The discharge patterns of neurons in auditory centers encode information about sounds.However,few studies have focused on the synaptic mechanisms underlying the shaping of discharge patterns using intracellular record...The discharge patterns of neurons in auditory centers encode information about sounds.However,few studies have focused on the synaptic mechanisms underlying the shaping of discharge patterns using intracellular recording techniques.Here,we investigated the discharge patterns of inferior collicular（IC）neurons using intracellular recordings to further elucidate the mechanisms underlying the shaping of discharge patterns.Under in vivo intracellular recording conditions,recordings were obtained from 66 IC neurons in 18 healthy adult mice（Mus musculus,Km）under free field-stimulation.Fiftyeight of these neurons fired bursts of action potentials（APs）to auditory stimuli and the remaining eight just generated local responses such as excitatory（n=4）or inhibitory（n=4）postsynaptic potentials.Based on the APs and subthreshold responses,the discharge patterns were classified into seven types：phasic（24/58,41.4%）,phasic burst（8/58,13.8%）,pauser（4/58,6.9%）,phasic-pauser（1/58,1.7%）,chopper（2/58,3.4%）,primary-like tonic（14/58,24.1%）and sound-induced inhibitory（5/58,8.6%）.We concluded that（1）IC neurons exhibit at least seven distinct discharge patterns;（2）inhibition participates in shaping the discharge pattern of most IC neurons and plays a role in sculpting the pattern,except for the primary-like tonic pattern which was not shapedby inhibition;and（3）local neural circuits are the likely structural basis that shapes the discharge patterns of IC neurons and can be formed either in the IC or in lower-level auditory structures.展开更多
The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation （i-LTP）, points to f...The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation （i-LTP）, points to functional reorganization after stroke. Little is known, however, about whether and how this i-LTP would affect subsequent induction of synaptic plasticity. Here, we first directly confirmed that i-LTP was induced in the endothelin-l-induced ischemia model as in other in vitro models. We also demonstrated increased expression of NR2B, CaMKII and p-CaMKII, which are reminiscent of i-LTP. We further induced LTP of field excitatory post- synaptic potentials （fEPSPs） on CA1 hippocampal neurons in peri-infarct regions of the endothelin-l-induced mini-stroke model. We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia. Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dam- pened at these two time points. These results suggest that i-LTP elevates the induction threshold of subsequent synap- tic plasticity. Our data helps to deepen the knowledge of meta-synaptic regulation of plasticity after focal ischemia.展开更多
基金supported by grants from the National Natural Science Foundation of China (31070971,31000959)
文摘The discharge patterns of neurons in auditory centers encode information about sounds.However,few studies have focused on the synaptic mechanisms underlying the shaping of discharge patterns using intracellular recording techniques.Here,we investigated the discharge patterns of inferior collicular（IC）neurons using intracellular recordings to further elucidate the mechanisms underlying the shaping of discharge patterns.Under in vivo intracellular recording conditions,recordings were obtained from 66 IC neurons in 18 healthy adult mice（Mus musculus,Km）under free field-stimulation.Fiftyeight of these neurons fired bursts of action potentials（APs）to auditory stimuli and the remaining eight just generated local responses such as excitatory（n=4）or inhibitory（n=4）postsynaptic potentials.Based on the APs and subthreshold responses,the discharge patterns were classified into seven types：phasic（24/58,41.4%）,phasic burst（8/58,13.8%）,pauser（4/58,6.9%）,phasic-pauser（1/58,1.7%）,chopper（2/58,3.4%）,primary-like tonic（14/58,24.1%）and sound-induced inhibitory（5/58,8.6%）.We concluded that（1）IC neurons exhibit at least seven distinct discharge patterns;（2）inhibition participates in shaping the discharge pattern of most IC neurons and plays a role in sculpting the pattern,except for the primary-like tonic pattern which was not shapedby inhibition;and（3）local neural circuits are the likely structural basis that shapes the discharge patterns of IC neurons and can be formed either in the IC or in lower-level auditory structures.
基金supported by Major State Basic Research Program of China(Grant No.2013CB733801)
文摘The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation （i-LTP）, points to functional reorganization after stroke. Little is known, however, about whether and how this i-LTP would affect subsequent induction of synaptic plasticity. Here, we first directly confirmed that i-LTP was induced in the endothelin-l-induced ischemia model as in other in vitro models. We also demonstrated increased expression of NR2B, CaMKII and p-CaMKII, which are reminiscent of i-LTP. We further induced LTP of field excitatory post- synaptic potentials （fEPSPs） on CA1 hippocampal neurons in peri-infarct regions of the endothelin-l-induced mini-stroke model. We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia. Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dam- pened at these two time points. These results suggest that i-LTP elevates the induction threshold of subsequent synap- tic plasticity. Our data helps to deepen the knowledge of meta-synaptic regulation of plasticity after focal ischemia.
