scholarly journals Long-term inhibitory plasticity in visual cortical layer 4 switches sign at the opening of the critical period

2013 ◽  
Vol 110 (47) ◽  
pp. E4540-E4547 ◽  
Author(s):  
S. Lefort ◽  
A. C. Gray ◽  
G. G. Turrigiano
Keyword(s):  
Critical Period ◽  
Cortical Layer ◽  
Layer 4 ◽  
Inhibitory Plasticity ◽  
Visual Cortical

scholarly journals Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity

2019 ◽  
Vol 30 (4) ◽  
pp. 2555-2572 ◽  
Author(s):  
Ming-fai Fong ◽  
Peter Sb Finnie ◽  
Taekeun Kim ◽  
Aurore Thomazeau ◽  
Eitan S Kaplan ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Visual Stimulation ◽  
Cortical Layer ◽  
Monocular Deprivation ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Layer 4 ◽  
Nmdar Activation ◽  
Visual Cortical

Abstract Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1. We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity. We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells. We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity.

scholarly journals Binocular matching of thalamocortical and intracortical circuits in the mouse visual cortex

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yu Gu ◽  
Jianhua Cang
Keyword(s):  
Cortical Neurons ◽  
Critical Period ◽  
Individual Layer ◽  
Adult Mice ◽  
Thalamic Input ◽  
Intracortical Circuits ◽  
Layer 4 ◽  
Binocular Matching ◽  
Cortical Inputs ◽  
Visual Cortical

Visual cortical neurons are tuned to similar orientations through the two eyes. The binocularly-matched orientation preference is established during a critical period in early life, but the underlying circuit mechanisms remain unknown. Here, we optogenetically isolated the thalamocortical and intracortical excitatory inputs to individual layer 4 neurons and studied their binocular matching. In adult mice, the thalamic and cortical inputs representing the same eyes are similarly tuned and both are matched binocularly. In mice before the critical period, the thalamic input is already slightly matched, but the weak matching is not manifested due to random connections in the cortex, especially those serving the ipsilateral eye. Binocular matching is thus mediated by orientation-specific changes in intracortical connections and further improvement of thalamic matching. Together, our results suggest that the feed-forward thalamic input may play a key role in initiating and guiding the functional refinement of cortical circuits in critical period development.

Age-Dependent Decline in Supragranular Long-Term Synaptic Plasticity by Increased Inhibition During the Critical Period in the Rat Primary Visual Cortex

2009 ◽  
Vol 101 (1) ◽  
pp. 269-275 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Kwang-Hyun Cho ◽  
Hyun-Sok Kim ◽  
Sang June Hahn ◽  
Myung-Suk Kim ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Excitatory Postsynaptic Potential ◽  
Age Dependent ◽  
Layer 4 ◽  
Old Rats ◽  
Synaptic Model

Supragranular long-term potentiation (LTP) and depression (LTD) are continuously induced in the pathway from layer 4 during the critical period in the rodent primary visual cortex, which limits the use of supragranular long-term synaptic plasticity as a synaptic model for the mechanism of ocular dominance (OD) plasticity. The results of the present study demonstrate that the pulse duration of extracellular stimulation to evoke a field potential (FP) is critical to induction of LTP and LTD in this pathway. LTP and LTD were induced in the pathway from layer 4 to layer 2/3 in slices from 3-wk-old rats when FPs were evoked by 0.1- and 0.2-ms pulses. LTP and LTD were induced in slices from 5-wk-old rats when evoked by stimulation with a 0.2-ms pulse but not by stimulation with a 0.1-ms pulse. Both the inhibitory component of FP and the inhibitory/excitatory postsynaptic potential amplitude ratio evoked by stimulation with a 0.1-ms pulse were greater than the values elicited by a 0.2-ms pulse. Stimulation with a 0.1-ms pulse at various intensities that showed the similar inhibitory FP component with the 0.2-ms pulse induced both LTD and LTP in 5-wk-old rats. Thus extracellular stimulation with shorter-duration pulses at higher intensity resulted in greater inhibition than that observed with longer-duration pulses at low intensity. This increased inhibition might be involved in the age-dependent decline of synaptic plasticity during the critical period. These results provide an alternative synaptic model for the mechanism of OD plasticity.

scholarly journals Sensory experience inversely regulates feedforward and feedback excitation-inhibition ratio in rodent visual cortex

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Nathaniel J Miska ◽  
Leonidas MA Richter ◽  
Brian A Cary ◽  
Julijana Gjorgjieva ◽  
Gina G Turrigiano
Keyword(s):  
Visual Cortex ◽  
Driving Force ◽  
Critical Period ◽  
Visual Experience ◽  
Feedback Inhibition ◽  
Intracortical Inhibition ◽  
Monocular Deprivation ◽  
Long Term Depression ◽  
Layer 4

