Neurons In Lateral Geniculate Nucleus Research Articles

The Mitochondrial Permeability Transition Pore Regulates Nitric Oxide-Mediated Apoptosis of Neurons Induced by Target Deprivation

Ablation of mouse occipital cortex induces precisely timed and uniform p53-modulated and Bax-dependent apoptosis of thalamocortical projection neurons in the dorsal lateral geniculate nucleus (LGN) by 7 d after lesion. We tested the hypothesis that this neuronal apoptosis is initiated by oxidative stress and the mitochondrial permeability transition pore (mPTP). Preapoptotic LGN neurons accumulate mitochondria, Zn(2+) and Ca(2+), and generate higher levels of reactive oxygen species (ROS), including superoxide, nitric oxide (NO), and peroxynitrite, than LGN neurons with an intact cortical target. Preapoptosis of LGN neurons is associated with increased formation of protein carbonyls, protein nitration, and protein S-nitrosylation. Genetic deletion of nitric oxide synthase 1 (nos1) and inhibition of NOS1 with nitroindazole protected LGN neurons from apoptosis, revealing NO as a mediator. Putative components of the mPTP are expressed in mouse LGN, including the voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), and cyclophilin D (CyPD). Nitration of CyPD and ANT in LGN mitochondria occurs by 2 d after cortical injury. Chemical cross-linking showed that LGN neuron preapoptosis is associated with formation of CyPD and VDAC oligomers, consistent with mPTP formation. Mice without CyPD are rescued from neuron apoptosis as are mice treated with the mPTP inhibitors TRO-19622 (cholest-4-en-3-one oxime) and TAT-Bcl-X(L)-BH4. Manipulation of the mPTP markedly attenuated the early preapoptotic production of reactive oxygen/nitrogen species in target-deprived neurons. Our results demonstrate in adult mouse brain neurons that the mPTP functions to enhance ROS production and the mPTP and NO trigger apoptosis; thus, the mPTP is a target for neuroprotection in vivo.

C-Fos Immunoreactivity in the Neurons of the Lateral Geniculate Nucleus in Albino Rats by Light Exposure after Dark Rearing

PurposeTo investigate the effect of dark rearing immediately after birth on the maturation of the visual relay neurons in the lateral geniculate nucleus.MethodsFifty neonatal rats were used. Neonates of the control groups were raised under a normal light/dark cycle. Neonates of the experiment groups were dark reared and isolated from light during the entire experimental period, then exposed to the sun light for 1 hour before sacrifice.ResultsIn the control groups, the neurons in the dorsal lateral geniculate nucleus developed normally at each age tested. In the experiment groups, the cytoplasm of the large neurons in the dorsal lateral geniculate nucleus of 2-week-old rats contained small vesicles, and the cytoplasm of the large neurons of 4-week-old rats was converted into a vacuole-like space. Moreover, c-Fos immunoreactivity of the large neurons in the dorsal lateral geniculate nucleus in the experiment groups was significantly increased compared to that of the control groups.ConclusionsWe suppose that the maturation of the neurons in the lateral geniculate nucleus might be influenced by light stimulation during the critical period. Furthermore, c-Fos could be a marker of the functional activity of the visual relay neurons of the lateral geniculate nucleus in albino rats.

Thalamic Gap Junctions Control Local Neuronal Synchrony and Influence Macroscopic Oscillation Amplitude during EEG Alpha Rhythms.

