The antinociceptive system. Endogenous mechanisms of pain control

2019 ◽  
pp. 130-136
Author(s):  
В.Г. Овсянников ◽  
А.Е. Бойченко ◽  
В.В. Алексеев ◽  
А.В. Каплиев ◽  
А.Е. Шумарин ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pain Control ◽  
Current Data ◽  
System Control ◽  
Control Mechanisms ◽  
Spinal Level ◽  
Inhibitory System ◽  
Antinociceptive System ◽  
The Central Nervous System

Представлен обзор современных данных по изучению антиноцицептивной системы и эндогенных механизмов обезболивания. Контроль болевой чувствительности осуществляется многими структурами ЦНС, каждая из которых функционирует как самостоятельное образование. В комплексе все они входят в состав сложной системы антиноцицепции, аналогично тому, как ощущение боли является результатом интегративной функции ЦНС. Данное сообщение посвящено анализу роли информации, поступающей по толстым миелиновым волокнам в задние рога спинного мозга и нисходящих тормозных влияний на уровне задних рогов спинного мозга. Охарактеризованы структуры, влияющие на антиноцицепцию. На уровне спинного мозга обнаружены два механизма подавления боли - это сегментарный контроль и система нисходящего тормозного контроля. По современным данным обезболивающие эффекты объясняются не только сегментарным контролем, но и включением надсегментарных механизмов контроля, в т.ч. и гуморальных. Центральные структуры головного мозга оказывают не только нисходящее влияние на спинальном уровне, но и модифицируют болевые сигналы в местах их переключения в различных структурах головного мозга. Нисходящая ингибиторная система тесно взаимосвязана с тремя нейротрансмиттерными системами: опиатной, норадренергической и серотонинергической. Возникновение боли зависит не только от интенсивности ноцицептивного повреждения, но и от состояния различных звеньев антиноцицептивной системы. На основании знаний о патогенезе острой боли, структуре и функции антиноцицептивной системы дается определение понятия «боль». This review focused on the antinociceptive system and endogenous mechanisms of pain control. Multiple structures of the central nervous system control the pain sensitivity, and each of them functions as an independent entity. Together they constitute a complex system of antinociception consistent with that the sensation of pain is provided by integrative functioning of the central nervous system. This review analyzed the role of information delivered through thick myelin fibers to posterior horns and descending inhibitory effects at the level of the posterior horns. Two pain relief mechanisms were found at the spinal level, the segmental control and the descending inhibitory control system. According to current data anesthetic effects are explained not only by the segmental control but also by involvement of suprasegmental control mechanisms, including humoral ones. Central structures both exert downstream effects at the spinal level and modify pain signals at the locations where they switch over in various cerebral structures. The descending inhibitory system is closely interrelated with three neurotransmitter systems, the opiate, noradrenergic and serotonergic ones. Emergence of pain depends on both the intensity of nociceptive damage and on the condition of multiple parts of the antinociceptive system.Based on studying the pathogenesis of acute pain and the structure and function of antinociceptive system the authors provided a definition for the term of pain.

scholarly journals Incorporation of 5-Bromo-2′-deoxyuridine into DNA and Proliferative Behavior of Cerebellar Neuroblasts: All That Glitters Is Not Gold

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1453
Author(s):  
Joaquín Martí-Clúa
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Current Data ◽  
Cellular Mechanisms ◽  
Dividing Cells ◽  
The Central Nervous System ◽  
Repeated Doses ◽  
Pyrimidine Analog

The synthetic halogenated pyrimidine analog, 5-bromo-2′-deoxyuridine (BrdU), is a marker of DNA synthesis. This exogenous nucleoside has generated important insights into the cellular mechanisms of the central nervous system development in a variety of animals including insects, birds, and mammals. Despite this, the detrimental effects of the incorporation of BrdU into DNA on proliferation and viability of different types of cells has been frequently neglected. This review will summarize and present the effects of a pulse of BrdU, at doses ranging from 25 to 300 µg/g, or repeated injections. The latter, following the method of the progressively delayed labeling comprehensive procedure. The prenatal and perinatal development of the cerebellum are studied. These current data have implications for the interpretation of the results obtained by this marker as an index of the generation, migration, and settled pattern of neurons in the developing central nervous system. Caution should be exercised when interpreting the results obtained using BrdU. This is particularly important when high or repeated doses of this agent are injected. I hope that this review sheds light on the effects of this toxic maker. It may be used as a reference for toxicologists and neurobiologists given the broad use of 5-bromo-2′-deoxyuridine to label dividing cells.