Brief (2-3d) monocular deprivation (MD) during the critical period induces a profound loss of responsiveness within binocular (V1b) and monocular (V1m) regions of rodent primary visual cortex. This has largely been ascribed to long-term depression (LTD) at thalamocortical synapses, while a contribution from intracortical inhibition has been controversial. Here we used optogenetics to isolate and measure feedforward thalamocortical and feedback intracortical excitation-inhibition (E-I) ratios following brief MD. Despite depression at thalamocortical synapses, thalamocortical E-I ratio was unaffected in V1b and shifted toward excitation in V1m, indicating that thalamocortical excitation was not effectively reduced. In contrast, feedback intracortical E-I ratio was shifted toward inhibition in V1m, and a computational model demonstrated that these opposing shifts produced an overall suppression of layer 4 excitability. Thus, feedforward and feedback E-I ratios can be independently tuned by visual experience, and enhanced feedback inhibition is the primary driving force behind loss of visual responsiveness.

scholarly journals Sensory Deprivation Independently Regulates Neocortical Feedforward and Feedback Excitation-Inhibition Ratio

2018 ◽  
Author(s):  
Nathaniel J. Miska ◽  
Leonidas M.A. Richter ◽  
Brian A. Cary ◽  
Julijana Gjorgjieva ◽  
Gina G. Turrigiano
Keyword(s):  
Critical Period ◽  
Visual Experience ◽  
Pyramidal Neurons ◽  
Feedback Inhibition ◽  
Sensory Deprivation ◽  
Intracortical Inhibition ◽  
Monocular Deprivation ◽  
Layer 4 ◽  
Postsynaptic Target

SUMMARYBrief (2-3d) monocular deprivation (MD) during the critical period induces a profound loss of responsiveness within layer 4 of primary visual cortex (V1). This has largely been ascribed to long-term depression (LTD) at thalamocortical synapses onto pyramidal neurons, while a contribution from intracortical inhibition has been controversial. Here we used optogenetics to probe feedforward thalamocortical and feedback intracortical excitation-inhibition (E-I) ratios following brief MD. While thalamocortical inputs onto pyramidal neurons were depressed, there was stronger depression onto PV+ interneurons, which shifted the thalamocortical-evoked E-I ratio toward excitation. In contrast, feedback intracortical E-I ratio was shifted toward inhibition, and a computational model of layer 4 demonstrated that these opposing shifts produced an overall suppression of layer 4 excitability. Thus, feedforward and feedback E-I ratios onto the same postsynaptic target can be independently regulated by visual experience, and enhanced feedback inhibition is the primary driving force behind loss of visual responsiveness.

Critical periods for functional and anatomical compensation in lateral suprasylvian visual area following removal of visual cortex in cats

1984 ◽  
Vol 52 (5) ◽  
pp. 941-960 ◽  
Author(s):  
L. Tong ◽  
R. E. Kalil ◽  
P. D. Spear
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Direction Selectivity ◽  
Visual Area ◽  
Critical Periods ◽  
Cortex Lesion ◽  
Thalamic Projections ◽  
Adult Cats ◽  
Visual Cortical

Previous experiments have found that neurons in the cat's lateral suprasylvian (LS) visual area of cortex show functional compensation following removal of visual cortical areas 17, 18, and 19 on the day of birth. Correspondingly, an enhanced retino-thalamic pathway to LS cortex develops in these cats. The present experiments investigated the critical periods for these changes. Unilateral lesions of areas 17, 18, and 19 were made in cats ranging in age from 1 day postnatal to 26 wk. When the cats were adult, single-cell recordings were made from LS cortex ipsilateral to the lesion. In addition, transneuronal autoradiographic methods were used to trace the retino-thalamic projections to LS cortex in many of the same animals. Following lesions in 18- and 26-wk-old cats, there is a marked reduction in direction-selective LS cortex cells and an increase in cells that respond best to stationary flashing stimuli. These results are similar to those following visual cortex lesions in adult cats. In contrast, the percentages of cells with these properties are normal following lesions made from 1 day to 12 wk of age. Thus the critical period for development of direction selectivity and greater responses to moving than to stationary flashing stimuli in LS cortex following a visual cortex lesion ends between 12 and 18 wk of age. Following lesions in 26-wk-old cats, there is a decrease in the percentage of cells that respond to the ipsilateral eye, which is similar to results following visual cortex lesions in adult cats. However, ocular dominance is normal following lesions made from 1 day to 18 wk of age. Thus the critical period for development of responses to the ipsilateral eye following a lesion ends between 18 and 26 wk of age. Following visual cortex lesions in 2-, 4-, or 8-wk-old cats, about 30% of the LS cortex cells display orientation selectivity to elongated slits of light. In contrast, few or no cells display this property in normal adult cats, cats with lesions made on the day of birth, or cats with lesions made at 12 wk of age or later. Thus an anomalous property develops for many LS cells, and the critical period for this property begins later (between 1 day and 2 wk) and ends earlier (between 8 and 12 wk) than those for other properties.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Critical periods in amblyopia