Although EEG alpha (α; 8–13 Hz) rhythms are often considered to reflect an “idling” brain state, numerous studies indicate that they are also related to many aspects of perception. Recently, we outlined a potential cellular substrate by which such aspects of perception might be linked to basic α rhythm mechanisms. This scheme relies on a specialized subset of rhythmically bursting thalamocortical (TC) neurons (high-threshold bursting cells) in the lateral geniculate nucleus (LGN) which are interconnected by gap junctions (GJs). By engaging GABAergic interneurons, that in turn inhibit conventional relay-mode TC neurons, these cells can lead to an effective temporal framing of thalamic relay-mode output. Although the role of GJs is pivotal in this scheme, evidence for their involvement in thalamic α rhythms has thus far mainly derived from experiments in in vitro slice preparations. In addition, direct anatomical evidence of neuronal GJs in the LGN is currently lacking. To address the first of these issues we tested the effects of the GJ inhibitors, carbenoxolone (CBX), and 18β-glycyrrhetinic acid (18β-GA), given directly to the LGN via reverse microdialysis, on spontaneous LGN and EEG α rhythms in behaving cats. We also examined the effect of CBX on α rhythm-related LGN unit activity. Indicative of a role for thalamic GJs in these activities, 18β-GA and CBX reversibly suppressed both LGN and EEG α rhythms, with CBX also decreasing neuronal synchrony. To address the second point, we used electron microscopy to obtain definitive ultrastructural evidence for the presence of GJs between neurons in the cat LGN. As interneurons show no phenotypic evidence of GJ coupling (i.e., dye-coupling and spikelets) we conclude that these GJs must belong to TC neurons. The potential significance of these findings for relating macroscopic changes in α rhythms to basic cellular processes is discussed.

Spike timing and information transmission at retinogeniculate synapses.

This study examines the rules governing the transfer of spikes between the retina and the lateral geniculate nucleus (LGN) with the goal of determining whether the most informative retinal spikes preferentially drive LGN responses and what role spike timing plays in the process. By recording from monosynaptically connected pairs of retinal ganglion cells and LGN neurons in vivo in the cat, we show that relayed spikes are more likely than nonrelayed spikes to be evoked by stimuli that match the receptive fields of the recorded cells and that an interspike interval-based mechanism contributes to the process. Relayed spikes are also more reliable in their timing and number where they often achieve the theoretical limit of minimum variance. As a result, relayed spikes carry more visual information per spike. Based on these results, we conclude that retinogeniculate processing increases sparseness in the neural code by selectively relaying the highest fidelity spikes to the visual cortex.

The Episodic Nature of Spike Trains in the Early Visual Pathway

An understanding of the neural code in a given visual area is often confounded by the immense complexity of visual stimuli combined with the number of possible meaningful patterns that comprise the response spike train. In the lateral geniculate nucleus (LGN), visual stimulation generates spike trains comprised of short spiking episodes ("events") separated by relatively long intervals of silence, which establishes a basis for in-depth analysis of the neural code. By studying this event structure in both artificial and natural visual stimulus contexts and at different contrasts, we are able to describe the dependence of event structure on stimulus class and discern which aspects generalize. We find that the event structure on coarse time scales is robust across stimulus and contrast and can be explained by receptive field processing. However, the relationship between the stimulus and fine-time-scale features of events is less straightforward, partially due to a significant amount of trial-to-trial variability. A new measure called "label information" identifies structural elements of events that can contain ≤30% more information in the context of natural movies compared with what is available from the overall event timing. The first interspike interval of an event most robustly conveys additional information about the stimulus and is somewhat more informative than the event spike count and much more informative than the presence of bursts. Nearly every event is preserved across contrast despite changes in their fine-time-scale features, suggesting that--at least on a coarse level--the stimulus selectivity of LGN neurons is contrast invariant. Event-based analysis thus casts previously studied elements of LGN coding such as contrast adaptation and receptive field processing in a new light and leads to broad conclusions about the composition of the LGN neuronal code.

