c-fos mediates antipsychotic-induced neurotensin gene expression in the rodent striatum

Robertson, George S.; Tetzlaff, Wolfram; Bedard, Annie M.; St-Jean, Martin; Wigle, N

doi:10.1016/0306-4522(95)00049-o

Cited by 47 publications

(20 citation statements)

References 59 publications

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“…USA 93 (1996) 14137 sence with the control oligonucleotides. This result establishes the effectiveness of the c-fos antisense oligonucleotide and confirm earlier observations by other groups using c-fos antisense oligonucleotides (12,13,(24)(25)(26)(27)(28). Data on c-fos mRNA levels after treatment with c-fos antisense oligonucleotides are rare.…”

Section: Discussionsupporting

confidence: 88%

“…Using immunohistochemistry no effects of the c-fos antisense oligonucleotides on the expression of fos B, c-jun, junB, and NGFI-A could be found in several studies (13,24,26,28). However, Dragunow et al (12,25) reported inhibitory effects on NGFI-A and junB expression of intrastriatal c-fos antisense treatment after stimulation with apomorphine or amphetamine, respectively.…”

Section: Discussionmentioning

confidence: 98%

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Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal γ-aminobutyric acid transmission in the conscious rat

Sommer

Rimondini

O’Connor

et al. 1996

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

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Antisense c-fos oligonucleotides injected into the neostriatum of conscious rats selectively inhibited c-fos expression associated with compensatory increases in striatal c-fos mRNA levels and also with increased expression of junB and NGFI-A mRNA, probably as a result of regulatory phenomena. Dual probe in vivo microdialysis was used to investigate ␥-aminobutyric acid (GABA) release in the substantia nigra and the globus pallidus, which represent the terminal sites of the dopamine D 1 receptor regulated striatonigral and the dopamine D 2 receptor regulated striatopallidal GABA pathways, respectively. Intrastriatal infusion of the c-fos antisense oligonucleotide profoundly decreased dialysate GABA levels in the ipsilateral substantia nigra within 60 min but did not inf luence the dialysate GABA levels in the globus pallidus compared with the sham and control oligonucleotide treated groups. The site of action of the antisense oligonucleotides was mainly restricted to striatal neurons as shown by the distribution of locally injected f luoresceine isothiocyanate and radiolabeled oligonucleotides. The findings demonstrate a facilitatory role for c-fos mediated gene regulation in striatonigral GABA transmission and strengthen the evidence that the regulation of neurotransmission is different in the striatonigral and striatopallidal GABA pathways.Neuronal plasticity is mediated by alterations in gene expression patterns. The first stage of this genomic reaction to environmental cues culminates in the selective short-term expression of transactivating proteins that influence the transcription of downstream genes involved in long-term changes in the cellular phenotype. This stimulus-transcription coupling in the brain is particularly well established for the c-fos gene and other members of the fos and jun gene families (1-3). Dopamine (DA) releasing drugs (indirect agonists) like amphetamine and cocaine but also high doses of the DA agonist apomorphine stimulate locomotion and induce c-fos in the medium sized spiny striatonigral ␥-aminobutyric acid (GABA) neurons (4-10). Suppression of striatal c-fos expression by antisense oligonucleotides has recently been demonstrated to attenuate the effects of DA agonists on motor function. We reported earlier that rats which received an unilateral c-fos antisense infusion in the neostriatum developed a strong ipsilateral turning behavior within 15-20 min after systemic amphetamine administration (11). Others have found similar inhibitory effects on DA agonist stimulated motor behavior after intrastriatal infusion of c-fos antisense oligonucleotides (12)(13)(14). While both the induction of c-fos expression in the neostriatum and the locomotor behavior are mediated by the DA D 1 receptors, no functional link between them has been established earlier and the mechanisms underlying the c-fos antisense-induced reduction in motor function is unclear. Since in the above-mentioned studies the behavioral consequences occurred very rapidly after the rats had been treated with the ps...

