Biogenic Amines in Neurotransmission and Human Disease最新文献

Introductory Chapter: Biogenic Amines in Neurotransmission and Human Disease from the Endocrinologist’s Perspective 导论章:从内分泌学家的角度看神经传递和人类疾病中的生物胺

Biogenic Amines in Neurotransmission and Human Disease Pub Date : 2019-11-13 DOI: 10.5772/intechopen.89244

A. Uçar

{"title":"Introductory Chapter: Biogenic Amines in Neurotransmission and Human Disease from the Endocrinologist’s Perspective","authors":"A. Uçar","doi":"10.5772/intechopen.89244","DOIUrl":"https://doi.org/10.5772/intechopen.89244","url":null,"abstract":"There are about 1011 neurons and 1014 synaptic connections in the human brain. The neural circuitry is continuously sculpted in response to experience, modified as we learn and store memories, and irreversibly altered by the gradual loss of neurons and connections as we age [1]. Neuronal signals are transmitted from cell to cell at synapses. When an action potential arrives at the presynaptic site, the depolarization of the membrane opens voltage-gated calcium channels that are clustered in the presynaptic membrane. Calcium influx triggers the release of neurotransmitters which are stored in membrane-enclosed synaptic vesicles and released by exocytosis. The neurotransmitter provokes an electrical change in the postsynaptic cell by binding to and opening transmitter-gated ion channels. After the neurotransmitter is secreted into the synaptic cleft, it is rapidly removed: it is either destroyed by specific enzymes in the synaptic cleft or taken up by the presynaptic nerve terminal or by surrounding glial cells. Reuptake is mediated by a variety of Na+-dependent neurotransmitter symporters. The cycling of neurotransmitters allows cells to keep up with the high rates of release [1–3]. The chemical or electrical synapses can be excitatory or inhibitory. Excitatory neurotransmitters open cation channels, causing an influx of Na+ and also Ca+ in many cases, which reduces the threshold to fire an action potential. Inhibitory neurotransmitters open Cl or K+ channels, thereby making it difficult to depolarize the cell membrane. Depending on the secretion milieu, the type of the receptors they bind to, and the ionic conditions that they encounter, transmitters may be either inhibitory or excitatory. For example, acetylcholine may have inhibitory or excitatory effects depending on the type of the receptor it binds to. Usually glutamate and serotonin are excitatory, whereas γ-aminobutyric acid and glycine are inhibitory [1–4]. All neurotransmitter receptors fall into one of these classes based on their signaling mechanisms:","PeriodicalId":190348,"journal":{"name":"Biogenic Amines in Neurotransmission and Human Disease","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133489925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kainate Receptors Modulating Glutamate Release in the Cerebellum 盐酸盐受体调节小脑谷氨酸释放

Biogenic Amines in Neurotransmission and Human Disease Pub Date : 2019-09-24 DOI: 10.5772/INTECHOPEN.87984

Pilar Losada-Ruiz, Rafael Falcón-Moya, A. Rodríguez-Moreno

{"title":"Kainate Receptors Modulating Glutamate Release in the Cerebellum","authors":"Pilar Losada-Ruiz, Rafael Falcón-Moya, A. Rodríguez-Moreno","doi":"10.5772/INTECHOPEN.87984","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.87984","url":null,"abstract":"Glutamate receptors of the kainate type (Kainate receptors, KARs), are mediators of ionotropic postsynaptic synaptic transmission, as well as presynaptic modulators of neurotransmitter release where they show both ionotropic and metabotropic actions regulating glutamate and γ -aminobutiric acid (GABA) release. The mechanisms underlying these modulatory roles are starting to be understood at some brain regions. Here we review the KARs roles and mechanisms involved in the modulation of glutamate release in the cerebellum at parallel fibers (PF)-Purkinje Cells (PuC) synapses. KARs activation mediate a biphasic effect on glutamate release at this synapse, with low kainate (KA) concentrations mediating a facilitation of glutamate release and higher KA concentrations mediating a depression of glutamate release. KA-mediated facilitation is prevented by antagonizing KARs, by inhibition of PKA or stimulation of adenylyl cyclase (AC), by blocking Ca 2+ permeant KARs, by depleting intracellular Ca 2+ stores and by blocking calmodulin. Thus, at cerebellar parallel fiber-Purkinje cell synapses, presynaptic KARs mediate glutamate release facilitation through Ca 2+ -calmodulin dependent activation of adenylyl cyclase/cAMP/protein kinase A signaling. KAR-mediated depression of glutamate release involves the AC/cAMP/PKA pathway as for facilitation but not Ca 2+ -calmodulin, being in this case AC activated by a Gi/o protein to mediate a depression of glutamate release.","PeriodicalId":190348,"journal":{"name":"Biogenic Amines in Neurotransmission and Human Disease","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124925429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Thrombotic Tendencies in Excess Catecholamine States 过量儿茶酚胺状态的血栓倾向

Biogenic Amines in Neurotransmission and Human Disease Pub Date : 2019-07-22 DOI: 10.5772/INTECHOPEN.81929