Sensitivity of V1 Neurons to Direction of Spectral Motion

Motion-in-depth causes changes in the size of retinal images in addition to producing optic flow patterns. A previous psychophysical study showed that human subjects can perceive expansion motion in texture stimuli that exhibit increases in the scale of image elements but no consistent optic flow pattern. The neural mechanisms by which the scale-change information is processed remain unknown. Here, we measured the responses of cat V1 and the lateral geniculate nucleus (LGN) neurons to a sequence of random images whose spatial frequency spectrum changed over time (i.e., average spatial scale expanded or contracted). We found that V1 neurons exhibit direction sensitivity to scale changes, with more cells preferring expansion than contraction motion. This direction sensitivity can be partly accounted for by the spectrotemporal receptive field of V1 neurons. Comparison of the direction sensitivity between V1 and LGN neurons showed that the sensitivity in V1 may originate from LGN neurons. Repetitive stimulation with expansion or contraction motion can decrease the sensitivity to the adapted direction in V1, and the effect can be transferred interocularly, suggesting that intracortical connections may be critically involved in the adaptation. Together, our results suggest that direction sensitivity to scale change in V1 may contribute to motion-in-depth processing.

Effect of retinal phototoxicity induced by blue light exposure on the response properties of neurons of the lateral geniculate nucleus of the rat

Abstract Purpose Exposure to bright blue light causes photochemical damage of rodent’s retina via the apoptotic pathway involved in retinitis pigmentosa and age‐related macular degeneration. This photochemical retinal damage occurs with a several different types of morphology and the severity of retinal damage induced by light has great variation among retinal regions. Rather than a mere decrease of the visual response blue light phototoxicity involves important changes on image processing at the retina. Higher visual areas, such as lateral geniculate nucleus (LGN) must adapt their physiology to the new situation. In the present work we will study the changes, and their temporal course, of the response of LGN neurons provoked by acute exposure to bright blue light. Methods We will stimulate the retina of Wistar rats at 7 different wavelengths and we will record extracellular multiunit activity of these neurons on three different groups: without exposure to bright light (control group), rats exposed to bright (5000 lux) blue light for 72 hours (exposed group) and rats exposed and let a week under control conditions (recovery group). Results Exposed group showed different profiles of the response parameters measured at the different stimulating wavelengths. These profiles were similar between control and recovery groups. Conclusion Data shows that retinal damage induced by blue light has a great impact on LGN physiology and that plasticity changes must occur at this area to adapt to the new situation.

A generalized linear model of the impact of direct and indirect inputs to the lateral geniculate nucleus

Relay neurons in the lateral geniculate nucleus (LGN) receive direct visual input predominantly from a single retinal ganglion cell (RGC), in addition to indirect input from other sources including interneurons, thalamic reticular nucleus (TRN), and the visual cortex. To address the extent of influence of these indirect sources on the response properties of the LGN neurons, we fit a Generalized Linear Model (GLM) to the spike responses of cat LGN neurons driven by spatially homogeneous spots that were rapidly modulated by a pseudorandom luminance sequence. Several spot sizes were used to probe the spatial extent of the indirect visual effects. Our extracellular recordings captured both the LGN spikes and the incoming RGC input (S potentials), allowing us to divide the inputs to the GLM into two categories: the direct RGC input and the indirect input to which we have access through the luminance of the visual stimulus. For spots no larger than the receptive field center, the effect of the indirect input is negligible, while for larger spots its effect can, on average, account for 5% of the variance of the data and for as much as 25% in some cells. The polarity of the indirect visual influence is opposite to that of the linear receptive field of the neurons. We conclude that the indirect source of response modulation of the LGN relay neurons arises from inhibitory sources, compatible with thalamic interneurons or TRN.

Dendrite plasticity in the lateral geniculate nucleus in primate glaucoma

Neural degeneration in glaucoma involves retinal ganglion cells and neurons of their major target, the lateral geniculate nucleus (LGN). Dendrites of relay LGN neurons projecting to the visual cortex were studied by immunocytochemical and quantitative Sholl analysis in combination with confocal microscopy and 3D-morphometry. In non-human adult primate glaucoma, relay LGN neurons showed reduced dendrite complexity and length, and these changes were modified by NMDA receptor blockade. Dendrite plasticity of LGN relay neurons in adult primate glaucoma has implications for potential disease modification by treatment interventions.

