title: Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala.
abstract: A large majority of neurons in the superficial layer of the dorsal horn projects to the lateral parabrachial nucleus (LPB). LPB neurons then project to the capsular part of the central amygdala (CeA; CeC), a key structure underlying the nociception-emotion link. LPB-CeC synaptic transmission is enhanced in various pain models by using electrical stimulation of putative fibers of LPB origin in brain slices. However, this approach has limitations for examining direct monosynaptic connections devoid of directly stimulating fibers from other structures and local GABAergic neurons. To overcome these limitations, we infected the LPB of rats with an adeno-associated virus vector expressing channelrhodopsin-2 and prepared coronal and horizontal brain slices containing the amygdala. We found that blue light stimulation resulted in monosynaptic excitatory postsynaptic currents (EPSCs), with very small latency fluctuations, followed by a large polysynaptic inhibitory postsynaptic current in CeC neurons, regardless of the firing pattern type. Intraplantar formalin injection at 24 h before slice preparation significantly increased EPSC amplitude in late firing-type CeC neurons. These results indicate that direct monosynaptic glutamatergic inputs from the LPB not only excite CeC neurons but also regulate CeA network signaling through robust feed-forward inhibition, which is under plastic modulation in response to persistent inflammatory pain.
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan;
authors.forename: Yae K
authors.initials: YK
authors.lastname: Sugimura
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan;
authors.forename: Yukari
authors.initials: Y
authors.lastname: Takahashi
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama, Japan; and Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Ayako M
authors.initials: AM
authors.lastname: Watabe
authors.affiliation: Department of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Nagoya University Graduate School of Medicine, Nagoya, Japan fusao@jikei.ac.jp.
authors.forename: Fusao
authors.identifier: 0000-0003-0031-9946
authors.initials: F
authors.lastname: Kato
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D066274:Central Amygdaloid Nucleus / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D053444:Inhibitory Postsynaptic Potentials / Q000502:physiology; D008297:Male; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000473:pathology / Q000502:physiology*; D059226:Nociceptive Pain / Q000473:pathology / Q000503:physiopathology*; D065823:Parabrachial Nucleus / Q000473:pathology / Q000503:physiopathology*; D017208:Rats, Wistar; D013569:Synapses / Q000473:pathology / Q000502:physiology*; D046509:Tissue Culture Techniques
chemical_list: D018698:Glutamic Acid
keywords: channelrhodopsin-2; excitatory postsynaptic current; feed-forward inhibition; pain; rat