NEUROTROPHIC EFFECTS OF ETIFOXINE

Abstract

Higher anxiety results in the decreased levels of various neurotrophic factors and enkephalins and in impaired production of proinflammatory cytokines. The anxiolytic etifoxine is used to treat anxiety states and adjustment disorders. Etifoxine modulates the GABAergic transmission and metabolism of neurosteroids. The latter determines the unique neurotrophic and neuroprotective properties of the drug, such as increased expression of neurotrophic factors, regeneration of nerve fibers, and preservation and regeneration of myelin sheaths. Other important pharmacological effects of an etifoxine molecule have been also discovered; these are to relieve allodynia related to 3α-steroids and GABA receptors and to effectively treat cerebral edema, experimental autoimmune encephalitis, and excessive nervous excitability in the presence of alcohol withdrawal. In addition, the chemoreactome simulation of the molecule of etifoxine has established that its attenuated side effects are due to its lower interaction with serotonin, acetylcholine, adrenergic and other neurotransmitter receptors than is shown by benzodiazepines. Etifoxine has been also found to have anti-inflammatory (due to antihistamine and antileukotriene effects) and antitumor activities and an ability to affect hemodynamics and vessel walls.The paper presents a systematic analysis of the results of trials of the neurotrophic properties of etifoxine. It considers how the drug stimulates the expression of neurotrophic factors, accelerates the maturation and regeneration of nerve fibers, and regenerates myelin sheaths.The neurotrophic effects of etifoxine along with its anxiolytic activity will accelerate the recovery of patients with different neurological diseases and enhance the quality of their neurorehabilitation.

Keywords

• anxiety
• adjustment disorders
• etifoxine
• neurotrophic and neuroprotective effects