EFFECT OF SEROTONIN AND NEUROPEPTIDES ON ADENYLATE CYCLASE OF THE CENTRAL NERVOUS SYSTEM AND PERIPHERAL ORGANS OF THE FRESHWATER SNAIL PLANORBARIUS CORNEUS

Prion disorders are infectious, neurodegenerative diseases that affect humans and animals. Susceptibility to some prion diseases such as kuru or the new variant of Creutzfeldt-Jakob disease in humans and scrapie in sheep and goats is influenced by polymorphisms of the coding region of the prion protein gene, while other prion disorders such as fatal familial insomnia, familial Creutzfeldt-Jakob disease, or Gerstmann-Straussler-Scheinker disease in humans have an underlying inherited genetic basis. Several prion strains have been demonstrated experimentally in rodents and sheep. The progression and pathogenesis of disease is influenced by both genetic differences in the prion protein and prion strain. Some prion diseases only affect the central nervous system whereas others involve the peripheral organs prior to neuroinvasion. Many experiments undertaken in different species and using different prion strains have postulated common pathways of neuroinvasion. It is suggested that prions access the autonomic nerves innervating peripheral organs and tissues to finally reach the central nervous system. We review here published data supporting this view and additional data suggesting that neuroinvasion may concurrently or independently involve the blood vascular system.

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Biochemical properties and kinetic parameters of dihydroxyphenyialanine – 5-hydroxytryptophan decarboxylase in brain, liver, and adrenals of cat

Canadian Journal of Biochemistry ◽

10.1139/o79-126 ◽

1979 ◽

Vol 57 (7) ◽

pp. 1014-1018 ◽

Cited By ~ 13

Author(s):

Sylvie Bouchard ◽

Andrée G. Roberge

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Enzyme Activity ◽

Kinetic Parameters ◽

Biochemical Properties ◽

Mechanisms Of Action ◽

Decarboxylase Activity ◽

Peripheral Organs ◽

Exogenous Addition ◽

The Central Nervous System

Biochemical properties and kinetic parameters of nonpurified dihydroxyphenylaianine –5-hydroxytryptophan decarboxylase extracted from brain and two peripheral organs, liver and adrenals, were studied in the cat. This study shows that decarboxylase activity in brain is lower than in peripheral organs and that 5-hydroxytryptophan can be decarboxylated without exogenous addition of pyridoxal-5′-phosphate (PLP). However, the addition of PLP substantially increases the enzyme activity. Excess of coenzyme (>60 μM) induces inhibition in adrenals and liver but not in the central nervous system (CNS). The observed inhibition might be related to the presence of a tetrahydroisoquinoline derivative formed in the medium. Differentiation between mechanisms of action of decarboxylase in the CNS and peripheral organs is suggested.

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The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/4028394 ◽

2019 ◽

Vol 2019 ◽

pp. 1-19 ◽

Cited By ~ 3

Author(s):

Chaoran Chen ◽

Xiang Zhou ◽

Jialiang He ◽

Zhenxing Xie ◽

Shufang Xia ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Vital Role ◽

Pathological Process ◽

Peripheral Organs ◽

Multiple Organs ◽

Long Time ◽

The Central Nervous System

Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.

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