PubMed · 13751498
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P KARLI. 1960. [Aggressiveness and tranquilizing agents].. https://pubmed.ncbi.nlm.nih.gov/13751498/
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The use of transgenic models in scientific research has made an enormous contribution to our understanding of the causes and symptoms of many diseases, including neurodegenerative conditions such as Alzheimer's Disease (AD) and Parkinson's Disease (PD). In the creation of transgenic models of neurodegenerative disease, effects of the background strain of the animal on the resulting genotype must be taken into consideration. This is particularly true for behavioural studies in which the background strain of the mouse may mask the phenotype of the genetic manipulation. Here, the behaviour of two mouse strains used in transgenic models, FVB/N and C57BL6/J, were compared. Studies of circadian wheel activity, cognition and aggression revealed considerable phenotypic differences between strains. These data also indicate that the FVB/N strain is not appropriate as a background strain in the behavioural assessment of transgenic mouse models.
Neuropeptide cholecystokinin (CCK) regulates the adaptation of rodents in the novel environment. In the present study we analysed the behavioural changes induced by the individual housing in mice, lacking CCK(2) receptors. The wild-type (+/+) and homozygous (-/-) CCK(2) receptor deficient mice of both gender were used throughout the study. The weight gain during the 21-day isolation period and changes in the locomotor activity following the social separation were measured. The elevated plus-maze and resident/intruder tests were also performed to test alterations in the emotional behaviour. Social isolation induced locomotor hyperactivity, reduced weight gain and increased aggressiveness in the wild-type (+/+) and homozygous (-/-) male mice. In the wild-type (+/+) female mice the significant reduction of exploratory activity in the plus-maze was evident. By contrast, in female mice, lacking CCK(2) receptors, the exploration of the plus-maze was not significantly affected by the individual housing. This finding demonstrates that the social isolation does not cause anxiety-like state in the CCK(2) receptor deficient mice. Moreover, the targeted invalidation of CCK(2) receptors increased in male mice the affinity of dopamine D(2) receptors in the sub-cortical structures, whereas in female mice the increased affinity of 5-hydroxytryptamine(2) (5-HT(2)) receptors in the frontal cortex was established. The increased affinity of 5-HT(2) receptors is probably the compensatory change to the lack of CCK(2) receptors in female mice and probably reflects the reduced sensitivity of these animals to the anxiogenic manipulations. In conclusion, targeted mutation of CCK(2) receptors selectively antagonised the behavioural changes induced by the individual housing in females, but not in male mice.
Transplantation of neural stem cells (NSCs) can replace lost neurons and improve the functional deficits. Cell transplantation strategies have been tried in the epileptic disorder, but the effect of exogenous NSCs is unknown. In this study, we attempted to test the anti-epileptogenic effect of NSCs in adult rats with status epilepticus. Experimental status epilepticus was induced by lithium-pilocarpine injection, and beta galactosidase-encoded human NSCs were transplanted intravenously on the next day of status epilepticus. Spontaneous recurrent seizures were monitored with Racine's seizure severity scale. Immunohistochemistry with anti-beta gal, Tuj-1, NeuN, GFAP, CNPase, GluR2, parvalbumin, and GABA were performed and extracellular field excitatory postsynaptic potentials (fEPSP) were recorded. Human NSCs suppressed spontaneous recurrent seizure formation and transplanted NSCs were differentiated into GABA-immunoreactive interneurons in the damaged hippocampus. Amplitude of fEPSP in the hippocampal CA1 was reduced, which was reversed by picrotoxin. These findings suggest that NSCs could be differentiated into inhibitory interneurons and decrease neuronal excitability, which could prevent spontaneous recurrent seizure formation in adult rats with pilocarpine-induced status epilepticus.