2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Ocular Dominance ◽  
Molecular Genetic ◽  
Monocular Deprivation ◽  
Critical Periods ◽  
Developmental Constraints ◽  
Early Postnatal Development ◽  
Visual Cortical

AbstractThe shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

scholarly journals Persistent, Ecotoxic and Bioaccumulative Compounds and their Possible Environmental Effects

1996 ◽  
Vol 68 (9) ◽  
pp. 1771-1780 ◽  
Author(s):  
K. Ballschmiter
Keyword(s):  
Critical Period ◽  
Environmental Fate ◽  
Body Burden ◽  
Substantial Part ◽  
Environmental Distribution ◽  
Major Class ◽  
The Relationship ◽  
Pollutant Transfer ◽  
Environmental Compartments

The relationship between physicochemical properties, environmental distribution and effects of organochlorine compounds as a major class of persistent organic pollutants (POPs) are discussed. The environmental fate of a compound includes its transport and dispersion in the environment as well as its accumulation and transformation in defined environmental compartments. Accumulation and transformation as the result of environmental distribution may have long-term consequences; this is indicated by the ultimate accumulation and long-term bioactivity of several widely spread organochlorines, and is clearly evident in the decomposition of chlorofluorocarbons in the stratosphere.Depending on the order of trophic levelsbiomagnifiaction factors of 10,000 up to 100,000 are encountered for persistentsemivolatile organochlorines such as 4,4'-DDE, PCB congeners or some Toxapheneconstituents. Mammals show intra-species pollutant transfer during thelactation period. While the mother animal is partly depleting its bodyburden, the calve accumulates in a critical period of its life via themilk a concentrated input of persistent organochlorines. A similar depletionphenomenon is also found for fish and crustacean which enrich in the eggsa substantial part of the accumulated body burden of the female.The air skimming of semivolatiles by plantsurfaces leads to surprisingly high levels of pollutants in the uppersoil layers of forests that otherwise would be considered pristine interms of human activities.

scholarly journals Seasonal plasticity in the adult somatosensory cortex

2020 ◽  
Vol 117 (50) ◽  
pp. 32136-32144
Author(s):  
Saikat Ray ◽  
Miao Li ◽  
Stefan Paul Koch ◽  
Susanne Mueller ◽  
Philipp Boehm-Sturm ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Activity Patterns ◽  
Adaptive Plasticity ◽  
Neural Systems ◽  
Mammalian Brain ◽  
Sensory Stimuli ◽  
Seasonal Plasticity ◽  
Layer 4 ◽  
Life On Earth

Seasonal cycles govern life on earth, from setting the time for the mating season to influencing migrations and governing physiological conditions like hibernation. The effect of such changing conditions on behavior is well-appreciated, but their impact on the brain remains virtually unknown. We investigate long-term seasonal changes in the mammalian brain, known as Dehnel’s effect, where animals exhibit plasticity in body and brain sizes to counter metabolic demands in winter. We find large seasonal variation in cellular architecture and neuronal activity in the smallest terrestrial mammal, the Etruscan shrew, Suncus etruscus. Their brain, and specifically their neocortex, shrinks in winter. Shrews are tactile hunters, and information from whiskers first reaches the somatosensory cortex layer 4, which exhibits a reduced width (−28%) in winter. Layer 4 width (+29%) and neuron number (+42%) increase the following summer. Activity patterns in the somatosensory cortex show a prominent reduction of touch-suppressed neurons in layer 4 (−55%), the most metabolically active layer. Loss of inhibitory gating occurs with a reduction in parvalbumin-positive interneurons, one of the most active neuronal subtypes and the main regulators of inhibition in layer 4. Thus, a reduction in neurons in layer 4 and particularly parvalbumin-positive interneurons may incur direct metabolic benefits. However, changes in cortical balance can also affect the threshold for detecting sensory stimuli and impact prey choice, as observed in wild shrews. Thus, seasonal neural adaptation can offer synergistic metabolic and behavioral benefits to the organism and offer insights on how neural systems show adaptive plasticity in response to ecological demands.

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