Abstract
Event Abstract Back to Event STEP (Striatal-enriched protein tyrosine phosphatase) is a critical component of the CRF system signaling in the extended amygdala of the rat brain. Joanna Dabrowska1*, Rimi Hazra1 and Donald G. Rainnie1 1 Yerkes Primate Research Center, Emory University, Department of Psychiatry and Center for Behavioral Neuroscience, United States STEP (Striatal-enriched protein tyrosine phosphatase), a recently discovered neuron-specific tyrosine phosphatase, is widely distributed in the rodent brain. STEP has been reported to be critically involved in the glutamate (NMDA receptor)-mediated regulation of the ERK (extracellular signal-regulated kinase) signaling cascade in rat neurons. Activation of the ERK cascade is thought to be an important signal transduction factor that regulates synaptic function, long-term potentation (LTP), and consequently learning and memory. STEP has been shown to downregulate the activity of ERK by dephosphorylation of ERK tyrosine residue. We have found robust somatodendritic expression of STEP in the extended amygdala: primarily in the anterolateral BNST (alBNST) and central amygdala (CeA). Because STEP distribution was highest in those regions of the extended amygdala that also show high corticotrophin releasing factor (CRF) expression, we performed dual immunofluorescence experiments to determine the relative co-localization of CRF and STEP. Dual labeling experiments revealed almost complete co-localization of CRF and STEP in alBNST and CeA. In contrast to CRF neurons of the extended amygdala, the population of CRF-positive neurons in paraventricular nucleus of the hypothalamus (PVN) did not express STEP. These data suggest that CRF neurons in the extended amygdala can utilize distinct second messenger pathways from CRF neurons of the PVN. CRF-expressing neurons in the extended amygdala are believed to be associated with the chronic affective (emotional) component of the stress response, in contrast to CRF neurons in the PVN, which are associated with acute mobilization of the hypothalamic-pituitary-adrenal (HPA) axis. Here, we used repeated stress paradigm to examine the effects of chronic stress on STEP expression in the alBNST. Rats were subjected to one-hour restraint stress for four consecutive days. Six days after the final stress manipulation (day 10), BNST samples from control and stressed animals were collected for protein assay (Western Blot), mRNA expression (RT-PCR) and immunohistochemistry. We have observed decreased levels of STEP in the BNST of stressed rats at the level of protein expression (STEP total protein content and STEP-positive neuronsâ expression) as well as significantly decreased mRNA expression. We conclude that STEP might be directly involved in stress-induced regulation of CRF signaling in the BNST, and deficits in STEP may therefore modulate the long-lasting effects of stress that are associated with states of fear and anxiety as well as etiology of PTSD, panic attacks and depression. Conference: 2010 South East Nerve Net (SENN) and Georgia/South Carolina Neuroscience Consortium (GASCNC) conferences, Atlanta , United States, 5 Mar - 7 Mar, 2010. Presentation Type: Poster Presentation Topic: Posters Citation: Dabrowska J, Hazra R and Rainnie DG (2010). STEP (Striatal-enriched protein tyrosine phosphatase) is a critical component of the CRF system signaling in the extended amygdala of the rat brain.. Front. Neurosci. Conference Abstract: 2010 South East Nerve Net (SENN) and Georgia/South Carolina Neuroscience Consortium (GASCNC) conferences. doi: 10.3389/conf.fnins.2010.04.00032 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 16 Mar 2010; Published Online: 16 Mar 2010. * Correspondence: Joanna Dabrowska, Yerkes Primate Research Center, Emory University, Department of Psychiatry and Center for Behavioral Neuroscience, Atlanta, United States, joanna.dabrowska@rosalindfranklin.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Joanna Dabrowska Rimi Hazra Donald G Rainnie Google Joanna Dabrowska Rimi Hazra Donald G Rainnie Google Scholar Joanna Dabrowska Rimi Hazra Donald G Rainnie PubMed Joanna Dabrowska Rimi Hazra Donald G Rainnie Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
Highlights
STEP (Striatal-enriched protein tyrosine phosphatase), a recently discovered neuronspecific tyrosine phosphatase, is widely distributed in the rodent brain
We have found robust somatodendritic expression of STEP in the extended amygdala: primarily in the anterolateral BNST and central amygdala (CeA)
Because STEP distribution was highest in those regions of the extended amygdala that show high corticotrophin releasing factor (CRF) expression, we performed dual immunofluorescence experiments to determine the relative co-localization of CRF and STEP
Summary
STEP (Striatal-enriched protein tyrosine phosphatase), a recently discovered neuronspecific tyrosine phosphatase, is widely distributed in the rodent brain. STEP has been reported to be critically involved in the glutamate (NMDA receptor)-mediated regulation of the ERK (extracellular signal-regulated kinase) signaling cascade in rat neurons. Activation of the ERK cascade is thought to be an important signal transduction factor that regulates synaptic function, long-term potentation (LTP), and learning and memory.
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