To analyze locomotor abilities of experimental animals, we estimated the grip strength. Our study found no significant differences of the motor functions in the knockout mice, which is consistent with previously published data obtained in different motor tasks . Intact grip strength by the knockouts suggests that muscle tone is not impaired in these mice.
We have shown that young mice with the target inactivation of γ-synuclein gene are characterized high working-memory capacity, but have no alterations in spatial learning and memory. Our previous study had revealed that behavioral phenotype of γ-KO mice can be characterized by low level of anxiety and enhanced habituation. These data can explain the improvement of learning in the passive and active avoidance models, used in the current investigation.
At the moment molecular and biochemical basis of the memory improvement in passive and active avoidance tests in γ-KO mice is not well understood. Several hypotheses can be assumed. Interestingly, inactivation of the expression of highly homologous to γ-synuclein, α-synuclein protein produces partially opposing phenotype – working and spatial memory impairment in adult mice . However in spite of high homology in the amino acid primary sequence α-synuclein and γ-synuclein proteins differ in their secondary structure: γ-synuclein has an increased α-helical propensity in the amyloid-forming region (NAC-region)  which is involved in trafficking of monoamine transporters . We can suggest that variations in the secondary structure are responsible for the opposite effects of α- and γ-synuclein gene knockout on expression of dopamine transporter (DAT) in the brain , that can in turn affect their cognitive ability . Moreover, inactivation of the gene expression of α- and γ-synuclein has opposite effects on the emotional status of animals [12, 29, 30], which may also be reflected in the observed changes in cognitive abilities. It has been shown previously using the same line of knockout mice that inactivation of γ-synuclein gene alone does not affect expression of α-synuclein mRNA or protein in neural tissue , therefore our results present a clear effect of γ-synuclein’s inactivation.
It is also possible that in the absence of γ-synuclein a general mechanism of synaptic vesicle turnover and neurotransmitter release are perturbed to the degree that does not noticeably alter animal physiology but affects certain types of behaviour. This idea is consistent with more pronounced changes in neurotransmission observed in α/γ-synuclein double knockout comparing to α-synuclein knockout mice  and in triple synuclein knockout comparing to α/β-synuclein double knockout mice [32–34].
γ-Synuclein inactivation did not affect spatial learning in the Morris water maze although γ-synuclein is highly expressed in the brain areas involved in spatial learning  and its inactivation was shown to cause developmental deficit in the number of dopamine neurons in the midbrain [27, 31] – an essential component for a water maze cued task learning . We also did not reveal alterations in spatial memory of γ-KO mice. The most obvious explanation for this fact can be based on different strategies used for the platform search. “Route navigation” strategy probably allows γ-KO mice to use their high performing working memory and thus compensate the deficient spatial memory which is critical in «locale navigation» strategy [37, 38]. This phenomenon as well as enhancement of working memory in γ-KO compared to WT mice needs further investigation.
Thus, our data provide the first evidence that γ-synuclein may be the important component of learning process which primarily based on the functioning of working memory.