Spike Timing and Visual Cortical Plasticity

2003 ◽  
pp. 255-267
Author(s):  
Yu-Xi Fu ◽  
Yang Dan
2021 ◽  
Vol 230 ◽  
pp. 26-37
Author(s):  
Michael S. Jacob ◽  
Brian J. Roach ◽  
Holly K. Hamilton ◽  
Ricardo E. Carrión ◽  
Aysenil Belger ◽  
...  

2021 ◽  
Vol 170 ◽  
pp. 11-21
Author(s):  
Rhiânan E. Ellis ◽  
Elizabeth Milne ◽  
Liat Levita

2020 ◽  
Author(s):  
Steven F. Grieco ◽  
Xin Qiao ◽  
Xiaoting Zheng ◽  
Yongjun Liu ◽  
Lujia Chen ◽  
...  

SummarySubanesthetic ketamine evokes rapid and long-lasting antidepressant effects in human patients. The mechanism for ketamine’s effects remains elusive, but ketamine may broadly modulate brain plasticity processes. We show that single-dose ketamine reactivates adult mouse visual cortical plasticity and promotes functional recovery of visual acuity defects from amblyopia. Ketamine specifically induces down-regulation of neuregulin-1 (NRG1) expression in parvalbumin-expressing (PV) inhibitory neurons in mouse visual cortex. NRG1 downregulation in PV neurons co-tracks both the fast onset and sustained decreases in synaptic inhibition to excitatory neurons, along with reduced synaptic excitation to PV neurons in vitro and in vivo following a single ketamine treatment. These effects are blocked by exogenous NRG1 as well as PV targeted receptor knockout. Thus ketamine reactivation of adult visual cortical plasticity is mediated through rapid and sustained cortical disinhibition via downregulation of PV-specific NRG1 signaling. Our findings reveal the neural plasticity-based mechanism for ketamine-mediated functional recovery from adult amblyopia.Highlights○ Disinhibition of excitatory cells by ketamine occurs in a fast and sustained manner○ Ketamine evokes NRG1 downregulation and excitatory input loss to PV cells○ Ketamine induced plasticity is blocked by exogenous NRG1 or its receptor knockout○ PV inhibitory cells are the initial functional locus underlying ketamine’s effects


2019 ◽  
Vol 116 (25) ◽  
pp. 12506-12515 ◽  
Author(s):  
Mohammad Bagher Khamechian ◽  
Vladislav Kozyrev ◽  
Stefan Treue ◽  
Moein Esghaei ◽  
Mohammad Reza Daliri

Efficient transfer of sensory information to higher (motor or associative) areas in primate visual cortical areas is crucial for transforming sensory input into behavioral actions. Dynamically increasing the level of coordination between single neurons has been suggested as an important contributor to this efficiency. We propose that differences between the functional coordination in different visual pathways might be used to unambiguously identify the source of input to the higher areas, ensuring a proper routing of the information flow. Here we determined the level of coordination between neurons in area MT in macaque visual cortex in a visual attention task via the strength of synchronization between the neurons’ spike timing relative to the phase of oscillatory activities in local field potentials. In contrast to reports on the ventral visual pathway, we observed the synchrony of spikes only in the range of high gamma (180 to 220 Hz), rather than gamma (40 to 70 Hz) (as reported previously) to predict the animal’s reaction speed. This supports a mechanistic role of the phase of high-gamma oscillatory activity in dynamically modulating the efficiency of neuronal information transfer. In addition, for inputs to higher cortical areas converging from the dorsal and ventral pathway, the distinct frequency bands of these inputs can be leveraged to preserve the identity of the input source. In this way source-specific oscillatory activity in primate cortex can serve to establish and maintain “functionally labeled lines” for dynamically adjusting cortical information transfer and multiplexing converging sensory signals.


2003 ◽  
Vol 23 (31) ◽  
pp. 10002-10012 ◽  
Author(s):  
Alexandre E. Medina ◽  
Thomas E. Krahe ◽  
David M. Coppola ◽  
Ary S. Ramoa

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