A crustacean serotonin receptor: Cloning and distribution in the thoracic ganglia of crayfish and freshwater prawn

2004 ◽  
Vol 473 (4) ◽  
pp. 526-537 ◽  
Author(s):  
Mar�a A. Sosa ◽  
Nadja Spitzer ◽  
Donald H. Edwards ◽  
Deborah J. Baro
Keyword(s):  
Serotonin Receptor ◽  
Freshwater Prawn ◽  
Thoracic Ganglia ◽  
Receptor Cloning

scholarly journals Mouse 5HT1B serotonin receptor: cloning, functional expression, and localization in motor control centers.

1992 ◽  
Vol 89 (7) ◽  
pp. 3020-3024 ◽  
Author(s):  
L. Maroteaux ◽  
F. Saudou ◽  
N. Amlaiky ◽  
U. Boschert ◽  
J. L. Plassat ◽  
...  
Keyword(s):  
Motor Control ◽  
Serotonin Receptor ◽  
Functional Expression ◽  
Receptor Cloning

Assessment for the Role of Serotonin Receptor Subtype 3 for the Analgesic Action of Morphine at the Spinal Level

2005 ◽  
Vol 18 (2) ◽  
pp. 113
Author(s):  
Myung Ha Yoon ◽  
Hong Buem Bae ◽  
Jeong Il Choi ◽  
Seok Jae Kim ◽  
Chang Mo Kim ◽  
...  
Keyword(s):  
Serotonin Receptor ◽  
Receptor Subtype ◽  
Analgesic Action ◽  
Spinal Level ◽  
Subtype 3

Adding perphenazine to increase effectiveness of standard glioblastoma chemoirradiation. (Preprint)

2020 ◽  
Author(s):  
Richard Kast
Keyword(s):  
Dopamine Receptor ◽  
Subventricular Zone ◽  
Serotonin Receptor ◽  
Treatment Effectiveness ◽  
Short Note ◽  
Recurrent Glioblastoma ◽  
Current Standard ◽  
Medically Ill ◽  
Current Standard Treatment ◽  
Protein Phosphatase 2

UNSTRUCTURED In the effort to improve treatment effectiveness in glioblastoma, this short note reviewed collected data on the pathophysiology of glioblastoma with particular reference to intersections with the pharmacology of perphenazine. That study identified five areas of potentially beneficial intersection. Data showed seemingly 5 independent perphenazine attributes of benefit to glioblastoma treatment - i) blocking dopamine receptor 2, ii) reducing centrifugal migration of subventricular zone cells by blocking dopamine receptor 3, iii) blocking serotonin receptor 7, iv) activation of protein phosphatase 2, and v) nausea reduction. Perphenazine is fully compatible with current chemoirradiation protocols and with the commonly used ancillary medicines used in clinical practice during the course of glioblastoma. All these attributes argue for a trial of perphenazine’s addition to current standard treatment with temozolomide and irradiation. The subventricular zone seeds the brain with mutated cells that become recurrent glioblastoma after centrifugal migration. The current paper shows how perphenazine might reduce that contribution. Perphenazine is an old, generic, cheap, phenothiazine antipsychotic drug that has been in continuous clinical use worldwide since the 1950’s. Clinical experience and research data over these decades have shown perphenazine to be well-tolerated in psychiatric populations, in normals, and in non-psychiatric, medically ill populations for whom perphenazine is used to reduce nausea. For now (Summer, 2020) the nature of glioblastoma requires a polypharmacy approach until/unless a core feature and means to address it can be identified in the future. Conclusions: Perphenazine possesses a remarkable constellation of attributes that recommend its use in GB treatment.

scholarly journals Vitamin B6 deficiency disrupts serotonin signaling in pancreatic islets and induces gestational diabetes in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ashley M. Fields ◽  
Kevin Welle ◽  
Elaine S. Ho ◽  
Clementina Mesaros ◽  
Martha Susiarjo
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Glucose Intolerance ◽  
Vitamin B6 ◽  
Serotonin Receptor ◽  
Dependent Manner ◽  
Β Cell ◽  
Vitamin B6 Deficiency ◽  
Maternal Glucose

AbstractIn pancreatic islets, catabolism of tryptophan into serotonin and serotonin receptor 2B (HTR2B) activation is crucial for β-cell proliferation and maternal glucose regulation during pregnancy. Factors that reduce serotonin synthesis and perturb HTR2B signaling are associated with decreased β-cell number, impaired insulin secretion, and gestational glucose intolerance in mice. Albeit the tryptophan-serotonin pathway is dependent on vitamin B6 bioavailability, how vitamin B6 deficiency impacts β-cell proliferation during pregnancy has not been investigated. In this study, we created a vitamin B6 deficient mouse model and investigated how gestational deficiency influences maternal glucose tolerance. Our studies show that gestational vitamin B6 deficiency decreases serotonin levels in maternal pancreatic islets and reduces β-cell proliferation in an HTR2B-dependent manner. These changes were associated with glucose intolerance and insulin resistance, however insulin secretion remained intact. Our findings suggest that vitamin B6 deficiency-induced gestational glucose intolerance involves additional mechanisms that are complex and insulin independent.

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