Linear and Nonlinear Contributions to the Visual Sensitivity of Neurons in Primate Lateral Geniculate Nucleus

Several parallel pathways convey retinal signals to the visual cortex of primates. The signals of the parvocellular (P) and magnocellular (M) pathways are well characterized; the properties of other rarely encountered cell types are distinctive in many ways, but it is not clear that they can provide signals with the same fidelity. Here we study this by characterizing the temporal receptive field of neurons in the lateral geniculate nucleus of anesthetized marmosets. For each neuron, we measured the response to a flickering uniform field, and, from this, estimated the linear and nonlinear receptive fields using spike-triggered average (STA) and spike-triggered covariance (STC) analyses. As expected the response of most P-cells was dominated by the STA, but the response of most M-cells required additional nonlinear components, and these usually acted to suppress cell responses. The STC analysis showed stronger suppressive axes in suppressed-by-contrast cells, and both suppressive and excitatory axes in on-off cells. Together, the STA and the STC analyses form a model of the temporal response to a large uniform field: under this model, the information that was provided by suppressed-by-contrast cells or on-off cells approached that provided by the P- and M-cells. However, whereas P- and M-cells provided more information about luminance, the nonlinear cells provided more information about the contrast energy. This suggests that the nonlinear cells provide complimentary signals to those of P- and M-cells, with reasonably high fidelity, and may play an important role in normal visual processing.

Eigenvalue distributions for a class of covariance matrices with application to Bienenstock-Cooper-Munro neurons under noisy conditions

We analyze the effects of noise correlations in the input to, or among, Bienenstock-Cooper-Munro neurons using the Wigner semicircular law to construct random, positive-definite symmetric correlation matrices and compute their eigenvalue distributions. In the finite dimensional case, we compare our analytic results with numerical simulations and show the effects of correlations on the lifetimes of synaptic strengths in various visual environments. These correlations can be due either to correlations in the noise from the input lateral geniculate nucleus neurons, or correlations in the variability of lateral connections in a network of neurons. In particular, we find that for fixed dimensionality, a large noise variance can give rise to long lifetimes of synaptic strengths. This may be of physiological significance.

Spatial organization of L- and M-cone inputs to neurons in the macaque lateral geniculate nucleus

Spatial organization of L- and M-cone inputs to neurons in the macaque lateral geniculate nucleus

Organization of Concentric Double-Opponent Receptive Fields in the Primary Visual Cortex by Using Independent Component Analysis