The development of central nervous system control of the gill withdrawal reflex evoked by siphon stimulation in Aplysia

1979 ◽  
Vol 57 (9) ◽  
pp. 987-997 ◽  
Author(s):  
Ken Lukowiak
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Abdominal Ganglion ◽  
System Control ◽  
Reflex Amplitude ◽  
Withdrawal Reflex ◽  
Reflex Latency ◽  
Neural Processes ◽  
The Central Nervous System ◽  
Cns Control

In older Aplysia, the central nervous system (CNS) (abdominal ganglion) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) which initially mediates the gill withdrawal reflex and its subsequent habituation evoked by tactile stimulation of the siphon. In young animals, both the suppressive and facilitatory CNS control were found to be absent. In older animals, removal of branchial nerve (Br) input to the gill resulted in a significantly reduced reflex latency and, with ctenidial (Ct) and siphon (Sn) nerves intact, a significantly increased reflex amplitude and an inability of the reflex to habituate with repeated siphon stimulation. In young animals, removal of Br had no effect on reflex latency and with Ct and Sn intact, the reflex amplitude latency was not increased and the reflex habituated. Older animals can easily discriminate between different intensity stimuli applied to the siphon as evidenced by differences in reflex amplitude, rates of habituation, and evoked neural activity. On the other hand, young animals cannot discriminate well between different stimulus intensities. The lack of CNS control in young animals was found to be due to incompletely developed neural processes within the abdominal ganglion and not the PNS. The lack of CNS control in young Aplysia results in gill reflex behaviours being less adaptive in light of changing stimulus conditions, but may be of positive survival value in that the young will not habituate as easily. The fact that CNS control is present in older animals strengthens the idea that in any analysis of the underlying neural mechanisms of habituation the entire integrated CNS–PNS must be taken into account.

Diabetes mellitus and the central nervous system

2016 ◽  
Vol 88 (10) ◽  
pp. 82-86 ◽  
Author(s):  
E V Surkova
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose Control ◽  
Current Data ◽  
Treatment And Prevention ◽  
Imaging Results ◽  
The Central Nervous System ◽  
Considerable Impact ◽  
Relationship Of

The review considers the current views on the central nervous system (CNS) in diabetes mellitus (DM). It discusses an attitude towards the term «diabetic encephalopathy». The data of investigations of cognitive functions in types 1 and 2 DM and the brain structural imaging results obtained using up-to-date technologies are considered. The results of studies of the factors that induce cerebral changes in DM and their associated cognitive impairments are given. There is evidence that hyperglycemia has a more considerable impact on the above processes than hypoglycemia; other possible factors, apart from blood glucose control, are set out. The current views on the function of insulin in the CNS and the relationship of central insulin resistance to Alzheimer’s disease are outlined. There are current data on intranasal insulin application that is still exploratory, but, as might be judged from the findings, may by a promising method for the treatment and prevention of cognitive decline in both patients with DM and those without this condition.

scholarly journals INSULIN AND INSULIN RESISTANCE: NEW MOLECULE MARKERS AND TARGET MOLECULE FOR THE DIAGNOSIS AND THERAPY OF DISEASES OF THE CENTRAL NERVOUS SYSTEM

2013 ◽  
Vol 12 (5) ◽  
pp. 104-118 ◽  
Author(s):  
A. B. Salmina ◽  
N. A. Yauzina ◽  
N. V. Kuvacheva ◽  
M. M. Petrova ◽  
T. Ye. Taranushenko ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Central Nervous System ◽  
Nervous System ◽  
Current Data ◽  
Nad Metabolism ◽  
Metabolic Coupling ◽  
Proliferation And Differentiation ◽  
Insulin Activity ◽  
The Central Nervous System

