scholarly journals Neonatal administration of a subanaesthetic dose of JM-1232(−) in mice results in no behavioural deficits in adulthood

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Koji Iwanaga ◽  
Yasushi Satoh ◽  
Ryosuke Akai ◽  
Toshiaki Ishizuka ◽  
Tomiei Kazama ◽  
...  
Keyword(s):  
Adenosine Diphosphate ◽  
Neonatal Exposure ◽  
Long Term Effects ◽  
Intravenous Anaesthetic ◽  
Neonatal Administration ◽  
Paediatric Practice ◽  
The Brain ◽  
Intravenous Anaesthetics ◽  
Behavioural Deficits

AbstractIn animal models, neonatal exposure of general anaesthetics significantly increases apoptosis in the brain, resulting in persistent behavioural deficits later in adulthood. Consequently, there is growing concern about the use of general anaesthetics in obstetric and paediatric practice. JM-1232(−) has been developed as a novel intravenous anaesthetic, but the effects of JM-1232(−) on the developing brain are not understood. Here we show that neonatal administration of JM-1232(−) does not lead to detectable behavioural deficits in adulthood, contrarily to other widely-used intravenous anaesthetics. At postnatal day 6 (P6), mice were injected intraperitoneally with a sedative-equivalent dose of JM-1232(−), propofol, or midazolam. Western blot analysis of forebrain extracts using cleaved poly-(adenosine diphosphate-ribose) polymerase antibody showed that JM-1232(−) is accompanied by slight but measurable apoptosis 6 h after administration, but it was relatively small compared to those of propofol and midazolam. Behavioural studies were performed in adulthood, long after the neonatal anaesthesia, to evaluate the long-term effects on cognitive, social, and affective functions. P6 administration to JM-1232(−) was not accompanied by detectable long-term behavioural deficits in adulthood. However, animals receiving propofol or midazolam had impaired social and/or cognitive functions. These data suggest that JM-1232(−) has prospects for use in obstetric and paediatric practice.

scholarly journals Functional Connectivity within Brain Networks of Long Term and Short term Meditators

2019 ◽  
Vol 9 (2S) ◽  
pp. 29-34
Keyword(s):  
Functional Connectivity ◽  
Temporal Correlation ◽  
Brain Regions ◽  
Invasive Technique ◽  
Long Term Effects ◽  
Short Term ◽  
Statistical Concept ◽  
The Brain ◽  
Meditative Practices

Meditation refers to a state of mind of relaxation and concentration, where generally the mind and body is at rest. The process of meditation reflects the state of the brain which is distinct from sleep or typical wakeful states of consciousness. Meditative practices usually involve regulation of emotions and monitoring of attention. Over the past decade there has been a tremendous increase in an interest to study the neural mechanisms involved in meditative practices. It could also be beneficial to explore if the effect of meditation is altered by the number of years of meditation practice. Functional Magnetic Resonance Imaging (fMRI) is a very useful imaging technique which can be used to perform this analysis due to its inherent benefits, mainly it being a non-invasive technique. Functional activation and connectivity analysis can be performed on the fMRI data to find the active regions and the connectivity in the brain regions. Functional connectivity is defined as a simple temporal correlation between anatomically separate, active neural regions. Functional connectivity gives the statistical dependencies between regional time series. It is a statistical concept and is quantified using metrics like Correlation. In this study, a comparison is made between functional connectivity in the brain regions of long term meditation practitioners (LTP) and short-term meditation practitioners (STP) to see the differences and similarities in the connectivity patterns. From the analysis, it is evident that in fact there is a difference in connectivity between long term and short term practitioners and hence continuous practice of meditation can have long term effects.

