Rapid Critical Period Induction by Tonic Inhibition in Visual Cortex

Iwai, Yoshio; Fagiolini, Michela; Obata, Kunihiko; Hensch, Takao K.

doi:10.1523/jneurosci.23-17-06695.2003

Cited by 172 publications

(161 citation statements)

References 56 publications

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“…In V1, BDNF (Hanover et al, 1999) and the development of GABAergic projections have been shown to play a key role in the onset of the critical period (Fagiolini and Hensch, 2000;Fagiolini et al, 2004). Similarly, dark-rearing delays the onset of the critical period (Mower, 1991;Iwai et al, 2003). Strikingly, once triggered, the critical period is always of a fixed duration.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, in the visual system of several species, the onset of monocular deprivation-related plasticity is closely linked to the completion of visual acuity development (Berardi et al, 2000(Berardi et al, , 2003Stern et al, 2001). Further supporting the concept that regulation of the CP window is tied to sensory experience, normally patterned inputs are necessary for the development of normal cortical columnar organization and the timing of CP offset (Fagiolini et al 1994;Zhang et al, 2002;Iwai et al 2003;Chang and Merzenich, 2003). This way, a premature closure of the CP could be prevented if insufficient or incoherent inputs are present during development.…”

Section: Introductionmentioning

confidence: 90%

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Critical Period Window for Spectral Tuning Defined in the Primary Auditory Cortex (A1) in the Rat

Villers-Sidani¹,

Chang²,

Bao³

et al. 2007

J. Neurosci.

339

346

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Experience-dependent plasticity during development results in the emergence of highly adapted representations of the external world in the adult brain. Previous studies have convincingly shown that the primary auditory cortex (A1) of the rat possesses a postnatal period of sensory input-driven plasticity but its precise timing (onset, duration, end) has not been defined. In the present study, we examined the effects of pure-tone exposure on the auditory cortex of developing rat pups at different postnatal ages with a high temporal resolution. We found that pure-tone exposure resulted in profound, persistent alterations in sound representations in A1 only if the exposure occurred during a brief period extending from postnatal day 11 (P11) to P13. We also found that postnatal sound exposure in this epoch led to striking alterations in the cortical representation of sound intensity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 90%

Critical Period Window for Spectral Tuning Defined in the Primary Auditory Cortex (A1) in the Rat

Villers-Sidani¹,

Chang²,

Bao³

et al. 2007

J. Neurosci.

339

346

View full text Add to dashboard Cite

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“…Such possibilities may be further examined in developmental studies to compare the critical periods between wild-type and GAD67-GFP mice. In the visual cortex, enhancing or reducing tonic levels of GABA by diazepam (selective GABA agonist) infusion prematurely closes critical periods for monocular deprivation (Iwai et al, 2003).…”

Section: Network and Developmental Consequences Of Altered Intracortimentioning

confidence: 99%

Major Effects of Sensory Experiences on the Neocortical Inhibitory Circuits

Jiao¹,

Zhang²,

Yanagawa³

et al. 2006

J. Neurosci.

152

164

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During postnatal development, sensory experiences play critical roles in the refinement of cortical connections. However, both the process of postnatal experience-dependent maturation of neocortical inhibitory networks and its underlying mechanisms remain elusive. Here, we examined the differential properties of intracortical inhibitory networks of layer IV in "sensory-spared" and "sensorydeprived" cortices of glutamate acid decarboxylase 67 (GAD67)-green fluorescent protein (GFP) (⌬neo) and wild-type mouse. Our results showed that row D whisker trimming (WT) begun at postnatal day 7 (P7), but not after P15, induced a robust reduction of parvalbumin (PV) expression, measured by the PV/GFP ratio and PV cell densities, in the deprived barrels. WT also induced a robust reduction in the number of inhibitory perisomatic varicosities and synaptic GAD65/67 immunoreactivities in spiny neurons of the deprived barrels. Although the GAD65/67 expressions in interneurons were also downregulated in the deprived barrels, the GFP expression remained unchanged. Patch-clamp recording from spiny cells showed a 1.5-fold reduction of intracortical evoked IPSCs (eIPSCs) in deprived versus spared cortices. The reduction in eIPSCs occurred via changes in presynaptic properties and unitary IPSC amplitudes. Miniature IPSCs showed subtle but significant differences between the two experimental conditions. In addition, properties of the IPSCs in deprived barrels resemble those of IPSCs recorded in immature brains (P7). Together, these results suggest that the properties of local intracortical inhibitory networks are modified by sensory experiences. Perisomatic inhibition mediated by PV-positive basket cells is pruned by sensory deprivation.