The review summarizes current data on the role of insulin in the regulation of t glucose metabolism in the central nervous system at physiologic and pathologic conditions. For many years, the brain has been considered as an insulin-independent organ which utilizes glucose without insulin activity. However, it is become clear now that insulin not only regulates glucose transport and metabolism, but also has modulatory efftects in impact on excitability, proliferation and differentiation of brain progenitor cells, synaptic plasticity and memory formation, secretion of neurotransmitters, apoptosis. We have critically reviewed literature information and our own data on the role of insulin and insulin resistance in neuron-glia metabolic coupling, regulation of NAD+ metabolism and action of NAdependent enzymes, neurogenesis, brain development in (patho)physiological conditions. The paper clarifies interrelations between alterations in glucose homeostasis, development of insulin resistance and development of neurodegeneration (Alzheimer's disease and Parkinson's disease), autism, stroke, and depression. We discuss the application of novel molecular markers of insulin resistance (adipokines, α-hydroxybutyrate, BDNF, insulin-regulated aminopeptidase, provasopressin) and molecular targets for diagnostics and treatment of brain disorders associated with insulin resistance.

Modeling and Simulation of the Central Nervous System Control with Generic Fuzzy Models

SIMULATION ◽  
2003 ◽  
Vol 79 (11) ◽  
pp. 648-669 ◽  
Author(s):  
Angela Nebot ◽  
Francisco Mugica ◽  
François E. Cellier ◽  
Montserrat Vallverdú
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Modeling And Simulation ◽  
System Control ◽  
Fuzzy Models ◽  
The Central Nervous System ◽  
Central Nervous System Control

Central nervous system control of airway tone in guinea pigs: the role of histamine

1988 ◽  
Vol 65 (5) ◽  
pp. 2024-2029 ◽  
Author(s):  
P. J. Mauser ◽  
N. H. Edelman ◽  
R. W. Chapman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pigs ◽  
Lung Compliance ◽  
System Control ◽  
The Central Nervous System ◽  
Dose Dependent Decrease ◽  
Airway Tone ◽  
Dynamic Lung Compliance ◽  
H1 Antagonist

The central nervous system (CNS) plays an important role in the reflex control of bronchomotor tone, but the relevant neurotransmitters and neuromodulators have not been identified. In this study we have investigated the effect of histamine. Anesthetized male guinea pigs were prepared with a chronically implanted intracerebroventricular (icv) cannula and instrumented for the measurement of pulmonary resistance (RL), dynamic lung compliance (Cdyn), tidal volume (VT), respiratory rate (f), blood pressure (BP), and heart rate (HR). Administration of histamine (2-30 micrograms) icv caused a significant (P less than 0.05) reduction of Cdyn with no change in RL, VT, and f. At a dose of 100 micrograms icv, histamine caused an increase in RL (202 +/- 78%), a reduction of Cdyn (77 +/- 9%), an increase in f (181 +/- 64%), and a reduction of VT (53 +/- 18%). There were no changes in BP and HR after 100 micrograms of icv histamine. In contrast, intravenous administration of histamine (0.1-2 micrograms/kg) caused a dose-dependent decrease in Cdyn and increase in RL that was associated with tachypnea at each bronchoconstrictor dose. Intravenous histamine (2 micrograms/kg) produced a fall in BP and an increase in HR. The bronchoconstrictor responses to icv histamine were completely blocked by vagotomy and significantly reduced by atropine (0.1 mg/kg iv), whereas vagotomy and atropine did not block the bronchospasm due to intravenous histamine. Additional studies indicated that the pulmonary responses due to icv histamine (100 micrograms) were blocked by pretreatment with the H1-antagonist chlorpheniramine (1 and 10 micrograms, icv). These data indicate that histamine may serve a CNS neurotransmitter function in reflex bronchoconstriction in guinea pigs.

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