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Biological Activities of Peptides in Brain Tissues
Published in Gerard O’Cuinn, Metabolism of Brain Peptides, 2020
Neuropeptide Y (also known as neuropeptide tyrosine or NPY) was first identified by Tatemoto and Mutt8. This 36-amino-acid peptide is the most widely distributed of the neuropeptides discovered to date and has generated a huge number of scientific publications over the last decade. NPY fulfills the main neurotransmitter criteria: storage in synaptic granulae9, release triggered by electrical nerve stimulation10, action at specific receptors. Much of the research relating to NPY has concerned its coexistence with classic neurotransmitters (e.g., norepinephrine) and possible role in cotransmission, in line with the generally accepted view that neurons use multiple messenger molecules, at least one of which is usually a peptide. NPY has frequently been used to study cotransmission, particularly as a mediator of sympathetic neurotransmission in conjunction with the classic neurotransmitter norepinephrine.
Psychiatric Side Effects
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Joshua Schimmel, Evren Burakgazi-Dalkilic, Hatice Burakgazi-Yilmaz
The effects of RA on dopamine within the striatum may also play a role in alterations in mood and emotion. Abnormal dopaminergic transmission is well known to play a role in depression and psychosis. Alterations in dopamine signaling could be due to decreased presynaptic release or impaired signal transduction (13). RA has been proven to increase dopamine signal transduction through the induction of various proteins in the developing striatum (14). Assuming these effects can be applied to the adult brain, this would indicate that RA has a role in improving dopaminergic transmission. This evidence supports the argument that RA may diminish depression rather than worsen it; however, the important consideration is the association RA has in a system proven to be central to the etiology of depression. Increased levels of dopaminergic signaling are found in patients with schizophrenia and psychosis, suggesting that improved dopaminergic transmission in the striatum could also explain the many reports of psychosis seen with retinoid treatment.
Effects of Neuropeptides on Intestinal Ion Transport
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
However, if stimulation leads to release of both transmitters, potential for interactions occur. Campbell43 argues cogently that cotransmission involves the clear demonstration “that two or more coreleased transmitters act on the same target cell, so that the net result of transmission incorporates interactive effects of the transmitters”. His analysis thus holds both coexistence and corelease to be necessary but insufficient conditions for demonstrating cotransmission. Such interactions could be synergistic (additive) or antagonistic. Corelease may not necessarily imply release from the same site. In the feline jejunum, 5-HT and substance P were released into the lumen following vagal stimulation, but pharmacological antagonists were used to demonstrate that the release of the two transmitters was independent and from two different sources (the EC cell for 5-HT and peptidergic neurons for substance P).48
Quantification methods for viruses and virus-like particles applied in biopharmaceutical production processes
Published in Expert Review of Vaccines, 2022
Keven Lothert, Friederike Eilts, Michael W. Wolff
Regarding the imaging methods, the application of electron microscopy, i.e. transmission (TEM) and scanning electron microscopy (SEM), has to be mentioned. Investigations by TEM are helpful in virus and VLP productions to confirm the product integrity, if titers were determined only based on antigen contents [139]. As an example, negative staining electron microscopy was successfully applied for counting Influenza A particles [7]. This quantification may be optimized by automation, but the number of counted particles, as well as drawing a conclusion on particle concentrations from the initial sample volume, is rather challenging [157]. Furthermore, due to tedious sample preparation, a highly limited throughput and the considerable costs of appropriate equipment must be taken into account. Consequently, the method might be considered as a niche application, and is only stated in the interest of completeness. A striking benefit, however, is the specificity, as viruses can be identified fairly easily, according to specific visible surface characteristics [44].
Dopaminergic and glutamatergic biomarkers disruption in addiction and regulation by exercise: a mini review
Published in Biomarkers, 2022
Muhammad Abdullah, Li-Chung Huang, Shih-Hsien Lin, Yen Kuang Yang
In our view, the integrated dopaminergic and glutamatergic model of addiction may serve better to understand the complexities of addiction. For example, some stages of addiction (i.e. addiction development and maintenance) can be better explained by the decreased transmission of the dopaminergic system, which is acutely increased by addictive substances. Similarly, relapse and cue-induced craving have been reported to be more accurately defined by glutamatergic modulations than dopaminergic ones (Tzschentke and Schmidt 2003, Kalivas 2009). The lack of pharmaceutical agents that target a broad range of these multiple therapeutic targets, and the limited efficacies of that they do, contribute to the current problem of treatment failure and relapse. Exercise intervention could be an effective treatment for addition (Lynch et al.2013, Zhang and Yuan 2019). Owing to therapeutic roles in multiple stages of addiction, dopaminergic and glutamatergic modulations could be very important mechanisms of exercise that combat drug addiction (Lynch et al.2013). Literature reviews focussed on mechanistic therapeutic outcomes and biomarker level studies enabling construction of a conceptual framework for exercise-based efficacy are scarce. Our aim was to provide a focussed review of the pathological mechanisms of drug-associated damage to the dopaminergic and glutamatergic nervous systems and the multi-level therapeutic mechanisms of exercise. We also propose clinical and scientific implications in this review.
The levels of nitrite, nitrate and lipid peroxidation in diabetic mouse brain: the effect of melatonin and pentoxifylline
Published in Archives of Physiology and Biochemistry, 2022
Ahmet S. Yalçınkaya, Mehmet Ramazan Şekeroğlu, Zübeyir Huyut, Erdem Çokluk, Hanefi Özbek, Gürkan Öztürk, Ragıp Balahoroğlu
There are many indicators of oxidative damage. These include the lipid peroxidation end product MDA (Sekeroglu et al.2012, Sekeroglu et al.2017, Huyut et al.2018), NO with known significant physiological functions and its derivatives, NO2, NO3 (Damghanian et al.2019). Previous studies reported that reactive oxygen and nitrogen species were increased and antioxidant capacity was decreased in the plasma or other tissues of diabetic patients (Godin et al.1988, Konukoğlu et al. 1999). In these studies, NO was showed to play an effective role in various complications of diabetes (Salas et al.1992, Şekeroğlu et al.2000). NO is a very important regulatory molecule, secondary messenger and transmitter and it is found in nerve, digestive, immune, cardiovascular and urogenital systems and synthesise from L-arginine by NO synthase (NOS) activity (Ghasemi and Jeddi 2017). NO has been reported to play a role especially in neurodegenerative diseases such as Parkinson, Huntington, Alzheimer and Epilepsy. It mediates the transmission of pain sensation and plays an important role long-term depression and in long-term potency and therefore in learning (Joyce 2017). NO also plays an important role in many physiological processes, including exercise performance, regulation of blood pressure, metabolic health and cardiovascular changes, tissue blood flow, glucose and calcium homeostasis, neurotransmission, skeletal muscle contractility, mitochondrial respiration and biogenesis (McDonagh et al.2019).