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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=CGN</id>
	<title>CGN - История изменений</title>
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	<updated>2026-06-08T11:26:45Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=CGN&amp;diff=5124&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Cingulin [KIAA1319]  ==Publications==  {{medline-entry |title=Effect of N-methyl-D-aspartate receptor blockade on caspase activation and neuronal death in the dev...»</title>
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		<updated>2021-05-12T13:30:15Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Cingulin [KIAA1319]  ==Publications==  {{medline-entry |title=Effect of N-methyl-D-aspartate receptor blockade on caspase activation and neuronal death in the dev...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Cingulin [KIAA1319]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Effect of N-methyl-D-aspartate receptor blockade on caspase activation and neuronal death in the developing rat cerebellum.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16781062&lt;br /&gt;
|abstract=In vitro studies have demonstrated that N-methyl-D-aspartate (NMDA) receptor activation rescue cerebellar granule neurons ([[CGN]]) from apoptotic death. It has been suggested that this effect mimics the transient glutamate receptors activation by mossy fibers during cerebellar development. We reported previously that [[CGN]] from postnatal days 2-4 (P2-P4) rats increased cell survival in response to NMDA treatment. In this study, we evaluated the effect of dizocilpine (MK-801) administrated for three consecutive days on the apoptotic death of [[CGN]] during development. MK-801 treatment decreased the large number of [[CGN]] condensed nuclei found at P8, but this drug increased the proportion of condensed nuclei at P16. We also found a high activity of caspases during the first postnatal week that decreased during development. MK-801 treatment did not modify the activity of caspase-8 at any age, but decreased caspase-9 activity at P8 and increased the activity of caspase-1 (76%) at P8, caspase-3 (160%) at P16 and caspase-9 (50%) at P12. These results suggest that NMDA receptor stimulation regulates the activity of caspases in a differential way and plays an important role in the in vivo [[CGN]] death during postnatal development.&lt;br /&gt;
|mesh-terms=* Aging&lt;br /&gt;
* Animals&lt;br /&gt;
* Caspases&lt;br /&gt;
* Cerebellum&lt;br /&gt;
* Dizocilpine Maleate&lt;br /&gt;
* Enzyme Activation&lt;br /&gt;
* Excitatory Amino Acid Antagonists&lt;br /&gt;
* Models, Animal&lt;br /&gt;
* Rats&lt;br /&gt;
* Rats, Wistar&lt;br /&gt;
* Receptors, N-Methyl-D-Aspartate&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1016/j.neulet.2006.05.039&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
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