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Cognitive deficit is considered to be a part of core dysfuncions in schizophrenia. It is associated with social impairment and influences the long-term course of the disorder. In addition to neuropsychological methods, event-related potentials can be used to study cognitive functions. In patients with schizophrenia an association was found between amplitude changes in slow negative component of evoked responses and infrequent deviations in a series of uniform stimuli. This amplitude change is known as „mismatch negativity“ (MMN). It is supposed to be independent of the focused attention and effort that otherwise interfere with neuropsychological testing. Recently accumulated knowledge on MMN as a possible preattentive measure of cognition supports its potential significance for neuropsychological assessment. It may be helpful in more precise diagnosis and functional evaluation of schizophrenia.

Článek online

Different sensitivity of miniature endplate currents of the rat extensor digitorum longus, soleus and diaphragm muscles to a novel acetylcholinesterase inhibitor C-547

Physiological research. 2006 ; 55 (5) : 585-589.

ISSN 0862-8408
Medvik
Zdroj

A novel derivative of 6-methyluracil, C-547, increased the amplitude and prolonged the duration of miniature endplate currents (MEPCs) which is typical for acetylcholinesterase inhibition. In the soleus and extensor digitorum longus significant potentiation was detected at nanomolar concentrations. In contrast, in the diaphragm muscle, the increase in the amplitudes of the MEPCs and the decay time constant ? appeared only when the concentration of C-547 was elevated to 1x10-7 M. Possible consequences for the exploitation of this drug, which can selectively inhibit AChE in particular synapses, are discussed.

MeSH
acetylcholinesterasa farmakokinetika účinky léků MeSH
bránice fyziologie účinky léků MeSH
cholinesterasové inhibitory farmakokinetika chemie MeSH
elektrofyziologie metody statistika a číselné údaje MeSH
financování vládou MeSH
interpretace statistických dat MeSH
nervosvalová ploténka enzymologie fyziologie chemie MeSH
potkani Wistar fyziologie MeSH
svaly fyziologie účinky léků MeSH
zvířata MeSH
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zvířata MeSH
Publikační typ
srovnávací studie MeSH

Článek online

Genetické a elektrofyziologické pozadí vnímání tinnitu u pacientů s kochleární percepční poruchou sluchu
[Genetic electrophysiological background of perception of tinnitus in patients with cochlear perception disorder of hearing]

Otorinolaryngologie a foniatrie. 2006 ; Roč. 55 (č. 2) : s. 96-102.

ISSN 1210-7867
Medvik
Zdroj

Desinhibiční hypotéza vzniku tinnitu je založena na existenci zpětnovazebné regulace neurální aktivity v ascendentní části sluchové dráhy cestou inhibice nebo aktivace descendentními neurálními spoji. Abychom mohli podpořit nebo vyvrátit tuto hypotézu, studovali jsme vztah mezi markery desinhibice ve sluchové dráze při registraci AEP a manifestací tinnitu. Variabilita genetického pozadí receptorů sluchové dráhy ve vztahu k manifestaci tinnitu může rovněž napomoci ke zjištění místa a struktury odpovědné za vznik tinnitu. Soubor 105 pacientů s kochleární percepční nedoslýchavostí byl sledován z hlediska manifestace tinnitu, byly měřeny BAEP a MLR a byla provedena analýza genetických polymorfismů – Taq I polymorfismus DRD2 receptoru, +101 C/T v 10. intronu a 1275 A/G polymorfismus GRIN2a podjednotky a 2664 C/T polymorfismus GRIN2b podjednotky NMDA receptoru a CA repetitivní sekvence v genu pro GABRß3 podjednotku pro GABAA receptor. Byly nalezeny následující závislosti: manifestace tinnitu dobře korelovala s poměrem amplitud vln V/III (p<0,001) a s amplitudou vlny PA odpovědi MLR (p<0,001). Manifestace tinnitu závisela rovněž na genotypu u CA repetitivní sekvence genu pro GABRß3 podjednotku (p=0,04). Polymorfismus 2664 C/T GRIN2b podjednotky NMDA receptoru měl vliv na variabilitu elektrofyziologických markerů desinhibice, ale tato závislost byla pouze marginální (min. p=0,07). Tyto výsledky mohou podporovat desinhibiční hypotézu vzniku tinnitu.

The disinhibitory feedback hypothesis of the tinnitus generation is based on feedback regulation of neural activity in the ascendent part auditory pathways via inhibition or activation of descendent auditory connections. To support or reject this hypothesis the relationship between markers of disinhibition in AEP and tinnitus manifestation could be studied. Additionally, the differences in genetic background of receptor systems of the auditory pathways having influence to the tinnitus manifestation may establish the site and structure responsible for the tinnitus generation. A group of 105 patients with cochlear sensorineural hearing loss was studied from the standpoints of tinnitus manifestation, BAEP and MLR and analysis of genetic polymorphisms – Taq I polymorphism of DRD2 receptor, 10 intron +101 C/T and 1275 A/G polymorphism of GRIN2a subunit of NMDA receptor, 2664 C/T polymorphism in the GRIN2b subunit of NMDA receptor and CA repeat in gene of GABRß3 subunit of GABAA receptor. Following dependencies were found: the tinnitus manifestation correlated well with the V/III amplitude ratio of BAEP (p<0.001) and PA amplitude of MLR (p<0.001). The tinnitus manifestation differed significantly in dependence to genotype of CA repeat in gene of GABRß3 subunit (p=0.04). Polymorphism 2664 C/T in the GRIN2b subunit of NMDA receptor influenced the electrophysiological markers of disinhibition, but this difference was only marginally significant (min. p=0.07). These results may support the disinhibitory feedback hypothesis of tinnitus generation.