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the effect on serotonin metabolism and to activate dopamine metabolism in cerebrum (Shishkina
et al., 2005, 2006).
In Shishkina et al. (2006), the nootropic activity of luoxetine was established for the irst time.
Both complexes GA: FL 1:1 and 4:1 demonstrate the same effect but at a slightly lower level than
reference drugs.
Fluoxetine (30 μM) is known to suppress epileptiform activity, which is manifested by a 50%
decrease in the amplitude of the electric potential oscillation, which relects the activity of nerve
cells induced by electric stimulation of hippocampus under the action of picrotoxin.
Fluoglyzine (complex 4:1), similar to luoxetine, suppresses bicuculline-induced epileptiform
activity in the sections of rat hippocampus, demonstrating antiepileptic activity (Shishkina et al.,
2006).
Phenibut (PhB) (γ-amino-β-phenylbutyric acid hydrochloride) is a nootropic sedative medica-
tion, relieving tension and anxiety and improving sleep. In clinical practice it is used for asthenic
syndrome, anxious neurotic conditions, sleep disorders and as an anti-naupathia preparation in pre-
surgery procedures. As a nootropic drug Phenibut has serious laws, for example, it provokes sleepi-
ness and allergic reactions.
Complexes GA: PhB 2:1 and 4:1, the toxicity of which is twice as lower than that of Phenibut,
produce a cognitive effect similar to that of the pharmacon and GABA. Unlike Phenibut and
GABA, the complexes increase mnestic capabilities in animals by 20% and decrease sedative effect
(Shishkina et al., 2006).
Buspirone (BSP) is an anxiolytic drug. It is characterized by high afinity to pre- (agonist)
and postsynaptic (partial agonist) serotonin receptors of the 5-HT 1A subtype. It impedes the syn-
thesis and release of serotonin, the activity of serotonergic neurons, particularly in the dorsal
raphe nucleus. It selectively blocks (antagonist) the pre- and postsynaptic D2-dopamine recep-
tors (has a moderate afinity) and increases the speed of activations of dopamine neurons in the
mesencephalon. The pharmacological properties of the PSP:GA complex (1:10) were studied on
the model of social depression in sexually mature male mice of the C57BL/6J line. It was shown
that neither buspirone nor the complex inluenced the level of glucose and the protein content in
blood (Table 11.6).
Earlier it had been shown that the stress of social interaction in mice causes the increase in
glucose content in the blood plasma of the victims (Avgustinovich et al., 2003). It is known that a
prolonged emotionally negative social stress increases the need in glucose, as it serves as the main
source of energy for nerve cells. Considering this, it may be said that neither buspirone nor the com-
plex of buspirone with glycyrrhizic acid inluences the mobilization of the energetic and structural
resources of the body caused by chronic social stress.
TABLE 11.6
Effects of Chronic Agents Dosing on the Biochemical 
Blood Indices in Anxious-Depressed Mice
Blood Indices
Solvent
Buspiron
Buspiron + GA
Glucose (mmol/L)
5.53 ± 0.035
5.52 ± 0.049
5.29 ± 0.154
Protein (g/L)
18.32 ± 2.093
21.46 ± 2.843
19.14 ± 2.755
Triglyceride (μmol/L)
1.27 ± 0.394
1.24 ± 0.314
0.90 ± 0.259
Cholesterol (mmol/L)
1.69 ± 0.554
2.97 ± 1.054
2.09 ± 0.512
61.05 ± 1.567
53.25 ± 4.219 a
53.76 ± 3.877
MDA (μmol/L)
Catalase (U/L)
32.21 ± 2.842
38.39 ± 1.975 a
38.81 ± 2.703 a
a Signiicantly different ( P < 0.05) from solvent.
 
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