Neurotransmitter modulation of Fos‐ and Jun‐like proteins in the turtle retina
- 17 April 1995
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 354 (4) , 481-500
- https://doi.org/10.1002/cne.903540402
Abstract
The expression of the Fos and Jun families of nuclear phosphoproteins can be induced by a variety of extracellular stimuli and is known to participate in the transcriptional regulation of target genes. To examine the role of these transcription factors in retinal function, we used polyclonal antisera to localize these protein families in the turtle retina. Fos‐like immunoreactivity was in many somata in the inner nuclear and ganglion cell layers. In contrast, Jun‐like immunoreactivity was in a smaller number of amacrine cells and many somata in the ganglion cell layer. The monostratified dendritic arbors of one prominent amacrine cell type with Jun‐like immunoreactivity were also labeled. There were no dramatic differences in the levels of Fos‐like immunoreactivity or Jun‐like immunoreactivity between light‐ or dark‐adapted retinas. We examined the effects of excitatory amino acids and γ‐aminobutyric acid (GABA) on the expression of these proteins in vitro. In some experiments, cobalt was used to block synaptic transmission. The excitatory amino acids increased both Fos‐ and Jun‐like immunoreactivity, while GABA generally showed no such stimulatory effect. In cobalt‐treated retinas, the same cell types had Jun‐like immunoreactivity as seen in the controls, but overall levels of immunoreactivity were increased. In cobalt‐treated dark‐adapted retinas, some excitatory amino acids increased cytoplasmic Fos‐like immunoreactivity in the somata and processes of large cells in the ganglion cell layer. Our results suggest that Fos‐ and Jun‐related proteins may play an important role in the postsynaptic responses to amino acid transmitters in a wide variety of amacrine and ganglion cells.Keywords
This publication has 77 references indexed in Scilit:
- Identification of an AP-1 transcription factor binding site within the human cholecystokinin (CCK) promoterNeuroReport, 1993
- Epidermal growth factor and transforming growth factor α induce c‐fos gene expression in retinal muller cells in vivoJournal of Neuroscience Research, 1991
- The immediate-early genes c-fos and c-jun are differentially expressed in the rat adrenal gland after capsaicin treatmentNeuroscience Letters, 1991
- Expression of c-fos protein by in hypothalamus of immature female rats: blockade by MK-801 or neonatal treatment with monosodium glutamateDevelopmental Brain Research, 1990
- Photic and circadian regulation of c-fos gene expression in the hamster suprachiasmatic nucleusNeuron, 1990
- Spinal c-fos induction by sensory stimulation in neonatal ratsNeuroscience Letters, 1990
- MK801-induced antagonism of NMDA-preferring excitatory amino acid receptors in horizontal cells of the turtle retinaNeuroscience Letters, 1989
- Induction of protooncogene fos by extracellular signals in primary glial cell culturesJournal of Neuroscience Research, 1989
- Long-lasting and sequential increase of c-fos oncoprotein expression in kainic acid-induced status epilepticusNeuroscience Letters, 1988
- Inducible binding of a factor to the c-fos enhancerCell, 1986