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“…In addition, benzodiazepine sensitivity was investigated in animals lacking the ability to synthesize GABA. The GAD65 knock-out mouse fails to enter the CP but can be made plastic by treating with the GABA agonist diaz-epam (DZ) (Hensch et al, 1998;Iwai et al, 2003). Natural CP timing can similarly be accelerated with DZ in immature wildtype mice (Fagiolini and Hensch, 2000).…”

Section: Inhibitory Plasticity In Sensory Systemsmentioning

confidence: 99%

Developmental Plasticity of Inhibitory Circuitry

et al. 2006

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In 1949, Donald Hebb proposed a mechanism for use-dependent synaptic plasticity, suggesting that input neurons that reliably activate their postsynaptic target will strengthen their connections (Hebb, 1949). Since then, studies of use-dependent plasticity during development have been almost entirely focused on excitatory synapses, particularly those incorporating NMDA receptors (NMDARs). Neural circuits depend heavily on inhibition, however. Although there have been several in vitro studies of possible synaptic mechanisms underlying inhibitory plasticity Alger, 1992, 1994;Komatsu, 1994;Kano, 1995;Zilberter, 2000;Kreitzer and Regehr, 2001;Wilson and Nicoll, 2001;Kilman et al., 2002;Maffei et al., 2006), little is known at the systems level about use-dependent plasticity of inhibitory synapses. The realization that "inhibitory" neurotransmitters often depolarize immature neurons (Ben-Ari, 2002) further complicates the picture. This issue is important because clinical treatments for epilepsy, sensory dysfunction, or brain damage need to be informed by an understanding of both excitatory and inhibitory components of the circuits they are aimed at influencing. This mini-symposium, presented at the 36th Annual Meeting of the Society for Neuroscience, will address the roles and mechanisms of inhibitory synaptic plasticity during development of the mammalian CNS, using primarily in vivo approaches to examine circuit-level plasticity in a wide array of model systems. The goal of the mini-symposium is to bring this important research area into the spotlight and to encourage other investigators to participate in developing a better understanding of this underappreciated issue. Inhibitory plasticity in motor systemsThe transient presence of episodic bursts of spontaneous network activity (SNA) is observed throughout the developing CNS. In the spinal cord, SNA is important for axon guidance, motoneuron survival, neurochemical expression, and joint and muscle development . Despite its importance, the role of SNA in the maturation of spinal connectivity is poorly understood. In the laboratory of Peter Wenner, co-chair of the mini-symposium, postdoctoral fellow Carlos Gonzalez-Islas has been investigating the role of SNA in homeostatic plasticity within the embryonic chick spinal cord. Despite significant developmental challenges to the production of SNA, it is clear that the network is capable of maintaining its activity levels (Chub and O'Donovan, 1998). Wenner and Gonzalez-Islas hypothesized that SNA is maintained through compensatory changes in synaptic strength. To test this hypothesis, they reduced network activity with lidocaine for 2 d in ovo. This increased the strength of both glutamatergic synapses and immature, depolarizing GABAergic synapses (Gonzalez-Islas and Wenner, 2006) and accelerated the modulation of GABAergic synaptic strength normally observed between episodes of SNA. Together, these compensatory responses appeared to increase the excitability of the embryonic spinal cord in an attempt to maintain approp...

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Rapid Critical Period Induction by Tonic Inhibition in Visual Cortex

Cited by 172 publications

References 56 publications

Critical Period Window for Spectral Tuning Defined in the Primary Auditory Cortex (A1) in the Rat

Critical Period Window for Spectral Tuning Defined in the Primary Auditory Cortex (A1) in the Rat

Major Effects of Sensory Experiences on the Neocortical Inhibitory Circuits

Developmental Plasticity of Inhibitory Circuitry

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