Up regulation of calbindin-D28K mRNA in the rat hippocampus following focal stimulation of the perforant path

Lowenstein, Daniel H.; Miles, Michael F.; Hatam, Farahnaz; McCabe, Thomas

doi:10.1016/0896-6273(91)90065-8

Cited by 101 publications

(48 citation statements)

References 43 publications

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“…In other animal models of epilepsy, including kindling, kainic acid, and pilocarpine, calbindin expression is reduced in the stratum granulosum and CA1 stratum pyramidale in the few months following the initial injury (Baimbridge and Miller, 1984;Baimbridge et al, 1985;Shetty and Turner, 1995;Yang et al, 1997;Tang et al, 2006). Conversely, following acute seizures by electrical stimulation or kainic acid treatments, calbindin protein and mRNA levels are increased (Lowenstein et al, 1991;Lowenstein et al, 1994;Lee et al, 1997). Therefore, it is possible that a compensatory increase in calbindin occurs following acute seizures and this change may be related to neurogenesis or stimulated synthesis (Lowenstein et al, 1991;Lowenstein et al, 1994;Lee et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, following acute seizures by electrical stimulation or kainic acid treatments, calbindin protein and mRNA levels are increased (Lowenstein et al, 1991;Lowenstein et al, 1994;Lee et al, 1997). Therefore, it is possible that a compensatory increase in calbindin occurs following acute seizures and this change may be related to neurogenesis or stimulated synthesis (Lowenstein et al, 1991;Lowenstein et al, 1994;Lee et al, 1997). The animals used in these studies were not determined to have the SRSs characteristic of epilepsy.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of calbindin-D28k is altered by SE in granule cells of the dentate gyrus and CA1 neurons in the mouse pilocarpine model (Tang et al, 2006) and in the rat kindling model (Kohr et al, 1991). Alternatively, calbindin expression has been shown to increase immediately following acute seizures (Lowenstein et al, 1991;Lowenstein et al, 1994;Lee et al, 1997). These results indicate that SE causes significant changes in calbindin expression, but that these changes may vary depending on the time of observation, the region studied and the model employed for observation.…”

Section: Introductionmentioning

confidence: 95%

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Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus

et al. 2008

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SummaryAcquired epilepsy (AE) is characterized by spontaneous recurrent seizures and long-term changes that occur in surviving neurons following an injury such as status epilepticus (SE). Long-lasting alterations in hippocampal Ca 2+ homeostasis have been observed in both in vivo and in vitro models of AE. One major regulator of Ca 2+ homeostasis is the neuronal calcium binding protein, calbindinD28k that serves to buffer and transport Ca 2+ ions. This study evaluated the expression of hippocampal calbindin levels in the rat pilocarpine model of AE. Calbindin protein expression was reduced over 50% in the hippocampus in epileptic animals. This decrease was observed in the pyramidal layer of CA1, stratum lucidum of CA3, hilus, and stratum granulosum and stratum moleculare of the dentate gyrus when corrected for cell loss. Furthermore, calbindin levels in individual neurons were also significantly reduced. In addition, the expression of calbindin mRNA was decreased in epileptic animals. Time course studies demonstrated that decreased calbindin expression was initially present 1 month following pilocarpine-induced SE and lasted for up to 2 years after the initial episode of SE. The results indicate that calbindin is essentially permanently decreased in the hippocampus in AE. This decrease in hippocampal calbindin may be a major contributing factor underlying some of the plasticity changes that occur in epileptogenesis and contribute to the alterations in Ca 2+ homeostasis associated with AE.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus

et al. 2008

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“…Interestingly, neurogranin knockout mice are impaired in spatial learning as well as hippocampal synaptic plasticity (40). Retinoic acid has also been shown to induce expression of calbindin D28K (CaBD28K), a calcium-buffering protein found in hippocampal CA1 pyramidal neurons (41,42). CaBD28K-deficient mice suffer loss of LTP (43).…”

Section: Discussionmentioning

confidence: 99%

Vitamin A deprivation results in reversible loss of hippocampal long-term synaptic plasticity

