Living on the edge: Pain control by blood leukocytes at the borders of the central nervous system

2019 ◽  
Vol 106 (3) ◽  
pp. 509-511
Author(s):  
Felipe A. Pinho‐Ribeiro
2006 ◽  
Vol 69 (2) ◽  
pp. 79-100 ◽  
Author(s):  
Motohide Takemura ◽  
Shinichi Sugiyo ◽  
Masayuki Moritani ◽  
Masayuki Kobayashi ◽  
Norifumi Yonehara

Author(s):  
В.Г. Овсянников ◽  
А.Е. Бойченко ◽  
В.В. Алексеев ◽  
А.В. Каплиев ◽  
А.Е. Шумарин ◽  
...  

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.


Author(s):  
Gladys Harrison

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.


Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.


Author(s):  
Ezzatollah Keyhani

Acetylcholinesterase (EC 3.1.1.7) (ACHE) has been localized at cholinergic junctions both in the central nervous system and at the periphery and it functions in neurotransmission. ACHE was also found in other tissues without involvement in neurotransmission, but exhibiting the common property of transporting water and ions. This communication describes intracellular ACHE in mammalian bone marrow and its secretion into the extracellular medium.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


Sign in / Sign up

Export Citation Format

Share Document