Behavioral perseveration and impairment of long-term memory in rats after intrahippocampal injection of kainic acid in subconvulsive dose

Архипов, В. И.; Kulesskaja, Natalia; Lebedev, D. S.

doi:10.1016/j.pbb.2007.08.012

Cited by 28 publications

(17 citation statements)

References 39 publications

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“…This latter observation supports the notion that hippocampal A␤ injections induce behavioral perseverance or impairment in the ability to inhibit irrelevant exploratory behavior in rats. Behavioral perseverance has been linked to injury in the hippocampal system (Whishaw and Tomie, 1997;Arkhipov et al, 2008) but is even more closely associated with injury of the prefrontal cortex (Morgan et al, 2003;Clarke et al, 2004), where some neurons fire in synchrony with the hippocampal rhythm during learning (Jones and Wilson, 2005;Siapas et al, 2005;Sirota et al, 2008;Peyrache et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Decreased Rhythmic GABAergic Septal Activity and Memory-Associated θ Oscillations after Hippocampal Amyloid-β Pathology in the Rat

Villette¹,

Poindessous‐Jazat²,

Simon³

et al. 2010

J. Neurosci.

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The memory deficits associated with Alzheimer's disease result to a great extent from hippocampal network dysfunction. The coordination of this network relies on theta () oscillations generated in the medial septum. Here, we investigated in rats the impact of hippocampal amyloid ␤ (A␤) injections on the physiological and cognitive functions that depend on the septohippocampal system. Hippocampal A␤ injections progressively impaired behavioral performances, the associated hippocampal power, and frequency response in a visuospatial recognition test. These alterations were associated with a specific reduction in the firing of the identified rhythmic bursting GABAergic neurons responsible for the propagation of the rhythm to the hippocampus, but without loss of medial septal neurons. Such results indicate that hippocampal A␤ treatment leads to a specific functional depression of inhibitory projection neurons of the medial septum, resulting in the functional impairment of the temporal network.

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Section: Discussionmentioning

confidence: 99%

Decreased Rhythmic GABAergic Septal Activity and Memory-Associated θ Oscillations after Hippocampal Amyloid-β Pathology in the Rat

Villette¹,

Poindessous‐Jazat²,

Simon³

et al. 2010

J. Neurosci.

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“…Previously we selected a subconvulsive dose of KA (0.2 μg), causing no epileptization of the brain after injection into the dorsal hippocampus. It has been shown that this hippocampal injury leads to specifi c disorders in the animal long-term memory (mainly in information reproduction processes and in the capacity to inhibit the reactions which lost biological sense) [4]. With time the defects in animal behavior, caused by injection of this KA dose, are compensated for.…”

Section: Methodsmentioning

confidence: 99%

Expression of Mitochondrial Uncoupling Protein UCP2 in the Brain of Rats after Hippocampal Injury Inflicted by Kainic Acid

Lebedev

Архипов

2010

Bull Exp Biol Med

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The expression of mitochondrial protein UCP2 and cytochrome C-oxidase subunit III genes in the hippocampus and prefrontal cortex was evaluated by real-time PCR 3 and 7 days after microinjection of kainic acid into the dorsal hippocampus. In contrast to cytochrome C-oxidase subunit III mRNA, the level of UCP2 mRNA in the hippocampus increased 1 week after microinjection of kainic acid. The expression of both genes in the prefrontal cortex did not differ from the control. Presumably, activation of UCP2 synthesis in hippocampal injury indicates the neuroprotective effects of this protein.

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“…This hippocampal injury led to disorders in the reproduction of food-getting habit, trained before its injection; in addition, CA-inflicted injury induced the liability to persevering and reduction of the inhibitory processes [1,3]. These cognitive disorders were observed in the animals 1-2 weeks after CA injection, and hence, this period was the most interesting for us.…”

Section: Resultsmentioning

confidence: 99%

“…The animals performed 10 running episodes during each day. The methods for studies of the rat behavior have been described in detail previously [1,3]. Stereotaxic bilateral injection of CA (Sigma) was carried out under pentobarbital narcosis (30 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

Expression of mGluR5 and Synaptophysin Genes after Injury to the Dorsal Hippocampus, Inflicted by Cainic Acid

Lebedev

Архипов

2009

Bull Exp Biol Med

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The expression of synaptophysin (vesicular protein) and mGluR5 (metabotropic glutamate receptor) genes was studied 3, 7, and 20 days after cainic acid injury of the dorsal hippocampal area in Wistar rats. The expression of both genes was characteristically reduced in the hippocampus. Twenty days after the exposure the expression of mGluR5 in this brain area reached the control level, while synaptophysin expression remained low. An opposite trend was observed in the frontal cortex: synaptophysin expression 20 days after exposure did not differ from the control, while mGluR5 expression was reduced. The peculiar time course of both genes' expression in the hippocampus and frontal cortex indicates the involvement of the frontal cortex in mechanisms of functional recovery after hippocampal injuries.

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Behavioral perseveration and impairment of long-term memory in rats after intrahippocampal injection of kainic acid in subconvulsive dose

Cited by 28 publications

References 39 publications

Decreased Rhythmic GABAergic Septal Activity and Memory-Associated θ Oscillations after Hippocampal Amyloid-β Pathology in the Rat

Decreased Rhythmic GABAergic Septal Activity and Memory-Associated θ Oscillations after Hippocampal Amyloid-β Pathology in the Rat

Expression of Mitochondrial Uncoupling Protein UCP2 in the Brain of Rats after Hippocampal Injury Inflicted by Kainic Acid

Expression of mGluR5 and Synaptophysin Genes after Injury to the Dorsal Hippocampus, Inflicted by Cainic Acid

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