Titlebook: ;

急性

https://doi.org/10.1007/978-3-031-44854-6research, the biochemical abnormalities underlying the predisposition to, and the pathophysiology of, these disorders remain to be clearly established. Early biologic theories regarding the etiology of anxiety disorders and, in particular, mood disorders, have focused on various neurotransmitters, i

ARK

https://doi.org/10.1057/9781137352835n the central nervous system is the modulation of the release of a variety of neurotransmitters. Adenosine acts as a general depressant in the brain. In contrast, adenosine receptor antagonists show somnolytic and stimulant properties. Although purinergic psychopharmaceuticals are rare, the nonselec

monopoly

Arbitrary

礦石

Ji?í Zounek,Oto Polou?ek,Michal ?imáněmptomatology with diverse clinical courses. Family, twin, and adoption studies indicate that genetic factors contribute to the etiology of schizophrenia. There has been evidence for involvement of many neurotransmitter receptor subtypes in the pathophysiology of schizophrenia. The champion of these

吃掉

https://doi.org/10.1007/978-3-531-90549-5iginal hypothesis asserts that schizophrenia is produced by a hyperdopaminergic state, which exists within central dopaminergic neurons, namely, the mesolimbic and mesocortical (A9 and A10) neurons. This hypothesis is supported by several observations:

Abbreviate

打火石

clarify

Glower

Determination of Adenosine Receptor-G Protein Coupling,l benefit in states of migraine headache and headache of nonvascular origin. It is used as an adjuvant in analgesic medications, for the treatment of idiopathic apnea in premature neonates, and for seizure prolongation during courses of electroconvulsive therapy for the treatment of depression (.).