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Journal ArticleDOI

Expression of c-fos protein in brain: metabolic mapping at the cellular level

TLDR
Fos immunohistochemistry provides a cellular method to label polysynaptically activated neurons and thereby map functional pathways in response to polysynaptic activation.
Abstract
The proto-oncogene c-fos is expressed in neurons in response to direct stimulation by growth factors and neurotransmitters. In order to determine whether the c-fos protein (Fos) and Fos-related proteins can be induced in response to polysynaptic activation, rat hindlimb motor/sensory cortex was stimulated electrically and Fos expression examined immunohistochemically. Three hours after the onset of stimulation, focal nuclear Fos staining was seen in motor and sensory thalamus, pontine nuclei, globus pallidus, and cerebellum. Moreover, 24-hour water deprivation resulted in Fos expression in paraventricular and supraoptic nuclei. Fos immunohistochemistry therefore provides a cellular method to label polysynaptically activated neurons and thereby map functional pathways.

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Citations
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Journal ArticleDOI

A role for ghrelin in the central regulation of feeding.

TL;DR: It is shown that ghrelin is involved in the hypothalamic regulation of energy homeostasis and probably has a function in growth regulation by stimulating feeding and release of growth hormone.
Journal ArticleDOI

The regulation and function of c-fos and other immediate early genes in the nervous system.

TL;DR: This review highlights the importance of identifying the genes that are responsive to trans-synaptic stimulation and membrane electrical activity in neural cells and proposes that IEGs encode regulatory proteins that control the expression of late response genes.
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A role for glucagon-like peptide-1 in the central regulation of feeding

TL;DR: It is reported here that intracerebroventricular (ICV) GLP-1 powerfully inhibits feeding in fasted rats, and this findings suggest that central GLp-1 is a new physiological mediator of satiety.
Journal ArticleDOI

Transduction of psychosocial stress into the neurobiology of recurrent affective disorder.

TL;DR: The author postulates that both sensitization to stressors and episode sensitization occur and become encoded at the level of gene expression, suggesting that the biochemical and anatomical substrates underlying the affective disorders evolve over time as a function of recurrences, as does pharmacological responsivity.
References
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Journal ArticleDOI

Stimulation of 3T3 cells induces transcription of the c- fos proto-oncogene

TL;DR: Transcription of the c-fos proto-oncogene is greatly increased within minutes of administering purified growth factors to quiescent 3T3 cells, and this stimulation is the most rapid transcriptional response to peptide growth factors yet described, implying a role for c- fos in cell-cycle control.
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Induction of c-fos-like protein in spinal cord neurons following sensory stimulation.

TL;DR: Physiological stimulation of rat primary sensory neurons causes the expression of c-fos-protein-like immunoreactivity in nuclei of postsynaptic neurons of the dorsal horn of the spinal cord, suggesting that synaptic transmission may induce rapid changes in gene expression in certain post Synaptic neurons.
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Mapping patterns of c-fos expression in the central nervous system after seizure

TL;DR: A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole, and this effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital.
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Induction of c- fos gene and protein by growth factors precedes activation of c- myc

TL;DR: Stimulation of fibroblasts with serum or purified growth factors leads to a dramatic induction of expression of both c-fos mRNA and protein within a few minutes, followed by activation of c-myc.
Journal ArticleDOI

Role of ion flux in the control of c-fos expression.

TL;DR: It is demonstrated that c-fos is induced in PC12 cells either by receptor–ligand interaction or by agents or conditions that effect voltage-dependent calcium channels.
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