Long-term effects of early life stress on the brain monoamines level in the rats

2013 ◽  
Vol 43 (1) ◽  
pp. 79
Author(s):  
R. Ghalamghash ◽  
H.Z. Mammedov ◽  
H. Ashayeri ◽  
A. Hosseini
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Long Term Effects ◽  
Brain Monoamines ◽  
The Brain

Environments, Past and Present

2020 ◽  
Author(s):  
Angela Duckworth ◽  
Keyword(s):  
Allostatic Load ◽  
Acute Stress ◽  
The Body ◽  
Physiological Changes ◽  
Long Term Effects ◽  
Flight Response ◽  
Fight Or Flight Response ◽  
The Brain ◽  
Fight Or Flight

For more than a century, scientists have known that acute stress activates the fight-or-flight response. When your life is on the line, your body reacts instantly: your heart races, your breath quickens, and a cascade of hormones sets off physiological changes that collectively improve your odds of survival. More recently, scientists have come to understand that the fight-or-flight response takes a toll on the brain and the body—particularly when stress is chronic rather than acute. Systems designed to handle transient threats also react to stress that occurs again and again, for weeks, months, or years. It turns out that poverty, abuse, and other forms of adversity repeatedly activate the fight-or-flight response, leading to long-term effects on the immune system and brain, which in turn increase the risk for an array of illnesses, including asthma, diabetes, arthritis, depression, and cardiovascular disease. Pioneering neuroscientist Bruce McEwen called this burden of chronic stress “allostatic load.”

scholarly journals The Use of Botulinum Toxin for the Treatment of Chronic Joint Pain: Clinical and Experimental Evidence

Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 314 ◽  
Author(s):  
Nicole Blanshan ◽  
Hollis Krug
Keyword(s):  
Pain Relief ◽  
Joint Pain ◽  
Peripheral Sensitization ◽  
Long Term Effects ◽  
Neuropeptide Release ◽  
Osteoarthritis Pain ◽  
Catalytically Active ◽  
The Central Nervous System ◽  
The Brain

Chronic osteoarthritis pain is an increasing worldwide problem. Treatment for osteoarthritis pain is generally inadequate or fraught with potential toxicities. Botulinum toxins (BoNTs) are potent inhibitors of neuropeptide release. Paralytic toxicity is due to inhibition at the neuromuscular junction, and this effect has been utilized for treatments of painful dystonias. Pain relief following BoNT muscle injection has been noted to be more significant than muscle weakness and hypothesized to occur because of the inhibition of peripheral neuropeptide release and reduction of peripheral sensitization. Because of this observation, BoNT has been studied as an intra-articular (IA) analgesic for chronic joint pain. In clinical trials, BoNT appears to be effective for nociceptive joint pain. No toxicity has been reported. In preclinical models of joint pain, BoNT is similarly effective. Examination of the dorsal root ganglion (DRG) and the central nervous system has shown that catalytically active BoNT is retrogradely transported by neurons and then transcytosed to afferent synapses in the brain. This suggests that pain relief may also be due to the central effects of the drug. In summary, BoNT appears to be safe and effective for the treatment of chronic joint pain. The long-term effects of IA BoNT are still being determined.

scholarly journals Normalizing the Abnormal: Do Antipsychotic Drugs Push the Cortex Into an Unsustainable Metabolic Envelope?

2019 ◽  
Vol 46 (3) ◽  
pp. 484-495 ◽  
Author(s):  
Federico E Turkheimer ◽  
Pierluigi Selvaggi ◽  
Mitul A Mehta ◽  
Mattia Veronese ◽  
Fernando Zelaya ◽  
...  
Keyword(s):  
Psychotic Symptoms ◽  
Antipsychotic Treatment ◽  
Long Term Effects ◽  
Extrapyramidal Syndrome ◽  
Before And After ◽  
Cardiac Disorders ◽  
Positive Symptoms Of Psychosis ◽  
The Brain ◽  
Novel Model

Abstract The use of antipsychotic medication to manage psychosis, principally in those with a diagnosis of schizophrenia or bipolar disorder, is well established. Antipsychotics are effective in normalizing positive symptoms of psychosis in the short term (delusions, hallucinations and disordered thought). Their long-term use is, however, associated with side effects, including several types of movement (extrapyramidal syndrome, dyskinesia, akathisia), metabolic and cardiac disorders. Furthermore, higher lifetime antipsychotic dose-years may be associated with poorer cognitive performance and blunted affect, although the mechanisms driving the latter associations are not well understood. In this article, we propose a novel model of the long-term effects of antipsychotic administration focusing on the changes in brain metabolic homeostasis induced by the medication. We propose here that the brain metabolic normalization, that occurs in parallel to the normalization of psychotic symptoms following antipsychotic treatment, may not ultimately be sustainable by the cerebral tissue of some patients; these patients may be characterized by already reduced oxidative metabolic capacity and this may push the brain into an unsustainable metabolic envelope resulting in tissue remodeling. To support this perspective, we will review the existing data on the brain metabolic trajectories of patients with a diagnosis of schizophrenia as indexed using available neuroimaging tools before and after use of medication. We will also consider data from pre-clinical studies to provide mechanistic support for our model.