Misner

Jacobs

Shimizu

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

228

179

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Despite its long history, the central effects of progressive depletion of vitamin A in adult mice has not been previously described. An examination of vitamin-deprived animals revealed a progressive and ultimately profound impairment of hippocampal CA1 longterm potentiation and a virtual abolishment of long-term depression. Importantly, these losses are fully reversible by dietary vitamin A replenishment in vivo or direct application of all transretinoic acid to acute hippocampal slices. We find retinoid responsive transgenes to be highly active in the hippocampus, and by using dissected explants, we show the hippocampus to be a site of robust synthesis of bioactive retinoids. In aggregate, these results demonstrate that vitamin A and its active derivatives function as essential competence factors for long-term synaptic plasticity within the adult brain, and suggest that key genes required for long-term potentiation and long-term depression are retinoid dependent. These data suggest a major mental consequence for the hundreds of millions of adults and children who are vitamin A deficient.V itamin A and its derivatives (the retinoids) activate signaling pathways necessary for development, differentiation, and homeostasis of several tissues, including the nervous system (1, 2). Known impairments caused by the lack of dietary vitamin A include blindness, infertility, embryonic malformations, and compromised immunity. Vitamin A deficiency (VAD) is currently a risk for over 100 million children in over 75 countries, and results in nearly 3.2 million associated childhood deaths annually (refs. 3 and 4, and http:͞͞www.unicef.org͞sowc98).The biological effects of retinoids are mediated by retinoid receptors, a subgroup of the nuclear receptor superfamily. The retinoid receptor family includes the retinoic acid receptors (RARs; ␣, ␤, and ␥), which bind all trans-retinoic acid and 9-cis retinoic acid, and the retinoid X receptors (RXRs; ␣, ␤, and ␥), which bind 9-cis retinoic acid only. RAR͞RXR heterodimers, and to some extent RXR homodimers, act as transcription factors by binding to retinoid response elements in the promoters of target genes and activating gene expression in the presence of ligand (1, 4, 5). Multiple combinations of RAR͞RXR heterodimers are possible, depending on the overlapping expression of receptor subtypes within tissues (1).Each RAR and RXR exhibits a specific expression pattern in the adult central nervous system (CNS), distinct from that found in the developing nervous system (2, 6-10), indicating that, in addition to the modulation of neuronal development during embryogenesis, retinoids are likely to regulate activities in the mature brain. Supporting this notion, evidence suggests that RAR␤, RXR␤, and RXR␥ modulate locomotor behavior by regulating the expression of dopamine receptors in the adult striatum (11). Additionally, retinoic acid production is required in distinct regions of the adult songbird brain for song maturation, a learned behavior (12). Moreover, we recently found that RAR␤ ϪϪ ...

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“…One potential mechanism mediating the shift in the modification threshold is a change in calcium buffering at the synaptic sites. It has been proposed that changes in the concentration of calcium-binding proteins such as calbindin D 28k , which has been shown to be regulated by activity (14,15), might serve as a mechanism regulating free calcium levels and thus the ease of synaptic plasticity (16). Because dentate granule cells amply express calbindin D 28k (14), immunoblot analysis was used to test the prediction that CS of the medial path would increase levels of calbindin D 28k .…”

Section: Nmda Receptors Versus Cell Firing In Adjusting the Modificationmentioning

confidence: 99%

Heterosynaptic metaplasticity in the hippocampus in vivo : A BCM-like modifiable threshold for LTP

Abraham

Mason-Parker²,

Bear³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

154

125

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The homeostatic maintenance of the ''modification threshold'' for inducing long-term potentiation (LTP) is a fundamental feature of the Bienenstock, Cooper, and Munro (BCM) model of synaptic plasticity. In the present study, two key features of the modification threshold, its heterosynaptic expression and its regulation by postsynaptic neural activity, were tested experimentally in the dentate gyrus of awake, freely moving rats. Conditioning stimulation ranging from 10 to 1,440 brief 400-Hz trains, when applied to medial perforant path afferents, raised the threshold for LTP induction heterosynaptically in the neighboring lateral perforant path synapses. This effect recovered slowly over a 7-to 35-day period. The same conditioning paradigms, however, did not affect the reversal of long-term depression. The inhibition of LTP by medial-path conditioning stimulation was N-methyl-D-aspartate (NMDA) receptor-dependent, but antidromic stimulation of the granule cells could also inhibit lateral path LTP induction, independently of NMDA receptor activation. Increased calcium buffering is a potential mechanism underlying the altered LTP threshold, but the levels of two important calcium-binding proteins did not increase after conditioning stimulation, nor was de novo protein synthesis required for generating the threshold shift. These data confirm, in an in vivo model, two key postulates of the BCM model regarding the LTP threshold. They also provide further evidence for the broad sensitivity of synaptic plasticity mechanisms to the history of prior activity, i.e., metaplasticity.M any experimental observations now support the suggestion that long-term potentiation (LTP) and long-term depression (LTD) underlie not only long-term information storage important for learning and memory but also the experiencedependent adaptations important for tuning the patterns of synaptic connectivity in the developing nervous system (1, 2). However, for these mechanisms to store information optimally, regulatory processes must exist to maintain the modifiable synapses of the network within a useful dynamic range. One proposal to account for such homeostatic regulation was made by Bienenstock, Cooper, and Munro (BCM; ref. 3) in their model of visual cortical receptive field plasticity during development. These authors suggested that the ''modification threshold'' (the level of postsynaptic response below which gives LTD and above which gives LTP) is itself dynamically regulated by the average level of postsynaptic activity. For example, if visual cortical neurons suffered a prolonged reduction in their activity because of visual deprivation, then the modification threshold would be correspondingly reduced. This adaptive response allows the preservation of a broad range of LTP and LTD responses despite treatments that restrict the firing repertoire of those neurons. A converse process, involving an elevated modification threshold, occurs if a neuron's level of activity is increased over a prolonged period. The term ''metaplasticity'' has ...

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Up regulation of calbindin-D28K mRNA in the rat hippocampus following focal stimulation of the perforant path

Cited by 101 publications

References 43 publications

Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus

Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus

Vitamin A deprivation results in reversible loss of hippocampal long-term synaptic plasticity

Heterosynaptic metaplasticity in the hippocampus in vivo : A BCM-like modifiable threshold for LTP

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