Effects of chronic nimodipine on working memory of old rats in relation to defects in synaptosomal calcium homeostasis

Batuecas, Alicia; Pereira, Rodolfo; Centeno, Carlos; Pulido, J.A.; Hernández, Miguel Cruz; Bollati, Alicia; Bogónez, Elena; Satrústegui, Jorgina

doi:10.1016/s0014-2999(98)00250-7

Cited by 32 publications

(22 citation statements)

References 53 publications

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“…It is important to appreciate that the effects of L-type VDCC antagonism on memory appear to be dependent on the dose regimen: chronically repeated low doses have been reported to have, if any, beneficial effects on memory (Disterhoft et al, 1996;Batuecas et al, 1998;Meneses and Hong, 1998;Kane and Robinson, 1999;Veng et al, 2003;Lashgari et al, 2006)-although these might be indirect, because of improved cardiac performance. Thus, the amnesic effects of single acute doses in rats should not be taken as directly relevant to the chronic treatment of human cardiovascular problems.…”

Section: Discussionmentioning

confidence: 99%

L-Type Voltage-Dependent Calcium Channel Antagonists Impair Perirhinal Long-Term Recognition Memory and Plasticity Processes

Seoane

Massey²,

Keen³

et al. 2009

J. Neurosci.

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The perirhinal cortex of the temporal lobe is essential for the familiarity discrimination component of recognition memory. In view of the importance of changes in calcium ion concentration for synaptic plasticity, the present study examined the effects of L-type voltagedependent calcium channel (VDCC) antagonism on rat perirhinal-based familiarity discrimination processes and plasticity including long-term depression (

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Section: Discussionmentioning

confidence: 99%

L-Type Voltage-Dependent Calcium Channel Antagonists Impair Perirhinal Long-Term Recognition Memory and Plasticity Processes

Seoane

Massey²,

Keen³

et al. 2009

J. Neurosci.

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“…-binding proteins calbindin-D 28K and calreticulin in cerebral cortex [120]. Nimodipine improved motor performance on balance, hanging and climbing tests and age-related alterations in limb coordination were delayed [128].…”

Section: Ion Channels and General Brain Agingmentioning

confidence: 98%

“…K ? channel activity also increases as cognitive ability declines and neuropathologies increase [116,[120][121][122][123][124].…”

Section: Ion Channels and General Brain Agingmentioning

confidence: 99%

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Dopamine and Aging: Intersecting Facets

Rollo

2008

Neurochem Res

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Aging encompasses life itself so understanding requires frameworks that forge unity amidst complexity. The free radical theory of aging is one example. The original focus on damage was augmented recently by appreciation that reactive oxygen and nitrogen species are essential to normal signaling and cell function. This paradigm is currently undergoing an explosive expansion fueled by the discovery that regulatory organization is a merry-go-round of redox cycling seamlessly fused to endogenous clocks. This might best be described as an "Electroplasmic Cycle." This is certainly applicable to dopaminergic neurons with their exceptional metabolic, electrical and rhythmic properties. Here I review normal aging of dopamine systems to highlight them as a valuable model. I then examine the possible integration of free radical and ion channel theories of aging. Finally, I incorporate clocks and explore the multifaceted implications of electroplasmic cycles with special emphasis on dopamine.

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“…During aging, L-VDCC activity and expression increases in the CA1 hippocampal subfield (Thibault and Landfield, 1996) which is related to increases in the slow afterhyperpolarization (sAHP) and reduced neuronal excitability (Disterhoft et al, 1996; Power et al, 2002). These electrophysiological changes are correlated with age-associated memory deficits (Thibault and Landfield, 1996), which can be improved with antagonism of L-VDCCs with nimodipine (Thompson et al, 1990; Moyer et al, 1992; Batuecas et al, 1998). Notably, blockade of the L-VDCC reduces the sAHP to a similar extent in both young and aged rats (Power et al, 2002) and improves memory in young and aged rats as well (Levy et al, 1991; Ingram et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Differential rescue of spatial memory deficits in aged rats by L-type voltage-dependent calcium channel and ryanodine receptor antagonism

et al. 2014

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Age-associated memory impairments may result as a consequence of neuroinflammatory induction of intracellular calcium (Ca+2) dysregulation. Altered L-type voltage dependent calcium channel (L-VDCC) and ryanodine receptor (RyR) activity may underlie age-associated learning and memory impairments. Various neuroinflammatory markers are associated with increased activity of both L-VDCCs and RyRs, and increased neuroinflammation are associated with normal aging. In vitro, pharmacological blockade of L-VDCCs and RyRs has been shown to be anti-inflammatory. Here, we examined whether pharmacological blockade of L-VDCCs or RyRs with the drugs nimodipine and dantrolene, respectively, could improve spatial memory and reduce age-associated increases in microglia activation. Dantrolene and nimodipine differentially attenuated age-associated spatial memory deficits but were not anti-inflammatory in vivo. Furthermore, RyR gene expression was inversely correlated with spatial memory, highlighting the central role of Ca+2 dysregulation in age-associated memory deficits.

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Effects of chronic nimodipine on working memory of old rats in relation to defects in synaptosomal calcium homeostasis

Cited by 32 publications

References 53 publications

L-Type Voltage-Dependent Calcium Channel Antagonists Impair Perirhinal Long-Term Recognition Memory and Plasticity Processes

L-Type Voltage-Dependent Calcium Channel Antagonists Impair Perirhinal Long-Term Recognition Memory and Plasticity Processes

Dopamine and Aging: Intersecting Facets

Differential rescue of spatial memory deficits in aged rats by L-type voltage-dependent calcium channel and ryanodine receptor antagonism

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