Neuropeptide S-mediated control of fear expression and extinction: role of intercalated GABAergic neurons in the amygdala. Export

@article{citeulike:3138512, abstract = {A deficient extinction of memory is particularly important in the regime of fear, where it limits the beneficial outcomes of treatments of anxiety disorders. Fear extinction is thought to involve inhibitory influences of the prefrontal cortex on the amygdala, although the detailed synaptic mechanisms remain unknown. Here, we report that neuropeptide S (NPS), a recently discovered transmitter of ascending brainstem neurons, evokes anxiolytic effects and facilitates extinction of conditioned fear responses when administered into the amygdala in mice. An NPS receptor antagonist exerts functionally opposing responses, indicating that endogenous NPS is involved in anxiety behavior and extinction. Cellularly, NPS increases glutamatergic transmission to intercalated GABAergic neurons in the amygdala via presynaptic NPS receptors on connected principal neurons. These results identify mechanisms of NPS in the brain, a key role of intercalated neurons in the amygdala for fear extinction, and a potential pharmacological avenue for treating anxiety disorders.}, address = {Institute of Physiology I (Neurophysiology), Westf\"{a}lische Wilhelms-University M\"{u}nster, Robert-Koch-Strasse 27a, D-48149 M\"{u}nster, Germany.}, author = {J\"{u}ngling, Kay and Seidenbecher, Thomas and Sosulina, Ludmila and Lesting, J\"{o}rg and Sangha, Susan and Clark, Stewart D. and Okamura, Naoe and Duangdao, Dee M. and Xu, Yan-Ling L. and Reinscheid, Rainer K. and Pape, Hans-Christian C.}, citeulike-article-id = {3138512}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.neuron.2008.07.002}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18667157}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18667157}, day = {31}, doi = {10.1016/j.neuron.2008.07.002}, issn = {1097-4199}, journal = {Neuron}, keywords = {080821, bj, jc}, month = {July}, number = {2}, pages = {298--310}, posted-at = {2008-08-20 06:14:54}, priority = {2}, title = {Neuropeptide S-mediated control of fear expression and extinction: role of intercalated GABAergic neurons in the amygdala.}, url = {http://dx.doi.org/10.1016/j.neuron.2008.07.002}, volume = {59}, year = {2008} }

TY - JOUR ID - citeulike:3138512 L3 - citeulike-article-id:3138512 N2 - A deficient extinction of memory is particularly important in the regime of fear, where it limits the beneficial outcomes of treatments of anxiety disorders. Fear extinction is thought to involve inhibitory influences of the prefrontal cortex on the amygdala, although the detailed synaptic mechanisms remain unknown. Here, we report that neuropeptide S (NPS), a recently discovered transmitter of ascending brainstem neurons, evokes anxiolytic effects and facilitates extinction of conditioned fear responses when administered into the amygdala in mice. An NPS receptor antagonist exerts functionally opposing responses, indicating that endogenous NPS is involved in anxiety behavior and extinction. Cellularly, NPS increases glutamatergic transmission to intercalated GABAergic neurons in the amygdala via presynaptic NPS receptors on connected principal neurons. These results identify mechanisms of NPS in the brain, a key role of intercalated neurons in the amygdala for fear extinction, and a potential pharmacological avenue for treating anxiety disorders. IS - 2 JF - Neuron SN - 1097-4199 AD - Institute of Physiology I (Neurophysiology), Westfälische Wilhelms-University Münster, Robert-Koch-Strasse 27a, D-48149 Münster, Germany. EP - 310 TI - Neuropeptide S-mediated control of fear expression and extinction: role of intercalated GABAergic neurons in the amygdala. VL - 59 SP - 298 KW - 080821 KW - bj KW - jc AU - Jüngling, Kay AU - Seidenbecher, Thomas AU - Sosulina, Ludmila AU - Lesting, Jörg AU - Sangha, Susan AU - Clark, Stewart AU - Okamura, Naoe AU - Duangdao, Dee AU - Xu, Yan-Ling AU - Reinscheid, Rainer AU - Pape, Hans-Christian PY - 2008/07/31/ UR - http://dx.doi.org/10.1016/j.neuron.2008.07.002 ER -