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The Journal of Neuroscience, January 19, 2005, 25(3):577-583; doi:10.1523/JNEUROSCI.4196-04.2005

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Behavioral/Systems/Cognitive
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor₂ Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum

Jie Liu,¹ Baojian Yu,¹ Luis Orozco-Cabal,¹ Dimitri E. Grigoriadis,² Jean Rivier,³ Wylie W. Vale,³ Patricia Shinnick-Gallagher,¹ and Joel P. Gallagher¹

¹Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555-1031, ²Neurocrine Biosciences Incorporated, San Diego, California 92121, and ³Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, Peptide Biology Laboratory, La Jolla, California 92037

Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF₁ and CRF₂. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse.

In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF₁ receptors with CRF but was depressed after activation of CRF₂ receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF₁ activation remained facilitatory, but CRF₂ activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF₂ effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF₁ and CRF₂ coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF₂-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA_A-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABA_A-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.

Key words: cocaine; CRF; facilitation of transmission; glutamatergic excitatory transmission; urocortin; CRF₂; CRF₁; GABA_A inhibitory transmission; acute withdrawal

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Received May 7, 2004; revised November 17, 2004; accepted November 22, 2004.

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