonal transmission. They also show that high levels of lactate, albeit causing suppression of synaptic transmission, do not cause irreversible damage. However, acidosis associated with lactic acid release may damage synaptic transmission irreversibly.Key words: acidosis, hippocampal slice, ischemia, lactate, lactic acid, neuronal transmission, synapse.

scholarly journals Catecholamines: Knowledge and understanding in the 1960s, now, and in the future

2019 ◽  
Vol 3 ◽  
pp. 239821281881068 ◽  
Author(s):  
S. Clare Stanford ◽  
David J. Heal
Keyword(s):  
First Generation ◽  
Dopaminergic Transmission ◽  
Hyperactivity Disorder ◽  
Rational Development ◽  
Technological Developments ◽  
Neuronal Transmission ◽  
The 1960S ◽  
New Treatments ◽  
The Brain ◽  
Distribution Of Noradrenaline

The late 1960s was a heyday for catecholamine research. Technological developments made it feasible to study the regulation of sympathetic neuronal transmission and to map the distribution of noradrenaline and dopamine in the brain. At last, it was possible to explain the mechanism of action of some important drugs that had been used in the clinic for more than a decade (e.g. the first generation of antidepressants) and to contemplate the rational development of new treatments (e.g. l-dihydroxyphenylalanine therapy, to compensate for the dopaminergic neuropathy in Parkinson’s disease, and β1-adrenoceptor antagonists as antihypertensives). The fact that drug targeting noradrenergic and/or dopaminergic transmission are still the first-line treatments for many psychiatric disorders (e.g. depression, schizophrenia, and attention deficit hyperactivity disorder) is a testament to the importance of these neurotransmitters and the research that has helped us to understand the regulation of their function. This article celebrates some of the highlights of research at that time, pays tribute to some of the subsequent landmark studies, and appraises the options for where it could go next.

scholarly journals Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice

2018 ◽  
Vol 115 (36) ◽  
pp. 9002-9007 ◽  
Author(s):  
Te-Chen Tzeng ◽  
Yuto Hasegawa ◽  
Risa Iguchi ◽  
Amy Cheung ◽  
Daniel R. Caffrey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Seizure Activity ◽  
Synaptic Proteins ◽  
Amyloid Peptide ◽  
Spine Density ◽  
Central Neurons ◽  
Chemically Induced ◽  
Neuronal Transmission ◽  
Selective Increase

Alzheimer’s disease (AD) is characterized by the progressive destruction and dysfunction of central neurons. AD patients commonly have unprovoked seizures compared with age-matched controls. Amyloid peptide-related inflammation is thought to be an important aspect of AD pathogenesis. We previously reported that NLRP3 inflammasome KO mice, when bred into APPswe/PS1ΔE9 (APP/PS1) mice, are completely protected from amyloid-induced AD-like disease, presumably because they cannot produce mature IL1β or IL18. To test the role of IL18, we bred IL18KO mice with APP/PS1 mice. Surprisingly, IL18KO/APP/PS1 mice developed a lethal seizure disorder that was completely reversed by the anticonvulsant levetiracetam. IL18-deficient AD mice showed a lower threshold in chemically induced seizures and a selective increase in gene expression related to increased neuronal activity. IL18-deficient AD mice exhibited increased excitatory synaptic proteins, spine density, and basal excitatory synaptic transmission that contributed to seizure activity. This study identifies a role for IL18 in suppressing aberrant neuronal transmission in AD.

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