| Autor: |
Kolik LG; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia. lgkolik@mail.ru., Konstantinopolsky MA; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Nadorova AV; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Kruglov SV; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Antipova TA; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Gudasheva TA; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Seredenin SB; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia. |
| Jazyk: |
angličtina |
| Zdroj: |
Bulletin of experimental biology and medicine [Bull Exp Biol Med] 2020 Nov; Vol. 170 (1), pp. 30-34. Date of Electronic Publication: 2020 Nov 22. |
| DOI: |
10.1007/s10517-020-04998-0 |
| Abstrakt: |
Activity of compound GSB-106, a low-molecular mimetic of loop 4 of the brain neurotrophic factor (BDNF), was studied in experimental morphine withdrawal syndrome simulated in outbred rats. Single and subchronic (5 intraperitoneal injections) administration of GSB-106 in a dose of 0.1 mg/kg significantly reduced the total index of morphine withdrawal syndrome by 55.2 and 45.6%, respectively. GSB-106 reduced the severity of some behavioral signs (piloerection, gnashing of teeth, wet-dog shaking, and runaway attempts), but had no effect on mechanical allodynia formed in the rats with dependence. Subchronic treatment with GSB-106 prevented the increase in the content of ΔFosB (product of early response gene) in the striatum induced by morphine withdrawal. The results confirmed the concept on the involvement of neurotrophins, specifically BDNF and its analogs, in the mechanisms associated with the formation of opiate dependence. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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