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Introduction: Developmental dysphasia (DD) is a developmental language disorder with high prevalence, but also with low publication index and confusion of the terminology (including the Czech version of ICD - "speech" disorder instead of "language" disorder). The scientific view has passed the development from a symptom, through the specific nozologic unit to the current term Developmental language disorder (DLD) and its classification among a new category of diseases in ICD-11 (existing in DSM-5) called Neurodevelopmental disorders. Another disorder with the characteristic pathology in communication is the autism spectrum disorder (ASD) which is classified as a disease of the same category as DD. Compared to DD, it has a higher publication index, lower prevalence, and even more serious consequences. Three different domains that cause confusion, both in ASD and DD, are "speech", "language", and "communication". The same confusion applies to the current subtypes in ICD-11 with the term "functional language". In the Czech Republic there are very few studies dealing with the patients with DD, their profile of a clinic picture has not been processed so far. In spite of the increase of Czech research of ASD there is a missing speech, language, and communication profile of these individuals. This has...

Perinatal insult may lead to a permanent impairment of brain function resulting in the development of epilepsy. Status epilepticus (SE) in immature rats leads to hippocampal hyperexcitability. The functional and morphological changes of the hippocampus are similar to those seen in human temporal lobe epilepsy. The excitability may be influenced by adenosine. Adenosine acts its anticonvulsant effect by activation of A1 receptors (A1R). The concentration of adenosine is regulated by adenosine kinase (ADK) present in two isoforms - ADK-L and -S. The main goal of the thesis is to elucidate the changes in A1R and ADK isoforms expression during intact brain development and after SE. A1R agonist 2-chloro-N6- cyclopentyladenosine (CCPA), as well as inhibition of ADK by 5-iodotubercidin (5-ITU), may bolster the anticonvulsant effect, but their action may correspond with the level of A1R and ADK. Hippocampal excitability in immature rats after LiCl-pilocarpine SE was studied by the model of hippocampal afterdischarges (ADs) and correlated with changes of A1R and ADK in the hippocampus. ADs demonstrated significantly decreased hippocampal excitability shortly after SE induction, whereas significant hyperexcitability accompanied by spontaneous seizures in older rats was shown. Increasing ADK-S expression...