scholarly journals Developmental Regulation of Homeostatic Plasticity in Mouse Primary Visual Cortex

2021 ◽  
Author(s):  
Wei Wen ◽  
Gina Turrigiano
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Neurons ◽  
Neural Circuit ◽  
Developmental Regulation ◽  
Visual Deprivation ◽  
Homeostatic Plasticity ◽  
Designer Drugs ◽  
Inhibitory Input ◽  
Synaptic Scaling

Homeostatic plasticity maintains network stability by adjusting excitation, inhibition, or the intrinsic excitability of neurons, but the developmental regulation and coordination of these distinct forms of homeostatic plasticity remains poorly understood. A major contributor to this information gap is the lack of a uniform paradigm for chronically manipulating activity at different developmental stages. To overcome this limitation, we utilized Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to directly suppress neuronal activity in layer (L) 2/3 of mouse primary visual cortex (V1) at two important developmental timepoints: the classic visual system critical period (CP, P24-29), and adulthood (P45-55). We show that 24 hours of DREADD-mediated activity suppression simultaneously induces excitatory synaptic scaling up and intrinsic homeostatic plasticity in L2/3 pyramidal neurons during the CP, consistent with previous observations using prolonged visual deprivation. Importantly, manipulations known to block these forms of homeostatic plasticity when induced pharmacologically or via visual deprivation also prevented DREADD-induced homeostatic plasticity. We next used the same paradigm to suppress activity in adult animals. Surprisingly, while excitatory synaptic scaling persisted into adulthood, intrinsic homeostatic plasticity was completely absent. Finally, we found that homeostatic changes in quantal inhibitory input onto L2/3 pyramidal neurons were absent during the CP but present in adults. Thus, the same population of neurons can express distinct sets of homeostatic plasticity mechanisms at different development stages. Our findings suggest that homeostatic forms of plasticity can be recruited in a modular manner according to the evolving needs of a developing neural circuit.

scholarly journals Homeostatic plasticity mechanisms in mouse V1

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Neuronal Activity ◽  
Dynamic Range ◽  
Ocular Dominance ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
The Brain

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

Experience-dependent changes in NMDAR1 expression in the visual cortex of an animal model for amblyopia

2004 ◽  
Vol 21 (4) ◽  
pp. 653-670 ◽  
Author(s):  
KATHRYN M. MURPHY ◽  
KEVIN R. DUFFY ◽  
DAVID G. JONES
Keyword(s):  
Visual Cortex ◽  
Neural Plasticity ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Cortical Circuits ◽  
Central Visual Field ◽  
Binocular Competition ◽  
Binocular Deprivation ◽  
Cortical Representations

When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.

scholarly journals Developmental switch in the polarity of experience-dependent synaptic changes in layer 6 of mouse visual cortex

2011 ◽  
Vol 106 (5) ◽  
pp. 2499-2505 ◽  
Author(s):  
Emily Petrus ◽  
Terence T. Anguh ◽  
Huy Pho ◽  
Angela Lee ◽  
Nicholas Gammon ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Light Exposure ◽  
Visual Deprivation ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Synapses ◽  
Thalamic Nuclei ◽  
Developmental Age

Layer 6 (L6) of primary sensory cortices is distinct from other layers in that it provides a major cortical input to primary sensory thalamic nuclei. L6 pyramidal neurons in the primary visual cortex (V1) send projections to the lateral geniculate nucleus (LGN), as well as to the thalamic reticular nucleus and higher order thalamic nuclei. Although L6 neurons are proposed to modulate the activity of thalamic relay neurons, how sensory experience regulates L6 neurons is largely unknown. Several days of visual deprivation homeostatically adjusts excitatory synapses in L4 and L2/3 of V1 depending on the developmental age. For instance, L4 exhibits an early critical period during which visual deprivation homeostatically scales up excitatory synaptic transmission. On the other hand, homeostatic changes in L2/3 excitatory synapses are delayed and persist into adulthood. In the present study we examined how visual deprivation affects excitatory synapses on L6 pyramidal neurons. We found that L6 pyramidal neurons homeostatically increase the strength of excitatory synapses following 2 days of dark exposure (DE), which was readily reversed by 1 day of light exposure. This effect was restricted to an early critical period, similar to that reported for L4 neurons. However, at a later developmental age, a longer duration of DE (1 wk) decreased the strength of excitatory synapses, which reversed to normal levels with light exposure. These changes are opposite to what is predicted from the homeostatic plasticity theory. Our results suggest that L6 neurons differentially adjust their excitatory synaptic strength to visual deprivation depending on the age of the animals.

