Optical Imaging of Plastic Changes Induced by Fear Conditioning in Auditory, Visual, and Somatosensory Cortices

Author(s):  
Yoshinori Ide ◽  
Muneyoshi Takahashi ◽  
Johan Lauwereyns ◽  
Minoru Tsukada ◽  
Takeshi Aihara
2011 ◽  
Vol 6 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Yoshinori Ide ◽  
Takashi Miyazaki ◽  
Johan Lauwereyns ◽  
Guy Sandner ◽  
Minoru Tsukada ◽  
...  

Synapse ◽  
2022 ◽  
Author(s):  
Yuki Kirihara ◽  
Manabu Zama ◽  
Satoshi Fujita ◽  
Shouhei Ogisawa ◽  
Shuichi Nishikubo ◽  
...  

2021 ◽  
Vol 11 (10) ◽  
pp. 1294
Author(s):  
Ichiro Takashima ◽  
Riichi Kajiwara

Studies using functional magnetic resonance imaging assume that hemodynamic responses have roughly linear relationships with underlying neural activity. However, to accurately investigate the neurovascular transfer function and compare its variability across brain regions, it is necessary to obtain full-field imaging of both electrophysiological and hemodynamic responses under various stimulus conditions with superior spatiotemporal resolution. Optical imaging combined with voltage-sensitive dye (VSD) and intrinsic signals (IS) is a powerful tool to address this issue. We performed VSD and IS imaging in the primary (S1) and secondary (S2) somatosensory cortices of rats to obtain optical maps of whisker-evoked responses. There were characteristic differences in sensory responses between the S1 and S2 cortices: VSD imaging revealed more localized excitatory and stronger inhibitory neural activity in S1 than in S2. IS imaging revealed stronger metabolic responses in S1 than in S2. We calculated the degree of response to compare the sensory responses between cortical regions and found that the ratio of the degree of response of S2 to S1 was similar, irrespective of whether the ratio was determined by VSD or IS imaging. These results suggest that neurovascular coupling does not vary between the S1 and S2 cortices.


2005 ◽  
Vol 94 (2) ◽  
pp. 1199-1211 ◽  
Author(s):  
Weiqing Ji ◽  
Nobuo Suga ◽  
Enquan Gao

In big brown bats, tone-specific plastic changes [best frequency (BF) shifts] of cortical and collicular neurons can be evoked by auditory fear conditioning, repetitive acoustic stimuli or cortical electric stimulation. It has been shown that acetylcholine (ACh) plays an important role in evoking large long-term cortical BF shifts. However, the role of N-methyl-d-aspartate (NMDA) receptors in evoking BF shifts has not yet been studied. We found 1) NMDA applied to the auditory cortex (AC) or inferior colliculus (IC) augmented the auditory responses, as ACh did, whereas 2-amino-5-phosphovalerate (APV), an antagonist of NMDA receptors, reduced the auditory responses, as atropine did; 2) although any of these four drugs did not evoke BF shifts, they influenced the development of the long-term cortical and short-term collicular BF shifts elicited by conditioning; 3) like ACh, NMDA augmented the cortical and collicular BF shifts regardless of whether it was applied to the AC or IC; 4) endogenous ACh of the AC and IC is necessary to produce the long-term cortical and short-term collicular BF shifts; 5) blockade of collicular NMDA receptors by APV abolished the development of the collicular BF shift and made the cortical BF shift small and short-term; 6) blockade of cortical NMDA receptors by APV reduced the cortical and collicular BF shifts and made the cortical BF shift short-term; and 7) conditioning with NMDA + atropine applied to the AC evoked the small, short-term cortical BF shift, whereas conditioning with APV + ACh applied to the AC evoked the small, but long-term cortical BF shift.


2009 ◽  
Vol 102 (2) ◽  
pp. 941-952 ◽  
Author(s):  
Weiqing Ji ◽  
Nobuo Suga

Experience-dependent plasticity in the central sensory systems depends on activation of both the sensory and neuromodulatory systems. Sensitization or nonspecific augmentation of central auditory neurons elicited by pseudo-conditioning with unpaired conditioning tonal (CS) and unconditioned electric leg (US) stimuli is quite different from tone-specific plasticity, called best frequency (BF) shifts, of the neurons elicited by auditory fear conditioning with paired CS and US. Therefore the neural circuits eliciting the nonspecific augmentation must be different from that eliciting the BF shifts. We first examined plastic changes in the response properties of collicular neurons of the big brown bat elicited by pseudo-conditioning and found that it elicited prominent nonspecific augmentation—an auditory response increase, a frequency-tuning broadening, and a threshold decreas—and that, in addition, it elicited a small short-lasting BF shift only when the CS frequency was 5 kHz lower than the BF of a recorded neuron. We examined the role of acetylcholine and the auditory and somatosensory cortices in these collicular changes. The development of the nonspecific augmentation was affected little by a muscarinic acetylcholine receptor antagonist applied to the inferior colliculus and by a GABAA receptor agonist applied to the auditory or somatosensory cortex. However, these drugs abolished the small short-lasting BF shift as they abolished the large long-lasting cortical and short-lasting collicular BF shifts elicited by the conditioning. These results indicate that, different from the BF shift, the nonspecific augmentation of the inferior colliculus depends on neither the cholinergic neuromodulator nor the auditory and somatosensory cortices.


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