Event Abstract Back to Event Organization of Concentric Double-Opponent Receptive Fields in the Primary Visual Cortex by Using Independent Component Analysis Yasunobu Igarashi1*, Takaaki Aoki2, Rui Kimura3 and Shin Ishii4 1 National Center for Neurology and Psychiatry, Japan 2 Nara Institute of Science and Technology, Japan 3 RIKEN Brain Science Institute, Japan 4 Kyoto University, Japan Previous experimental studies showed that neurons in the primary visual cort ex (V1) have four firing properties to represent visual information. Four fi ring properties are named luminance gabor, oriented double-opponent, concent ric single-opponent, and concentric double-opponent receptive fields. Previo us theoretical studies demonstrated that redundancy compressions like indepe ndent component analysis (ICA) and sparse coding can derive basic functions corresponding to luminance gabor and oriented double-opponent receptive fiel ds from natural images. On the other hand, emergences of basic functions cor responding to two concentric receptive fields via redundancy compression of natural images have not been reported. In this study, we propose a low pass filtering function of neurons in lateral geniculate nucleus (LGN) is importa nt to derive concentric basic functions in addition to redundancy compressio n. Neurons in LGN project their axons to neurons in V1. Therefore, it is pla usible that LGN contributes to form receptive fields of V1. We show that the concentric double-opponent basis function can be obtained by applying the l ow pass filtering and Fast ICA to natural images in a computer simulation. H owever, the concentric single-opponent basis function cannot be not obtained . This reason is thought that the concentric double-opponent basis function functionally includes the concentric single-opponent basis function from the view point of redundancy compression. We also clarify how shapes of basic f unctions depend on ones of learning images, and how color components of basi c functions depend on a color distribution of learning images. Conference: Neuroinformatics 2010 , Kobe, Japan, 30 Aug - 1 Sep, 2010. Presentation Type: Poster Presentation Topic: Computational Neuroscience Citation: Igarashi Y, Aoki T, Kimura R and Ishii S (2010). Organization of Concentric Double-Opponent Receptive Fields in the Primary Visual Cortex by Using Independent Component Analysis. Front. Neurosci. Conference Abstract: Neuroinformatics 2010 . doi: 10.3389/conf.fnins.2010.13.00055 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Jun 2010; Published Online: 11 Jun 2010. * Correspondence: Yasunobu Igarashi, National Center for Neurology and Psychiatry, Tokyo, Japan, igalab1@j-adni.org Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Yasunobu Igarashi Takaaki Aoki Rui Kimura Shin Ishii Google Yasunobu Igarashi Takaaki Aoki Rui Kimura Shin Ishii Google Scholar Yasunobu Igarashi Takaaki Aoki Rui Kimura Shin Ishii PubMed Yasunobu Igarashi Takaaki Aoki Rui Kimura Shin Ishii Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Temporal dynamics of orientation and spatial frequency tuning of neurons in the cat lateral geniculate nucleus

Temporal dynamics of orientation and spatial frequency tuning of neurons in the cat lateral geniculate nucleus

The role of inhibition in formatting visual information in the retina and LGN

The role of inhibition in formatting visual information in the retina and LGN

Burst-Time-Dependent Plasticity Robustly Guides ON/OFF Segregation in the Lateral Geniculate Nucleus

Spontaneous retinal activity (known as “waves”) remodels synaptic connectivity to the lateral geniculate nucleus (LGN) during development. Analysis of retinal waves recorded with multielectrode arrays in mouse suggested that a cue for the segregation of functionally distinct (ON and OFF) retinal ganglion cells (RGCs) in the LGN may be a desynchronization in their firing, where ON cells precede OFF cells by one second. Using the recorded retinal waves as input, with two different modeling approaches we explore timing-based plasticity rules for the evolution of synaptic weights to identify key features underlying ON/OFF segregation. First, we analytically derive a linear model for the evolution of ON and OFF weights, to understand how synaptic plasticity rules extract input firing properties to guide segregation. Second, we simulate postsynaptic activity with a nonlinear integrate-and-fire model to compare findings with the linear model. We find that spike-time-dependent plasticity, which modifies synaptic weights based on millisecond-long timing and order of pre- and postsynaptic spikes, fails to segregate ON and OFF retinal inputs in the absence of normalization. Implementing homeostatic mechanisms results in segregation, but only with carefully-tuned parameters. Furthermore, extending spike integration timescales to match the second-long input correlation timescales always leads to ON segregation because ON cells fire before OFF cells. We show that burst-time-dependent plasticity can robustly guide ON/OFF segregation in the LGN without normalization, by integrating pre- and postsynaptic bursts irrespective of their firing order and over second-long timescales. We predict that an LGN neuron will become ON- or OFF-responsive based on a local competition of the firing patterns of neighboring RGCs connecting to it. Finally, we demonstrate consistency with ON/OFF segregation in ferret, despite differences in the firing properties of retinal waves. Our model suggests that diverse input statistics of retinal waves can be robustly interpreted by a burst-based rule, which underlies retinogeniculate plasticity across different species.

