Hostname: page-component-78c5997874-j824f Total loading time: 0 Render date: 2024-11-10T05:12:08.379Z Has data issue: false hasContentIssue false
  • English
  • Français

The significance of the expression of Fos protein in the brain for the classification of antipsychotics

Published online by Cambridge University Press:  18 September 2015

J. Korf  and
J.B. Sebens
Get access Rights & Permissions [Opens in a new window]

Samenvatting

In de afgelopen zes jaar is veel onderzoek verficht naar de effecten van antipsychotica op de regionale c-fos-expressie in de hersenen. Deze benadering biedt in een dierexperimentele proefopzet de mogelijkheid op cellulair niveau de effecten van psychofarmaca te bestuderen. Het fos-gen behoort tot de groep ‘immediate early genes’. Dit zijn genen die de transcriptie van andere, vaak onbekende genen reguleren. Een aantal aspecten van dit mechanisme wordt in deze bijdrage beschreven. Het onderzoek naar de effecten van antipsychotica op c-fos-expressie wordt samengevat en de betekenis voor de classificatie van antipsychotica benadrukt. Het blijkt dat deze farmaca effectief zijn in zowel de (meso)limbische gebieden (als nucleus accumbens, septum en amygdala) als ook in de basale ganglia. De relatieve effecten, wat betreft de c-fos-reactie, van de atypische antipsychotica (als clozapine en risperidon) zijn hoger in de limbische structuren, vergeleken met de effecten van de typische (als haloperidol). De potentie van de c-fos-methodiek voor verdere ontwikkelingen in dit gebied wordt aangegeven.

Keywords

AntipsychoticaFos-eiwittengen-expressielimbische structurenbasale gangliaimmunohistochemieAntipsychotic drugsFos proteinsgene expressionlimbic systembasal gangliaimmunohistochemistry
Type
Research Article
Information
Acta Neuropsychiatrica , Volume 9 , Issue 4 , December 1997 , pp. 143 - 150
Copyright
Copyright © Scandinavian College of Neuropsychopharmacology 1997