V. Nambiar, Drisya Rajan Chalappurath

{"title":"Thrombotic Tendencies in Excess Catecholamine States","authors":"V. Nambiar, Drisya Rajan Chalappurath","doi":"10.5772/INTECHOPEN.81929","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81929","url":null,"abstract":"Catecholamines are neurotransmitters distributed throughout the body including adrenal glands, chromaffin tissues and other tissues innervated by post ganglionic adrenergic neurons. The rate of release of medullary hormones is responsible for the control of serum catecholamines. Thrombogenicity of catecholamines are due various mechanisms including hypercoagulable states, endothelial damage, blood stasis and platelet aggregation. Oxidative stress generated by catecholamine excess causes coronary spasm, ultrastructural cell damage and arrhythmias. Elevated plasminogen activator inhibitor-1 during catecholamine excess causes hypercoagulability by hypofi-brinosis. During stress, Catecholamines released in procoagulant environment causes vasoconstriction in adrenal veins resulting in venous thrombosis. Catecholamines generate moderately elevated levels of platelet count which enhances the risk of thrombosis. Hypercoagulability results in formation of coronary thrombus, rupture of atherosclerotic plaque and plaque progression due to gradual fibrinogen accumulation in the vessel walls. High levels of circulating catecholamines produce elevated levels thrombomodulin, the biomarkers of endothelial cell damage. In patients with hypertension in catecholamine excess, resistance to blood flow and damage to the integrity of blood vessels lead to atherosclerosis. A case report has been discussed which suggests an association of thrombotic tendency and catecholamine excess.","PeriodicalId":190348,"journal":{"name":"Biogenic Amines in Neurotransmission and Human Disease","volume":"308 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123399312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Homeostatic Plasticity and Therapeutic Approaches in Neurodegeneration 神经变性的内稳态可塑性和治疗方法

Biogenic Amines in Neurotransmission and Human Disease Pub Date : 2019-07-02 DOI: 10.5772/INTECHOPEN.86415

S. Martín-Aragón, P. Bermejo-Bescós, P. González, J. Benedí

{"title":"Homeostatic Plasticity and Therapeutic Approaches in Neurodegeneration","authors":"S. Martín-Aragón, P. Bermejo-Bescós, P. González, J. Benedí","doi":"10.5772/INTECHOPEN.86415","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.86415","url":null,"abstract":"The synapses transmit signals between neurons in an ever-changing fashion. Changes of synaptic transmission arise from numerous mechanisms known as synaptic plasticity. The importance and complexity of the synapse has fueled research into the molecular mechanisms underlying synaptogenesis, synaptic transmission, and plasticity. Particularly, homeostatic plasticity refers to the local changes in synaptic activation to generate local synaptic adaptations and network-wide changes in activity to generate adjustments between excitation and inhibition. This review chapter will focus on synaptic phenomena and mechanisms that are likely to contribute to network homeostasis. In addition, it will be discussed a putative modulation of the signaling mechanisms serving a homeostatic function as a viable therapeutic approach for disease modification in neurological and neurodegenerative disorders. To sum up, the main role of the following players in homeostatic plasticity will be analyzed, based on what a growing body of evidence has suggested recently: BDNF-mediated TrkB system activation; adenosine modulation system; nitric oxide/soluble GC/cGMP signaling; astrocyte involvement astroglial CB1 receptors; the microtubule-associated neuronal protein Tau; the signaling of the Wnt protein family; extracellular vesicles in the intercellular communication; and estrogen involvement in non-reproductive functions.","PeriodicalId":190348,"journal":{"name":"Biogenic Amines in Neurotransmission and Human Disease","volume":"249 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114479739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Pharmacological Effects of Herbs on Catecholamine Signaling 中药对儿茶酚胺信号传导的药理作用

Biogenic Amines in Neurotransmission and Human Disease Pub Date : 2018-12-31 DOI: 10.5772/INTECHOPEN.81510

N. Yanagihara, Xiaoja Li, Y. Toyohira, N. Satoh, Hui Shao, Y. Nozaki, Shin Ishikane, Fumi Takahashi, Ryo Okada, Hideyuki Kobayashi, M. Tsutsui, T. Kita

{"title":"The Pharmacological Effects of Herbs on Catecholamine Signaling","authors":"N. Yanagihara, Xiaoja Li, Y. Toyohira, N. Satoh, Hui Shao, Y. Nozaki, Shin Ishikane, Fumi Takahashi, Ryo Okada, Hideyuki Kobayashi, M. Tsutsui, T. Kita","doi":"10.5772/INTECHOPEN.81510","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81510","url":null,"abstract":"Herbs have many biologically and pharmacologically active compounds such as flavonoids and stilbenes. They have been used in remedies for various disorders. Here we review the effects of herbs on catecholamine synthesis and secretion in cultured bovine adrenal medullary cells. Ikarisoside A (1.0–100 μ M), a flavonol glycoside, inhibited the catecholamine secretion induced by acetylcholine (0.3 mM). This inhibition was associated with the suppression of 22 Na + and 45 Ca 2+ influx induced by acetylcholine. The ethanol extract (0.0003–0.005%) of matsufushi (extract of pine nodules) inhibited the catecholamine secretion induced by acetylcholine. SJ-2, one of the stilbene compounds isolated from matsufushi, inhibited acetyl-choline-induced catecholamine secretion. Matsufushi extract and SJ-2 reversibly inhibited acetylcholine-induced Na + currents in Xenopus oocytes expressed with α 3 β 4nicotinic acetylcholine receptors. Sweet tea is the processed leaves of Hydrangea macrophylla . The extract of sweet tea (0.3–1.0 mg/ml) suppressed catecholamine secretion induced by acetylcholine (0.3 mM). Moreover, sweet tea (0.1–1.0 mg/ml), ikarisoside A (1.0–100 μ M), and matsufushi (0.001–0.003%) or SJ-2 (10–30 μ M) inhibited acetylcholine-induced 14 C-catecholamine synthesis from 14 C-tyrosine. These findings indicate that ikarisoside A, matsufushi (or SJ-2), and sweet tea inhibit the catecholamine secretion and synthesis induced by acetylcholine in cultured bovine adrenal medullary cells and probably in sympathetic neurons.","PeriodicalId":190348,"journal":{"name":"Biogenic Amines in Neurotransmission and Human Disease","volume":"41 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128218988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0