Difference in Binocularity and Ocular Dominance Plasticity between GABAergic and Excitatory Cortical Neurons

Kameyama, Katsuro; Sohya, Kazuhiro; Ebina, Teppei; Fukuda, Atsuo; Yanagawa, Yuchio; Tsumoto, Tadaharu

doi:10.1523/jneurosci.5025-09.2010

Cited by 86 publications

(111 citation statements)

References 49 publications

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“…As reported previously from spiking (Gordon and Stryker, 1996;Hanover et al, 1999;Tagawa et al, 2005) and calcium responses (Mrsic-Flogel et al, 2007;Kameyama et al, 2010), the contralateral bias in normal mice (Fig. 2E) shifted toward more equivalent monocular responses and a more uniform distribution of OD (Fig.…”

Section: Binocular Response Properties In Normal and Deprived Animalssupporting

confidence: 80%

Binocular Disparity Selectivity Weakened after Monocular Deprivation in Mouse V1

2017

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Experiences during the critical period sculpt the circuitry within the neocortex, leading to changes in the functional responses of sensory neurons. Monocular deprivation (MD) during the visual critical period causes shifts in ocular preference, or dominance, toward the open eye in primary visual cortex (V1) and disrupts the normal development of acuity. In carnivores and primates, MD also disrupts the emergence of binocular disparity selectivity, a cue resulting from integrating ocular inputs. This disruption may be a result of the increase in neurons driven exclusively by the open eye that follows deprivation or a result of a mismatch in the convergence of ocular inputs. To distinguish between these possibilities, we measured the ocular dominance (OD) and disparity selectivity of neurons from male and female mouse V1 following MD. Normal mouse V1 neurons are dominated by contralateral eye input and contralateral eye deprivation shifts mouse V1 neurons toward more balanced responses between the eyes. This shift toward binocularity, as assayed by OD, decreased disparity sensitivity. MD did not alter the initial maturation of binocularity, as disparity selectivity before the MD was indistinguishable from normal mature animals. Decreased disparity tuning was most pronounced in binocular and ipsilaterally biased neurons, which are the populations that have undergone the largest shifts in OD. In concert with the decline in disparity selectivity, we observed a shift toward lower spatial frequency selectivity for the ipsilateral eye following MD. These results suggest an emergence of novel synaptic inputs during MD that disrupt the representation of disparity selectivity.

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Section: Binocular Response Properties In Normal and Deprived Animalssupporting

confidence: 80%

Binocular Disparity Selectivity Weakened after Monocular Deprivation in Mouse V1

2017

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“…To clearly distinguish the activity of L2/3 excitatory neurons, which integrate and transmit sensory information to other cortical areas, the L2/3 excitatory neuronal activity elicited in response to hindpaw pressure stimulation was examined by fura-2 Ca 2ϩ imaging (Kameyama et al, 2010) (Fig. 2a,b).…”

Section: Resultsmentioning

confidence: 99%

“…Labeling procedure and in vivo Ca 2ϩ imaging. Multicell bolus loading of L2/3 neurons and astrocytes with membrane-permeable Ca 2ϩ indicator Oregon Green 488 BAPTA-1 (OGB-1) AM (Invitrogen) or fura-2 AM (Invitrogen) was performed as previously reported (Kerr et al, 2005;Kameyama et al, 2010). Ca 2ϩ indicators (OGB-1 or fura-2) were excited at 800 nm, and Venus and sulforhodamine 101(SR101) were excited at 950 nm.…”

Section: Methodsmentioning

confidence: 99%

Inter-regional Contribution of Enhanced Activity of the Primary Somatosensory Cortex to the Anterior Cingulate Cortex Accelerates Chronic Pain Behavior

et al. 2011

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Multiple cortical areas are involved in pain processing, including the primary somatosensory cortex (S1) and the anterior cingulate cortex (ACC). Although accumulations of evidence suggest that the S1 activity increases under chronic pain conditions, whether plastic change occurs or not within the S1, and whether and how the plastic change contributes to chronic pain behavior, is unknown. Here, we provide the first evidence that intra-regional remodeling within the mouse S1 accelerates chronic pain behavior by modulating neuronal activity in the ACC, one of the important cortical areas for chronic pain. Using two-photon Ca 2ϩ imaging, we found that the spontaneous activity of layer 2/3 neurons in the S1 and then response to sensory and layer 4 stimulations increased under chronic pain conditions. In addition, pharmacological attenuation and facilitation of S1 activity attenuated and facilitated the chronic pain behavior, respectively. Furthermore, electrical response of the ACC to peripheral stimulation successfully correlated with S1 neuronal activity, and inhibition of ACC activity alleviated the mechanical allodynia. The present results will provide development of efficient therapeutic strategies against chronic pain by focusing on the S1 and ACC.

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“…The mice older than P14 were male, although those younger than P12 were not identified as male or female. VGATVenus transgenic mice were generated as reported previously (Wang et al, 2009) and confirmed to express the normal level of the GABA synthesizing enzyme, glutamate decarboxylase 67 (Kameyama et al, 2010). In part of the experiments, we used CB1-KO mice.…”

Section: Methodsmentioning

confidence: 99%

Laminar-Specific Maturation of GABAergic Transmission and Susceptibility to Visual Deprivation Are Related to Endocannabinoid Sensitivity in Mouse Visual Cortex

Jiang¹,

Sohya²,

Sarihi³

et al. 2010

J. Neurosci.

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The developmental period when neuronal responses are modified by visual experience is reported to start and end earlier in layer 4 than in layer 2/3ofthevisualcortex,andthematurationofGABAergicinhibitorycircuitsissuggestedtodeterminethetimingofthisperiod.Here,weexamine whether the laminar difference in such timing corresponds to a difference in the time course of the functional maturation of GABAergic synaptic transmission to star pyramidal and pyramidal cells in layers 4 and 2/3, respectively, of the mouse visual cortex and whether the development of the strength of GABAergic transmission is affected by visual deprivation in a laminar-specific manner. Our analysis of developmental changes in inhibitory postsynaptic currents of star pyramidal and pyramidal cells evoked by electrical stimulation of afferents or action potentials of fast-spiking GABAergic neurons revealed that there was a sequential maturation of GABAergic function from layers 4 to 2/3. The maturation of inhibition in layer 4 occurred at postnatal week 3, which preceded by 1 week that of layer 2/3. Visual deprivation by dark rearing arrested the functional development of GABAergic transmission in layer 2/3, whereas dark rearing was not so effective in layer 4. GABAergic synapses in layer 2/3 were sensitive to an agonist for cannabinoid type 1 receptors and not normally matured in receptor knock-out mice, whereas those in layer 4werenotso.Theseresultssuggestlaminar-specificmaturationofinhibitionandsusceptibilitytovisualdeprivation,whichmayberelatedtothe laminar difference in sensitivity to endocannabinoids.

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Difference in Binocularity and Ocular Dominance Plasticity between GABAergic and Excitatory Cortical Neurons

Cited by 86 publications

References 49 publications

Binocular Disparity Selectivity Weakened after Monocular Deprivation in Mouse V1

Binocular Disparity Selectivity Weakened after Monocular Deprivation in Mouse V1

Inter-regional Contribution of Enhanced Activity of the Primary Somatosensory Cortex to the Anterior Cingulate Cortex Accelerates Chronic Pain Behavior

Laminar-Specific Maturation of GABAergic Transmission and Susceptibility to Visual Deprivation Are Related to Endocannabinoid Sensitivity in Mouse Visual Cortex

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