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Literatuur

1.Nyberg, S, Nakashima, Y, A-L, Nordström, et al.Positron emission tomography of in-vivo binding characteristics of atypical antipsychotic drugs. Review of D2 and 5-HT2 receptor occupancy studies and clinical response. Br J Psychiat 1996; 168: 40–4.CrossRefGoogle Scholar
2.Korf, J, Coppens, HJ, Louwerens, JW.Receptorblokkade bij antipsychotische medicatie. In: Dingemans, PMAJ, Van den Bosch, RJ, Kahn, RS, Schene, AH, red. Schizofrenie: Onderzoek en implicaties voor de behandeling. Houten: Bohn Stafleu Van Loghum, 1995: 122–33.Google Scholar
3.Pilowsky, LS, Costa, DC, Ell, PJ, et al.D2 dopamine receptor binding in the basal ganglia of antipsychotic-free schizophrenic patients. An 123I-IBZM single photon emission computerised tomography study. Br J Psychiat 1994; 164: 16–26.CrossRefGoogle ScholarPubMed
4.Scherer, J, Tatsch, K, Schwarz, J, et al.D2-dopamine receptor occupancy differs between patients with and without extrapyramidal side effects. Acta psychiat scand 1994; 90: 266–8.CrossRefGoogle ScholarPubMed
5.McCulloch, J, Savaki, H, Sokoloff, L. Distribution of effects of haloperidol on energy metabolism in the rat brain. Brain Res 1982; 243: 81–90.CrossRefGoogle ScholarPubMed
6.Pizzolato, G, Soncrant, TT, Rapoport, SI.Haloperidol and cerebral metabolism in the conscious rat: relation to pharmacokinetics. J Neurochem 1984; 43: 724–32.CrossRefGoogle ScholarPubMed
7.Morgan, JL, Curran, T. Stimulus-transcription coupling in the nervous system: involvement of the inducible proto-oncogenes fos and jun. Int Rev Neurosci 1991; 14: 421–51.CrossRefGoogle ScholarPubMed
8.Sheng, M, Greenberg, ME.The regulation and function of c-fos and other immediate early genes in the nervous system. Neuron 1990; 4: 477–85.CrossRefGoogle ScholarPubMed
9.Konradi, C, Heckers, S. Haloperidol-induced Fos expression in striatum is dependent upon transcription factor cyclic AMP response element binding protein. Neurosci 1995; 65: 1051–61.CrossRefGoogle ScholarPubMed
10.Robertson, GS, Jian, M. D1 and D2 dopamine receptors differentially increase Fos-like immunoreactivity in accumbal projections to the ventral pallidum and midbrain. Neurosci 1995; 64: 1019–34.CrossRefGoogle Scholar
11.Wirtshafter, D, Asin, KE.Dopamine antagonists induce fos-like-immunoreactivity in the substantia nigra and entopeduncular nucleus of the rat. Brain Res 1995; 670: 205–14.CrossRefGoogle ScholarPubMed
12.Asin, KE, Bednarz, L, Nikkei, A, et al.Rotation and striatal c-fos expression after repeated, daily treatment with selective dopamine receptor agonists and levodopa. J Pharmac exp Ther 1995; 273: 1483–90.Google ScholarPubMed
13.Morelli, M, Fenu, S, Pinna, A, et al.Opposite effects of NMDA receptor blockade on dopaminergic D1 - and D2-mediated behavior in the 6-hydroxydopamine model of turning with c-fos expression. J Pharmacol exp Therap 1992; 260: 402–7.Google ScholarPubMed
14.Deutch, AY, Duman, RS.The effects of antipsychotic drugs on Fos protein expression in the prefrontal cortex: cellular localization and pharmacological characterization. Neurosci 1996; 70: 377–89.CrossRefGoogle ScholarPubMed
15.Guo, N, Klitenick, MA, C-S, Tham, et al.Receptor mechanisms mediating clozapine-induced c-fos expression in the forebrain. Neurosci 1995; 65: 747–56.CrossRefGoogle ScholarPubMed
16.Fink-Jensen, A, Ludvigsen, TS, Korsgaard, N. The effects of clozapine on Fos protein immunoreactivity in the rat forebrain is not mimicked by the addition of a 1-adrenergic or 5HT2-receptor to haloperidol. Neurosci Lett 1995; 194: 77–80.CrossRefGoogle ScholarPubMed
17.Wan, W, Ennulat, DJ, Cohen, BC.Acute administration of typical antipsychotic drugs induces distinctive patterns of Fos expression in the rat forebrain. Brain Res 1995; 688: 95–104.CrossRefGoogle ScholarPubMed
18.Sebens, JB, Koch, T, Ter Horst, GJ, Korf, J. Differential Fos-protein induction in rat forebrain regions after acute and longterm haloperidol and clozapine treatment. Eur J Pharmacol 1995;273:175–82.CrossRefGoogle ScholarPubMed
19.Cohen, BM, Wan, W. The thalamus as a site of action of antipsychotic drugs. Am J Psychiat 1996; 152: 104–6.Google Scholar
20.Robertson, GS, Matsumura, H, Fibiger, H. Induction patterns of Fos-like immunoreactivity in the forebrain as predictors of atypical antipsychotic activity. J Pharmacol exp Ther 1994; 271: 1058–64.Google ScholarPubMed
21.MacGibbon, GA, Lawlor, PA, Bravo, R, et al.Clozapine and haloperidol produce different patterns of immediate early gene expression in rat caudate-putamen, nucleus accumbens, lateral septum and islands of Calleja. Mol Brain Res 1994; 23: 21–32.CrossRefGoogle ScholarPubMed
22.Ruskin, DN, Marshall, JF.D1 dopamine receptors influence Fos immunoreactivity in the globus pallidus and subthalamic nucleus of intact and nigrostriatal-lesioned rats. Brain Res 1995; 703: 156–64.CrossRefGoogle ScholarPubMed
23.Fenu, S, Carta, A, Morelli, M. Modulation of dopamine D1-mediated turning behavior and striatal c-fos expression by the substantia nigra. Synapse 1995; 19: 233–40.CrossRefGoogle ScholarPubMed
24.Westenberg, HGM, den Boer, JA.De neurochemische basis voor psychofarmaca: dopamine, serotonine, cholecystokinine en glutamaat. In: Den Boer, JA, Van den Bosch, RJ, eds. Leerboek Schizofrenie: een neurobiologische benadering. Utrecht: De Tijdstroom, 1996: 109–27.Google Scholar
25.Coppens, HJ, Sebens, JB, Korf, J. Catalepsy, Fos-protein, and dopamine receptor occupancy after long-term haloperidol treatment. Pharm Biochem Behav 1995; 51: 175–82.CrossRefGoogle ScholarPubMed
26.Sebens, JB, Koch, T, Korf, J. Lack of cross-tolerance between haloperidol and clozapine towards Fos-protein induction in rat forebrain regions. Eur J Pharmacol 1996; 315: 269–75.CrossRefGoogle ScholarPubMed
27.Marin, C, Bonastre, M, Tolosa, E. Striatal c-fos levels do not correlate with haloperidol-induced behavioral supersensitivity. Synapse 1996; 23: 89–93.3.0.CO;2-C>CrossRefGoogle Scholar
28.Robertson, GS, Fibiger, HC.Neuroleptics increase c-fos expression in the forebrain: contrasting effects of haloperidol and clozapine. Neurosci 1992; 46: 315–28.CrossRefGoogle ScholarPubMed
29.Bartlett, EJ, Brodie, JD, Simkowitz, P, et al.Effects of haloperidol challenge on regional cerebral glucose utilization in normal human subjects. Am J Psychiat 1994; 151: 5.Google ScholarPubMed