scholarly journals Subgroups of parvalbumin-expressing interneurons in layers 2/3 of the visual cortex

2013 ◽  
Vol 109 (6) ◽  
pp. 1600-1613 ◽  
Author(s):  
Jessica Helm ◽  
Gulcan Akgul ◽  
Lonnie P. Wollmuth
Keyword(s):  
Visual Cortex ◽  
Pyramidal Neurons ◽  
Neural Circuit ◽  
Membrane Properties ◽  
Shape Information ◽  
Firing Patterns ◽  
Excitatory Synaptic Input ◽  
Flow Through ◽  
The Difference ◽  
Output Characteristics

The input, processing, and output characteristics of inhibitory interneurons help shape information flow through layers 2/3 of the visual cortex. Parvalbumin (PV)-positive interneurons modulate and synchronize the gain and dynamic responsiveness of pyramidal neurons. To define the diversity of PV interneurons in layers 2/3 of the developing visual cortex, we characterized their passive and active membrane properties. Using Ward's and k-means multidimensional clustering, we identified four PV interneuron subgroups. The most notable difference between the subgroups was their firing patterns in response to moderate stimuli just above rheobase. Two subgroups showed regular and continuous firing at all stimulus intensities above rheobase. The difference between these two continuously firing subgroups was that one fired at much higher frequencies and transitioned into this high-frequency firing rate at or near rheobase. The two other subgroups showed irregular, stuttering firing patterns just above rheobase. Both of these subgroups typically transitioned to regular and continuous firing at intense stimulations, but one of these subgroups, the strongly stuttering subgroup, showed irregular firing across a wider range of stimulus intensities and firing frequencies. The four subgroups also differed in excitatory synaptic input, providing independent support for the classification of subgroups. The subgroups of PV interneurons identified here would respond differently to inputs of varying intensity and frequency, generating diverse patterns of PV inhibition in the developing neural circuit.

Silent Synapses in the Immature Visual Cortex: Layer-Specific Developmental Regulation

2004 ◽  
Vol 91 (2) ◽  
pp. 1097-1101 ◽  
Author(s):  
Simon Rumpel ◽  
Gunnar Kattenstroth ◽  
Kurt Gottmann
Keyword(s):  
Visual Cortex ◽  
Pyramidal Neurons ◽  
Developmental Regulation ◽  
Pyramidal Cells ◽  
Cortical Plate ◽  
Glutamatergic Synapses ◽  
Silent Synapses ◽  
Deep Layers ◽  
Further Development ◽  
Layer Vi

Central glutamatergic synapses are thought to initially form as immature, so-called silent synapses showing exclusively N-methyl-d-aspartate receptor-mediated synaptic transmission. Postsynaptic insertion of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors during further development leads to a conversion into functional, mature synapses. Here, we tested the hypothesis that, according to the “inside first–outside last” pattern of neocortical layer formation and synaptogenesis, pyramidal cells in the superficial layers might show a higher fraction of silent synapses compared with pyramidal cells in the deep layers. We performed an electrophysiological analysis of glutamatergic synapses in acute rat visual cortex slices during postnatal development. In layer VI pyramidal neurons the incidence of silent synapses was high during the first postnatal week and strongly declined during further development. Surprisingly, in superficial cortical plate pyramidal neurons (immature layers II/III), the fraction of silent synapses was initially very low and increased up to the second postnatal week. Thereafter, a similar decline as found in layer VI pyramidal neurons was observed. Thus the developmental regulation of silent synapses was clearly different in pyramidal neurons from different neocortical layers. The almost complete absence of silent synapses at early stages in layer II/III pyramidal neurons indicates that an initially formed subset of synapses is constitutively functional. This might be important to enable spontaneous activity and latter activity-dependent maturation of synapses.

