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This Article Full Text Full Text (PDF) All Versions of this Article: 97/6/3893    most recent 00135.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Ji, G. Articles by Neugebauer, V. Search for Related Content PubMed PubMed Citation Articles by Ji, G. Articles by Neugebauer, V.

Differential Effects of CRF1 and CRF2 Receptor Antagonists on Pain-Related Sensitization of Neurons in the Central Nucleus of the Amygdala

Department of Neuroscience and Cell Biology, The University of Texas Medical Branch, Galveston, Texas

Submitted 6 February 2007; accepted in final form 23 March 2007

As a hormone in the hypothalamic–pituitary–adrenocortical (HPA) axis corticotropin-releasing factor (CRF) mediates stress responses. CRF can also act as a neuromodulator of synaptic transmission outside the HPA axis. A major site of extrahypothalamic expression of CRF and its G-protein–coupled receptors is the amygdala, a key player in affect-related disorders such as anxiety. The laterocapsular division of the central nucleus of the amygdala (CeLC) is important for the modulation of pain affect. This study determined the effects of CRF1 and CRF2 receptor antagonists in CeLC neurons in an arthritis pain model. Extracellular single-unit recordings were made from CeLC neurons in anesthetized adult rats. All neurons responded more strongly to noxious than to innocuous mechanical stimulation (compression) of peripheral tissues, including the knee. Evoked responses and background activity were measured before and during the development of a kaolin/carrageenan-induced knee joint arthritis. Drugs were administered into the CeLC by microdialysis before and/or after arthritis induction. All CeLC neurons showed increased responses to mechanical stimuli ("sensitization") 5–6 h postinduction of arthritis. A selective CRF1 receptor antagonist (NBI27914; 1–100 µM, concentration in microdialysis probe; 15 min) inhibited evoked responses and background activity in arthritis (n = 9) but had no effect under normal conditions before arthritis (n = 9). In contrast, a selective CRF2 receptor antagonist (Astressin-2B; 1–100 µM, 15 min) had no effect in arthritis (n = 7) but increased the neurons' responses under normal conditions (n = 8). These data suggest that CRF1 receptors in the amygdala contribute to pain-related sensitization, whereas the normally inhibitory function of CRF2 receptors is lost in the arthritis pain model.

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