Behavioral and Adaptive Status in an Experimental Model of Alzheimer's Disease in Rats

Popovic, Marko; Jovanova-Nešić, Katica; Popović, Natalija; Bokonjić, Dubravko; Dobrić, Silva; Rosić, N.; Rakić, Ljubisav

doi:10.3109/00207459608986719

Cited by 17 publications

(7 citation statements)

References 62 publications

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“…The intertrial interval was 60 s in duration PopoviC et al, 1996). During this time one half of the rats received 60 inescapable 5 s (3 mA) shocks (preshocked animals), whereas non-preshocked rats were placed into the preshock apparatus without shock experiences.…”

Section: Methodsmentioning

confidence: 99%

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Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental alzheimer's disease in rats

Popovic

Caballero-Bleda

Popović

et al. 1997

International Journal of Neuroscience

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It is well known that disturbance of calcium homeostasis has a significant role in the development of neurodegenerative disorders, such as Alzheimer's disease (AD). Our recent data suggest that acute treatment with the calcium antagonist verapamil can improve some behavioral deficits in an experimental model of AD. Therefore, the present study was done to establish the effect of chronically administered verapamil on cognitive and noncognitive behavior of rats with bilateral electrolitical lesions of nucleus basalis manocellularis (NBM)--an animal model of AD. The NBM lesions produce a deficit in performance of diverse behavior tests: active avoidance (AA), low level of fear (the open field test) as well as aggressive (the test of foot-shock induced aggression) and depressive (the learned helplessness test) behavior. Verapamil (1.0, 2.5, 5.0 and 10.0 mg/kg i.p.) or saline solution (1 ml/kg i.p.) were injected 24 hr after the lesion of NBM and then repeatedly administered during the next 8 days (twice a day). Performance of the two-way active avoidance test, the open field test, the foot shock-induced aggression test and the learned helplessness test were done on day 4 after the last verapamil or saline treatment (day 13 after the lesion). Verapamil in doses of 2.5 and 5.0 mg/kg significantly ameliorated the deficit in the performance of AA, the open field behavior, and the depression, but not the aggressive behavior. The obtained beneficial effect of chronic administered verapamil suggests that the regulation of calcium homeostasis during the early period after NBM lesions might be a reasonable way to prevent the behavioral deficits in an experimental model of AD.

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Section: Methodsmentioning

confidence: 99%

“…The rats were exposed to ten 5 s shocks (3 mA) with shock-free intervals of 25 s for a total test time of 5 min (PopoviC et al, 1996). The rats were exposed to ten 5 s shocks (3 mA) with shock-free intervals of 25 s for a total test time of 5 min (PopoviC et al, 1996).…”

Section: Foot Shock Aggressionmentioning

confidence: 99%

Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental alzheimer's disease in rats

Popovic

Caballero-Bleda

Popović

et al. 1997

International Journal of Neuroscience

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“…On the day of sacrifice, the rats were exposed to the re-testing, i.e. to 1 £ 20 trial session [28,39].…”

Section: Acquisition and Performance Of Active Avoidance Responsementioning

confidence: 99%

Cognitive deficits following blast injury-induced neurotrauma: possible involvement of nitric oxide

Černak¹,

Wang²,

Jiang³

et al. 2001

Brain Inj.

145

113

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Blast injuries, that is injuries caused by the complex pressure wave generated by some explosions, show increasing frequency throughout the world. However, whether blast injury is capable of inducing memory dysfunction has not been previously investigated. The present study examines the effects of blast injury-induced neurotrauma on memory deficit in rats. Furthermore, it is hypothesized that blast injury, stimulating nitric oxide production in the medial mesodiencephalic reticular formation and the dorsal hippocampus, both structures being involved in memory processing, may induce memory deficits. Prior to blast injury, Wistar rats were trained for an active avoidance task for 6 days. On day 6, rats that had acquired the avoidance response were subjected to whole-body blast injury, using a BT-I shock tube. Neurotrauma was confirmed by electron microscopical examination. At the completion of cognitive testing, rats were sacrificed at 3, 24 hours and 5 days after injury. The nitric oxide production in the brain structures was determined by the total nitrite/nitrate concentration, and by the expression of inducible nitric oxide synthase mRNA. The rats with blast injury revealed significant deficits in performance of the active avoidance task that persisted up to 5 days post-injury. Electron microscopical findings in both brain structures showed swellings of neurons, glial reaction, myelin debris, and increased pinocytotic activity on the fifth day following trauma. In blast injured rats, there was a significant elevation in total nitrite/nitrate levels 3 and 24 hours following injury which was comparable with the changes in the expression of inducible nitric oxide synthase mRNA. The results indicate that blast injury-induced neurotrauma is able to cause cognitive deficits.

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“…The nucleus basalis magnocellularis (NBM) in rats, which is homologous to the nbM, provides cholinergic inputs to the cerebral cortex (2). Electrolytic lesions of this nucleus cause a decrease of cortical cholinergic activity, as well as cognitive impairment in rats (3)(4)(5).…”

Section: Discussionmentioning

confidence: 99%

“…Bilateral NBM lesions were made by using a direct current of 1 .O mA passed through an unipolar stainless steel electrode (0.15 mm in diameter) for 30 set by means of a Grass S88 stimulator (5). The coordinates for the NBM were 1.3 mm posterior to bregma, 2.2 mm from the midline on each side and 6.5 mm ventral from the dura (20).…”

Section: Experinzental Ctnimulsmentioning

confidence: 99%

NADPH‐diaphorase activity in the frontal cortex of NBM‐lesioned rats treated with verapamil

Caballero-Bleda

Redondo‐Aniorte

Aldeguer‐Montiel

et al. 2001

Neuroscience Res Communica

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The effect of the calcium antagonist verapamil on NADPH‐diaphorase activity was studied in the frontal cortex of rats with lesioned nucleus basalis magnocellularis (NBM). Treatment with verapamil (5 mg/kg/12h ip) started 24 h after NBM lesions and lasted 8 days. Animals were sacrificed on day 21 after NBM‐lesions. There were no significant differences between control, saline‐ and verapamil‐treated NBM‐lesioned rats in the total number of neurons expressing NADPH‐diaphorase. However, the number of neurons which show loss of enzymatic reaction in their processes was significantly higher in saline‐treated NBM‐lesioned rats. This may relate to incipient neurodegeneration in these neurons. The obtained reactive decrease of NADPH‐diaphorase staining was abolished by verapamil treatment, which suggests a significant neuroprotective effect of this calcium antagonist.

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Behavioral and Adaptive Status in an Experimental Model of Alzheimer's Disease in Rats

Cited by 17 publications

References 62 publications

Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental alzheimer's disease in rats

Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental alzheimer's disease in rats

Cognitive deficits following blast injury-induced neurotrauma: possible involvement of nitric oxide

NADPH‐diaphorase activity in the frontal cortex of NBM‐lesioned rats treated with verapamil

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