Differential Expression of Egr‐1‐Like DNA‐Binding Activities in the Naive Rat Brain and After Excitatory Stimulation

Beckmann, Alison M.; Davidson, M.; Goodenough, Sharon; Wilce, Peter A.

doi:10.1046/j.1471-4159.1997.69062227.x

Cited by 26 publications

(14 citation statements)

References 36 publications

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“…One of the hallmarks of the Egr family is transcriptional regulation by neural activity (Beckmann, Davidson, Goodenough, & Wilce, 1997; Honkaniemi & Sharp, 1999). We thus tested the effects of neural activity on transcriptional expression of ApEgr.…”

Section: Resultsmentioning

confidence: 99%

An Aplysia Egr homolog is rapidly and persistently regulated by long-term sensitization training

Cyriac¹,

Holmes²,

Lass³

et al. 2013

Neurobiology of Learning and Memory

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The Egr family of transcription factors plays a key role in long-term plasticity and memory in a number of vertebrate species. Here we identify and characterize ApEgr (GenBank: KC608221), an Egr homolog in the marine mollusk Aplysia californica. ApEgr codes for a predicted 593-amino acid protein with the highly conserved trio of zinc-fingered domains in the C-terminus that characterizes the Egr family of transcription factors. Promoter analysis shows that the ApEgr protein selectively recognizes the GSG motif recognized by vertebrate Egrs. Like mammalian Egrs, ApEgr is constitutively expressed in a range of tissues, including the CNS. Moreover, expression of ApEgr is bi-directionally regulated by changes in neural activity. Of most interest, the association between ApEgr function and memory may be conserved in Aplysia, as we observe rapid and long-lasting up-regulation of expression after long-term sensitization training. Taken together, our results suggest that Egrs may have memory functions that are conserved from mammals to mollusks.

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Section: Resultsmentioning

confidence: 99%

An Aplysia Egr homolog is rapidly and persistently regulated by long-term sensitization training

Cyriac¹,

Holmes²,

Lass³

et al. 2013

Neurobiology of Learning and Memory

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“…Fos induction also correlates with the mossy fibre sprouting (Kiessling & Gass, 1993; Popovici et al, 1990) that occurs during epileptogenesis and may play a role in the subsequent manifestation of seizure symptoms. Like Fos, Egr1 also activates transcription of other genes (Beckmann et al, 1997; Christy & Nathans, 1989) and is considered to play an important role in neuronal plasticity (Knapska & Kaczmarek, 2004). Furthermore, the expression of Fos and Egr1 in seizure onset regions in PWE strongly correlates with interictal spiking (Rakhade et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Cannabidivarin (CBDV) suppresses pentylenetetrazole (PTZ)-induced increases in epilepsy-related gene expression

Amada

Yamasaki

et al. 2013

PeerJ

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To date, anticonvulsant effects of the plant cannabinoid, cannabidivarin (CBDV), have been reported in several animal models of seizure. However, these behaviourally observed anticonvulsant effects have not been confirmed at the molecular level. To examine changes to epilepsy-related gene expression following chemical convulsant treatment and their subsequent control by phytocannabinoid administration, we behaviourally evaluated effects of CBDV (400 mg/kg, p.o.) on acute, pentylenetetrazole (PTZ: 95 mg/kg, i.p.)-induced seizures, quantified expression levels of several epilepsy-related genes (Fos, Casp 3, Ccl3, Ccl4, Npy, Arc, Penk, Camk2a, Bdnf and Egr1) by qPCR using hippocampal, neocortical and prefrontal cortical tissue samples before examining correlations between expression changes and seizure severity. PTZ treatment alone produced generalised seizures (median: 5.00) and significantly increased expression of Fos, Egr1, Arc, Ccl4 and Bdnf. Consistent with previous findings, CBDV significantly decreased PTZ-induced seizure severity (median: 3.25) and increased latency to the first sign of seizure. Furthermore, there were correlations between reductions of seizure severity and mRNA expression of Fos, Egr1, Arc, Ccl4 and Bdnf in the majority of brain regions in the CBDV+PTZ treated group. When CBDV treated animals were grouped into CBDV responders (criterion: seizure severity ≤3.25) and non-responders (criterion: seizure severity >3.25), PTZ-induced increases of Fos, Egr1, Arc, Ccl4 and Bdnf expression were suppressed in CBDV responders. These results provide the first molecular confirmation of behaviourally observed effects of the non-psychoactive, anticonvulsant cannabinoid, CBDV, upon chemically-induced seizures and serve to underscore its suitability for clinical development.

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“…Egr1 has been suggested as a critical factor for the establishment of long term neuronal plasticity in the hippocampal formation (46 -48). Intriguingly, Egr1 expression is also strongly increased in hippocampal neurons after SE (49,50). In addition, human twin studies showed a dysregulation of Egr1 mRNA expression in idiopathic absence epilepsies (51).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Regulation of T-type Calcium Channel CaV3.2

Loo

Schaub

Pernhorst

et al. 2012

Journal of Biological Chemistry

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Background: Expression of the T-type Ca 2ϩ -channel Ca V 3.2 has to be tightly regulated for proper calcium homeostasis. Results: Overexpression of the transcription factor Egr1 strongly activates the Ca V 3.2 promoter and can be counteracted by the repressor REST. Conclusion: Egr1 and REST "bi-directionally" regulate the Ca V 3.2 promoter. Significance: Our results have important implications for calcium homeostasis and dynamics in health and disease.

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Differential Expression of Egr‐1‐Like DNA‐Binding Activities in the Naive Rat Brain and After Excitatory Stimulation

Cited by 26 publications

References 36 publications

An Aplysia Egr homolog is rapidly and persistently regulated by long-term sensitization training

An Aplysia Egr homolog is rapidly and persistently regulated by long-term sensitization training

Cannabidivarin (CBDV) suppresses pentylenetetrazole (PTZ)-induced increases in epilepsy-related gene expression

Transcriptional Regulation of T-type Calcium Channel CaV3.2

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