During the critical period of activity-dependent plasticity in rat striatum (30-37 days after birth) physiological circling behavior induces delayed modifications in GAP-43/B-50 phosphorylation by PKC. Postexercise, ipsi- and contralateral striatum to the circling direction show a similar temporal pattern of GAP-43/B-50 phosphorylation, with an initial decrease followed by a subsequent increase. However, there is a lag between initiation of the phosphorylation response in this asymmetrical task which does not occur when animals are subjected to exercise under conditions of symmetrical motor activity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.molbrainres.2003.08.003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Delayed and bilateral changes of GAP-43/B-50 phosphorylation after circling training during a critical period in rat striatum.
Brain Res Mol Brain Res
October 2003
Laboratorio de Biología Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, 4th Piso, Pabellón II, Ciudad Universitaria (C1428EHA), Buenos Aires, Argentina.
During the critical period of activity-dependent plasticity in rat striatum (30-37 days after birth) physiological circling behavior induces delayed modifications in GAP-43/B-50 phosphorylation by PKC. Postexercise, ipsi- and contralateral striatum to the circling direction show a similar temporal pattern of GAP-43/B-50 phosphorylation, with an initial decrease followed by a subsequent increase. However, there is a lag between initiation of the phosphorylation response in this asymmetrical task which does not occur when animals are subjected to exercise under conditions of symmetrical motor activity.
View Article and Find Full Text PDFLong term depression in the CA1 field is associated with a transient decrease in pre- and postsynaptic PKC substrate phosphorylation.
J Biol Chem
September 2000
Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands.
Induction of homosynaptic long term depression (LTD) in the CA1 field of the hippocampus is thought to require activation of N-methyl-d-aspartate receptors, an elevation of postsynaptic Ca(2+) levels, and a subsequent increase in phosphatase activity. To investigate the spatial and temporal changes in protein phosphatase activity following LTD induction, we determined the in situ phosphorylation state of a pre- (GAP-43/B-50) and postsynaptic (RC3) protein kinase C substrate during N-methyl-d-aspartate receptor-dependent LTD in the CA1 field of rat hippocampal slices. We show that LTD is associated with a transient (<30 min) and D-AP5-sensitive reduction in GAP-43/B-50 and RC3 phosphorylation and that LTD is prevented by the phosphatase inhibitors okadaic acid and cyclosporin A.
View Article and Find Full Text PDFActivation of pre- and postsynaptic protein kinase C during tetraethylammonium-induced long-term potentiation in the CA1 field of the hippocampus.
Neurosci Lett
May 2000
Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands.
Tetraethylammonium (TEA) induces a form of long-term potentiation (LTP) that is independent on N-methyl-D-aspartate (NMDA) receptor activation (LTP(K)). LTP(K) may be a suitable chemical model to study molecular mechanisms underlying LTP. We monitored the phosphorylation state of two identified neural-specific protein kinase C (PKC) substrates (the presynaptic protein GAP-43/B-50 and postsynaptic protein RC3) after different chemical depolarisations.
View Article and Find Full Text PDFQuantification of neuromodulin (GAP-43, B-50) and synapsin I in rat striata.
Nihon Shinkei Seishin Yakurigaku Zasshi
December 1999
Department of Pharmacology, Faculty of Medicine, Kagoshima University, Japan.
We reported previously that phosphorylated neuromodulin and phosphorylated synapsin I content increased in the striata of amphetamine-sensitized rats; however, the neuronal pathways responsible for the increase were unclear. In the present study, changes in neuromodulin and synapsin I content resulting from the manipulation of lesions were quantified to elucidate the responsible pathways. Nerve terminals originating in the corticostriatal pathway, those from the nigrostriatal pathway and those from interneurons in the striatum, were impaired by unilateral cortical ablation, 6-hydroxydopamine (6-OHDA) treatment and kainic acid injection into the striatum, respectively.
View Article and Find Full Text PDFDifferential changes in the phosphorylation of the protein kinase C substrates myristoylated alanine-rich C kinase substrate and growth-associated protein-43/B-50 following Schaffer collateral long-term potentiation and long-term depression.
J Neurochem
November 1999
Department of Medical Pharmacology, Rudolf Magnus Institute for Neurosciences, Utrecht, The Netherlands.
Activation of protein kinase C (PKC) is one of the biochemical pathways thought to be activated during activity-dependent synaptic plasticity in the brain, and long-term potentiation (LTP) and long-term depression (LTD) are two of the most extensively studied models of synaptic plasticity. Here we have examined changes in the in situ phosphorylation level of two major PKC substrates, myristoylated alanine-rich C kinase substrate (MARCKS) and growth-associated protein (GAP)-43/B-50, after pharmacological stimulation or induction of LTP or LTD in the CA1 field of the hippocampus. We find that direct PKC activation with phorbol esters, K+-induced depolarization, and activation of metabotropic glutamate receptors increase the in situ phosphorylation of both MARCKS and GAP-43/B-50.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!