TY - JOUR
T1 - Glutamate transmission rather than cellular pacemaking propels excitatory-inhibitory resonance for ictogenesis in amygdala
AU - Wang, Guan Hsun
AU - Chou, Ping
AU - Hsueh, Shu Wei
AU - Yang, Ya Chin
AU - Kuo, Chung Chin
N1 - Publisher Copyright:
© 2020 The Authors
PY - 2021/1
Y1 - 2021/1
N2 - Epileptic seizures are automatic, excessive, and synchronized neuronal activities originating from many brain regions especially the amygdala, the allocortices and neocortices. This may reflect a shared principle for network organization and signaling in these telencephalic structures. In theory, the automaticity of epileptic discharges may stem from spontaneously active “oscillator” neurons equipped with intrinsic pacemaking conductances, or from a group of synaptically-connected collaborating “resonator” neurons. In the basolateral amygdalar (BLA) network of pyramidal-inhibitory (PN-IN) neuronal resonators, we demonstrated that rhythmogenic currents are provided by glutamatergic rather than the classic intrinsic or cellular pacemaking conductances (namely the h currents). The excitatory output of glutamatergic neurons such as PNs presumably propels a novel network-based “relay burst mode” of discharges especially in INs, which precondition PNs into a state prone to burst discharges and thus further glutamate release. Also, selective activation of unilateral PNs, but never INs, readily drives bilateral BLA networks into reverberating discharges which are fully synchronized with the behavioral manifestations of seizures (e.g. muscle contractions). Seizures originating in BLA and/or the other structures with similar PN-IN networks thus could be viewed as glutamate-triggered erroneous network oscillations that are normally responsible for information relay.
AB - Epileptic seizures are automatic, excessive, and synchronized neuronal activities originating from many brain regions especially the amygdala, the allocortices and neocortices. This may reflect a shared principle for network organization and signaling in these telencephalic structures. In theory, the automaticity of epileptic discharges may stem from spontaneously active “oscillator” neurons equipped with intrinsic pacemaking conductances, or from a group of synaptically-connected collaborating “resonator” neurons. In the basolateral amygdalar (BLA) network of pyramidal-inhibitory (PN-IN) neuronal resonators, we demonstrated that rhythmogenic currents are provided by glutamatergic rather than the classic intrinsic or cellular pacemaking conductances (namely the h currents). The excitatory output of glutamatergic neurons such as PNs presumably propels a novel network-based “relay burst mode” of discharges especially in INs, which precondition PNs into a state prone to burst discharges and thus further glutamate release. Also, selective activation of unilateral PNs, but never INs, readily drives bilateral BLA networks into reverberating discharges which are fully synchronized with the behavioral manifestations of seizures (e.g. muscle contractions). Seizures originating in BLA and/or the other structures with similar PN-IN networks thus could be viewed as glutamate-triggered erroneous network oscillations that are normally responsible for information relay.
KW - Epileptogenesis
KW - GABAergic transmission
KW - Glutamatergic transmission
KW - Network reverberation
KW - Relay burst mode
UR - http://www.scopus.com/inward/record.url?scp=85097474570&partnerID=8YFLogxK
U2 - 10.1016/j.nbd.2020.105188
DO - 10.1016/j.nbd.2020.105188
M3 - 文章
C2 - 33221531
AN - SCOPUS:85097474570
SN - 0969-9961
VL - 148
JO - Neurobiology of Disease
JF - Neurobiology of Disease
M1 - 105188
ER -