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 98%

Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal γ-aminobutyric acid transmission in the conscious rat

Sommer

Rimondini

O’Connor

et al. 1996

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

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“…In situ hybridization was performed using two antisense oligonucleotides complementary to the mouse utrophin mRNA (oligonucleotide 1, 5Ј-TGTGCCCCTCAGCCACTCTTCCTTCTCCTTGATGG-TCTCCTC-3Ј, and oligonucleotide 2, 5Ј-TGCTGCCTGGTGGAACTGTG-GGCCTGGGTCAGTGTCAAGTG-3Ј) according to Schalling et al (15). Analysis of in situ hybridization labeling was performed using an image analysis system equipped with Image 1.47 software (Wayne Rasband, NIMH) (16). The density of in situ hybridization labeling in synaptic versus extrasynaptic regions was determined by measuring the number of labeled pixels within a circular field of constant 100 m in diameter.…”

Section: Methodsmentioning

confidence: 99%

Local Transcriptional Control of Utrophin Expression at the Neuromuscular Synapse

Gramolini¹,

Dennis

Tinsley

et al. 1997

Journal of Biological Chemistry

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Recently, the use of a transgenic mouse model system for Duchenne muscular dystrophy has demonstrated the ability of utrophin to functionally replace dystrophin and alleviate the muscle pathology (see Tinsley, J. M., Potter, A. C., Phelps, S. R., Fisher, R., Trickett, J. I., and Davies, K. E. (1996) Nature 384, 349 -353). However, there is currently a clear lack of information concerning the regulatory mechanisms presiding over utrophin expression during normal myogenesis and synaptogenesis. Using in situ hybridization, we show that utrophin mRNAs selectively accumulate within the postsynaptic sarcoplasm of adult muscle fibers. In addition, we demonstrate that a 1.3-kilobase fragment of the human utrophin promoter is sufficient to confer synapse-specific expression to a reporter gene. Deletion of 800 base pairs from this promoter fragment reduces the overall expression of the reporter gene and abolishes its synapse-specific expression. Finally, we also show that utrophin is present at the postsynaptic membrane of ectopic synapses induced to form at sites distant from the original neuromuscular junctions. Taken together, these results indicate that nerve-derived factors regulate locally the transcriptional activation of the utrophin gene in skeletal muscle fibers and that myonuclei located in extrasynaptic regions are capable of expressing utrophin upon receiving appropriate neuronal cues.

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“…Recent reports have demonstrated the usefulness of antisense (AS) oligodeoxynucleotides (ODNs) to study in vivo the role of specific proteins in the nervous system in a behavioral context (Chiasson et al 1992;Dragunow et al 1993;Heilig et al 1993;Sommer et al 1993;Merchant 1994;M611er et al 1994;Suzuki et al 1994;Hunter et al 1995;Robertson et al 1995;Wollnik et al 1995;for review, see Wahlestedt 1994) and specifically during learning (Schmidt et al 1995). Thus, we used intracerebral antisense intervention to assess the physiological significance of lEG transcription factors during acquisition and consolidation of the brightness discrimination in rats.…”

Section: Introductionmentioning

confidence: 99%

Suppression of c-fos induction in rat brain impairs retention of a brightness discrimination reaction.

Grimm¹,

Schicknick²,

Riede³

et al. 1997

Learn. Mem.

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IntroductionRecently, the induction of transcription factor-encoding immediate-early genes such as c-fos was observed in distinct brain regions of rats trained to acquire a footshock-motivated brightness discrimination in a Y-maze. The functional relevance of inducible transcription factors for learning and memory formation is, however, not clear. To address this question in the present study, we have used a synthetic antisense phosphorothioate oligodeoxynucleotide to suppress in vivo the expression of c-fos in rat brain.

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c-fos mediates antipsychotic-induced neurotensin gene expression in the rodent striatum

Cited by 47 publications

References 59 publications

Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal γ-aminobutyric acid transmission in the conscious rat

Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal γ-aminobutyric acid transmission in the conscious rat

Local Transcriptional Control of Utrophin Expression at the Neuromuscular Synapse

Suppression of c-fos induction in rat brain impairs retention of a brightness discrimination reaction.

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