scholarly journals Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160157 ◽  
Author(s):  
Melanie A. Gainey ◽  
Daniel E. Feldman
Keyword(s):  
Visual Cortex ◽  
Sensory Deprivation ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Synaptic Scaling ◽  
Cellular Mechanisms ◽  
Firing Rates ◽  
Parvalbumin Interneuron ◽  
Activity Dependent ◽  
V1 Cortex

We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

scholarly journals VIP interneurons in mouse primary visual cortex selectively enhance responses to weak but specific stimuli

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Daniel J Millman ◽  
Gabriel Koch Ocker ◽  
Shiella Caldejon ◽  
India Kato ◽  
Josh D Larkin ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Neurons ◽  
Feedback Inhibition ◽  
Neuron Activity ◽  
Low Contrast ◽  
Visual Coding ◽  
Mutual Antagonism ◽  
Layer 2 ◽  
Highly Correlated

Vasoactive intestinal peptide-expressing (VIP) interneurons in the cortex regulate feedback inhibition of pyramidal neurons through suppression of somatostatin-expressing (SST) interneurons and, reciprocally, SST neurons inhibit VIP neurons. Although VIP neuron activity in the primary visual cortex (V1) of mouse is highly correlated with locomotion, the relevance of locomotion-related VIP neuron activity to visual coding is not known. Here we show that VIP neurons in mouse V1 respond strongly to low contrast front-to-back motion that is congruent with self-motion during locomotion but are suppressed by other directions and contrasts. VIP and SST neurons have complementary contrast tuning. Layer 2/3 contains a substantially larger population of low contrast preferring pyramidal neurons than deeper layers, and layer 2/3 (but not deeper layer) pyramidal neurons show bias for front-to-back motion specifically at low contrast. Network modeling indicates that VIP-SST mutual antagonism regulates the gain of the cortex to achieve sensitivity to specific weak stimuli without compromising network stability.

Homeostatic plasticity and human primary visual cortex: A tDCS/TMS study

2012 ◽  
Vol 85 (3) ◽  
pp. 379-380
Author(s):  
T. Bocci ◽  
M. Caleo ◽  
L. Briscese ◽  
S. Tognazzi ◽  
E.S. Perego ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Homeostatic Plasticity

Independence and merger of thalamocortical channels within macaque monkey primary visual cortex: Anatomy of interlaminar projections

1994 ◽  
Vol 11 (3) ◽  
pp. 467-489 ◽  
Author(s):  
Takashi Yoshioka ◽  
Jonathan B. Levitt ◽  
Jennifer S. Lund
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Neurons ◽  
Macaque Monkey ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Extrastriate Cortex ◽  
Efferent Neuron ◽  
Neuron Populations ◽  
Efferent Neurons ◽  
Different Response

AbstractAn important issue in understanding the function of primary visual cortex in the macaque monkey is how the several efferent neuron groups projecting to extrastriate cortex acquire their different response properties. To assist our understanding of this issue, we have compared the anatomical distribution of VI intrinsic relays that carry information derived from magno- (M) and parvocellular (P) divisions of the dorsal lateral geniculate nucleus between thalamic recipient neurons and interareal efferent neuron groups within area VI. We used small, iontophoretic injections of biocytin placed in individual cortical laminae of area VI to trace orthograde and retrograde inter- and intralaminar projections. In either the same or adjacent sections, the tissue was reacted for cytochrome oxidase (CO), which provides important landmarks for different efferent neuron populations located in CO rich blobs and CO poor interblobs in laminae ⅔, as well as defining clear boundaries for the populations of efferent neurons in laminae 4A and 4B. This study shows that the interblobs, but not the blobs, receive direct input from thalamic recipient 4C neurons; the interblobs receive relays from mid 4C neurons (believed to receive convergent M and P inputs), while blobs receive indirect inputs from either M or P (or both) pathways through layers 4B (which receives M relays from layer 4Cα) and 4A (which receives P relays directly from the thalamus as well as from layer 4Cβ). The property of orientation selectivity, most prominent in the interblob regions and in layer 4B, may have a common origin from oriented lateral projections made by mid 4C spiny stellate neurons. While layer 4B efferents may emphasize M characteristics and layer 4A efferents emphasize P characteristics, the dendrites of their constituent pyramidal neurons may provide anatomical access to the other channel since both blob and interblob regions in layers ⅔ have anatomical access to M and P driven relays, despite functional differences in the way these properties may be expressed in the two compartments.

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