scholarly journals Neonatal Desflurane Exposure Induces More Robust Neuroapoptosis than Do Isoflurane and Sevoflurane and Impairs Working Memory

2011 ◽  
Vol 115 (5) ◽  
pp. 979-991 ◽  
Author(s):  
Mitsuyoshi Kodama ◽  
Yasushi Satoh ◽  
Yukiko Otsubo ◽  
Yoshiyuki Araki ◽  
Ryuji Yonamine ◽  
...  
Keyword(s):  
Working Memory ◽  
Open Field ◽  
Elevated Plus Maze ◽  
Memory Task ◽  
Adenosine Diphosphate ◽  
Long Term Memory ◽  
Neonatal Exposure ◽  
Term Memory ◽  
Plus Maze

Background In animal models, neonatal exposure to volatile anesthetics induces neuroapoptosis, leading to memory deficits in adulthood. However, effects of neonatal exposure to desflurane are largely unknown. Methods Six-day-old C57BL/6 mice were exposed to equivalent doses of desflurane, sevoflurane, or isoflurane for 3 or 6 h. Minimum alveolar concentration was determined by the tail-clamp method as a function of anesthesia duration. Apoptosis was evaluated by immunohistochemical staining for activated caspase-3, and by TUNEL. Western blot analysis for cleaved poly-(adenosine diphosphate-ribose) polymerase was performed to examine apoptosis comparatively. The open-field, elevated plus-maze, Y-maze, and fear conditioning tests were performed to evaluate general activity, anxiety-related behavior, working memory, and long-term memory, respectively. Results Minimum alveolar concentrations at 1 h were determined to be 11.5% for desflurane, 3.8% for sevoflurane, and 2.7% for isoflurane in 6-day-old mice. Neonatal exposure to desflurane (8%) induced neuroapoptosis with an anatomic pattern similar to that of sevoflurane or isoflurane; however, desflurane induced significantly greater levels of neuroapoptosis than almost equivalent doses of sevoflurane (3%) or isoflurane (2%). In adulthood, mice treated with these anesthetics had impaired long-term memory, whereas no significant anomalies were detected in the open-field and the elevated plus-maze tests. Although performance in a working memory task was normal in mice exposed neonatally to sevoflurane or isoflurane, mice exposed to desflurane had significantly impaired working memory. Conclusions In an animal model, neonatal desflurane exposure induced more neuroapoptosis than did sevoflurane or isoflurane and impaired working memory, suggesting that desflurane is more neurotoxic than sevoflurane or isoflurane.

Neuropsychological Syndrome and long term effects of Exposure to Organophosphate Pesticides in Humans

2019 ◽  
Vol 10 (4) ◽  
pp. 1219-1227
Author(s):  
Dr.Maida Zameer ◽  
Dr. Sunbal Siddique ◽  
Dr.Maria Baig
Keyword(s):  
Brain Injury ◽  
Neuropsychological Assessment ◽  
Organophosphate Pesticides ◽  
Significant Morbidity ◽  
Long Term Effects ◽  
Neurological Illness ◽  
Organophosphorous Compounds ◽  
The Brain ◽  
Neuroimaging Techniques

Organophosphorous compounds, the anticholinesterases, produce significant morbidity and mortality in Pakistan. Neuropsychological assessment was traditionally carried out to assess the extent of impairment to a particular skill and to attempt to determine the area of the brain which may have been damaged following brain injury or neurological illness. With the advent of neuroimaging techniques, location of space-occupying lesions can now be more accurately determined through this method, so the focus has now moved on to the assessment of cognition and behaviour, including examining the effects of any brain injury or neuropathological process that a person may have experienced.

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