Nooglutyl powder has been determined to have effective and potent nootropic properties. Nooglutyl was observed to have a positive effect on memory creation and retention, and it was also able to improve most of the cognitive processes of the lab animals. The study also suggested that it had antiamnesic and antihypoxic abilities.
Experiments on rats demonstrate that nooglutyl exhibits pronounced vestibular-protective properties and by its antimotion activity does not rank below classic vestibular protectors, such as scopolamine and diprazine. Electrophysiological experiments on cats show that nooglutyl alters spontaneous activity in 80% of cortical neurons (somatosensory zone I and area 5 of the parietal association cortex) and considerably weakens effects caused by motion sickness: activation of single unit activity of somatosensory zone I and inhibition of neuron responses to somatic stimulation. This property of the preparation is believed to form the basis of its antimotion effect.
Nooglutyl has been shown to selectively modulate AMPA receptors, typical of an ampakine stimulant, with the neuroprotective aspects of a racetam. It has been demonstrated to have a stronger effect on glutamate receptors than Noopept
AMPA and D2 receptors
As other nootropics, Nooglutyl is a positive modulator of AMPA-subtype glutamatergic receptors which was described to be more efficient than Noopept when in competition with the selective agonist RO-48- 8587.
(IC50 of 6.4 mM vs 80 mM for Noopept)
Plus, a study revealed that it increases both the dissociation constant and the density of D2 receptors in rats following systemic administration at 50 mg/kg.
Voronina, T. A. et al. Effect of nooglutil on benzodiazepine withdrawal syndrome and binding of 3H-spiperone with D2 receptors in rat striatum. Bull Exp Biol Med 134, 448每450 (2002).
Firstova, I.I., Vasil*eva, E.V., and Kovalev, G.I. (2011). [Studying specific effects of nootropic drugs on glutamate receptors in the rat brain]. Eksp Klin Farmakol 74, 6每10.
Benzodiazepine withdrawal
Interestingly, although it has not been shown to directly interfere with any GABAergic receptors, it appeared to improve symptoms from diazepam withdrawal in rats, particularly anxiety.
Voronina, T. A. et al. Effect of nooglutil on benzodiazepine withdrawal syndrome and binding of 3Hspiperone with D2 receptors in rat striatum. Bull Exp Biol Med 134, 448每450 (2002)
Brain trauma & Mitochondrial Oxidative Phosphorylation
Two studies (on rats) put forward that Nooglutyl prevent the inhibition of oxidative phosphorylation in mitochondria following craniocerebral trauma (50 mg/kg)
In comparison, its protective effect surpassed these of picamilon, piritidol, piracetam and pantogam Novikov, V.E., and Kovaleva, L.A. (1998).
[The effect of nootropic agents on brain mitochondrial function in the dynamics of craniocerebral trauma from the age aspect]. Eksp Klin Farmakol 61, 65每68.
Dopaminergic and serotoninergic alteration following prenatal alcohol exposure
Two studies (on rats) have explored the impact of prenatal alcohol exposure and described that Nooglutyl administration at 25 mg/kg/day to offspring rats (8th to 20Th day) prevents ethanol-associated alteration of both serotoninergic system in the brain cortex and dopaminergic system in the hippocamp.
Nooglutyl also normalized dopamine released in the rat striatum, but they observed an opposite effect on the offsprings of non-alcoholized rats.
Trofimov, S.S., Ostrovskaia, R.U., Smol*nikova, N.M., Khromova, I.V., Krapivin, S.V., Krylova, A.M., Kovalev, G.I., Gaĭnetdinov, R.R., Liubimov, B.I., and Voronina, T.A. (1992). [The nooglutil correction of functional disorders of the central nervous system caused by prenatal alcoholization in rats]. Eksp Klin Farmakol 55, 18每21.
Kovalev, G.I., Budygin, E.A., Gaĭnetdinov, R.R., Kudrin, V.S., Trofimov, S.S., and Ostrovskaia, R.U. (1993). [The sodium oxybutyrate and nooglutil correction of dopamine release in the striatum of prenatally alcoholized rat pups]. Biull Eksp Biol Med 116, 56每58.
Hypoxia/Ischemia
In a stroke rat model, a study has shown that Nooglutyl completely prevented amnestic disorders. They also use a rat model of hypoxia-induced amnesia and observed that Nooglutyl ※fully blocked§ the development of amnesic disorders.
Iasnetsov, V. V., Krylova, I. N. & Provornova, N. A. [Pharmacological treatment of memory disorders caused by hypoxia and cerebral ischemia in rats]. Aviakosm Ekolog Med 32, 55每60 (1998)
Brain injury
In a rat model with post-traumatic hematoma the authors have shown that a single intraperitoneal injection of nooglutyl decreased neurological deficiency and restored the coordination of movements.
Passive avoidance reaction retrieval was also improved. Garibova, T.L., Galaeva, I.P., Voronina, T.A., Kraĭneva, V.A., Kapitsa, I.G., Kirichenko, S.V., Makarenko, A.N., Mirzoian, G.R., and Kuznetsova, E.A. (2003). [Effect of nooglutil on rats with intracerebral posttraumatic hematoma (hemorrhagic stroke)]. Eksp Klin Farmakol 66, 13每16.
Clonidine & Scopolamine-induced cognitive impairments
One study described that Nooglutyl abolish the memory-impairing effect of clonidine at 50mg/kg when administered once daily for 5 days, as well as scopolamine-provoked amnesia in step-through-trained mice.
However, the observation that interested me the most in this study is that the authors did not observe any influence of Nooglutyl on hippocampal and cortical BDNF levels, conversely to piracetam.
Voronina, T.A., Garibova, T.L., Trofimov, S.S., Sopyev, Z.A., Petkov, V.D., and Lazarova, M.B. (1991). Comparative studies on the influence of ONK (N(5-hydroxynicotinoil) glutamic acid), piracetam and meclofenoxate on the learning- and memory-impairing effect of scopolamine, clonidine, and methergoline. Acta Physiol Pharmacol Bulg 17, 8每16.
Impaired cognitive function associated with aging
While using a model of senescence-accelerated mice, Nooglutyl succeeded at 20 mg/kg to enhance locomotor activity in open field test and diminished their anxiety while improving retrieval of passive avoidance reflex. Garibova, T., Voronina, T., Litvinova, S., Grigor*ev, V., and Bachurin, S. (2007).