Cholinergic modulation of non- N-methyl- d-aspartic acid glutamatergic transmission in the chick ventral lateral geniculate nucleus

Neurotransmission between glutamatergic terminals of retinal ganglion cells and principal neurons of the ventral lateral geniculate nucleus (LGNv) was examined with patch clamp recordings in chick brain slices during electrical stimulation of the optic tract. Since muscarinic and nicotinic receptors are present in high densities in LGNv, the present study examined possible roles of both receptors in modulating retinogeniculate transmission. During whole-cell recordings from LGNv neurons, acetylcholine (ACh, 100 μM) caused an initial increase in amplitudes of optic tract-evoked non- N-methyl- d-aspartic acid (NMDA) glutamatergic postsynaptic currents (PSCs). This increase was unchanged when 1 μM atropine was present, indicating that this initial enhancement of PSCs was due entirely to activation of nicotinic receptors. However, during washout of ACh the amplitudes of evoked PSCs became significantly decreased by 40.4±5.0% for several minutes before recovering to their original amplitudes, an effect blocked by 1 μM atropine. Exogenously applied muscarine (10 μM) markedly depressed optic tract-evoked PSCs, and this decrease in amplitude was blocked by atropine. In a second set of experiments, we examined effects of releasing endogenous ACh prior to optic tract stimulation. This was accomplished by stimulation of the lateral portion of LGNv via a separate conditioning electrode. Following a brief train of low intensity conditioning stimuli, non-NMDA glutamatergic PSCs evoked by optic tract stimulation were potentiated. However, at higher conditioning stimulus intensities the PSCs were markedly decreased compared with control, and this decrease was partially blocked by atropine (1 μM). Neither ACh nor muscarine altered amplitudes of PSCs elicited by exogenously applied glutamate. Muscarine significantly reduced the frequency but not the amplitudes of miniature PSCs, consistent with a presynaptic location for muscarinic receptors mediating these effects. Thus while activation of nicotinic receptors potentiates retinogeniculate transmission, activation of muscarinic receptors mediates depression of transmission, demonstrating a complex cholinergic modulation of sensory information in LGNv.

Effect of correlated lateral geniculate nucleus firing rates on predictions for monocular eye closure versus monocular retinal inactivation

Monocular deprivation experiments can be used to distinguish between different ideas concerning properties of cortical synaptic plasticity. Monocular deprivation by lid suture causes a rapid disconnection of the deprived eye connected to cortical neurons whereas total inactivation of the deprived eye produces much less of an ocular dominance shift. In order to understand these results one needs to know how lid suture and retinal inactivation affect neurons in the lateral geniculate nucleus (LGN) that provide the cortical input. Recent experimental results by Linden showed that monocular lid suture and monocular inactivation do not change the mean firing rates of LGN neurons but that lid suture reduces correlations between adjacent neurons whereas monocular inactivation leads to correlated firing. These, somewhat surprising, results contradict assumptions that have been made to explain the outcomes of different monocular deprivation protocols. Based on these experimental results we modify our assumptions about inputs to cortex during different deprivation protocols and show their implications when combined with different cortical plasticity rules. Using theoretical analysis, random matrix theory and simulations we show that high levels of correlations reduce the ocular dominance shift in learning rules that depend on homosynaptic depression (i.e., Bienenstock-Cooper-Munro type rules), consistent with experimental results, but have the opposite effect in rules that depend on heterosynaptic depression (i.e., Hebbian/principal component analysis type rules).

The effect of orientation adaptation on responses of lateral geniculate nucleus neurons with high orientation bias in cats

Adaptation to stimulus orientation is assumed to have a cortical basis, but few studies have addressed whether it affects the activity of subcortical neurons. Using single-unit recording, we studied the effects of orientation adaptation on the responses of lateral geniculate nucleus (LGN) neurons with high orientation bias (OB) in anesthetized and paralyzed cats. Following adaptation to one stimulus orientation, the response at the adapting orientation was decreased, and the preferred orientation was shifted away from the adapting orientation. This phenomenon was similar to the effects observed for orientation adaptation in the primary visual cortex (V1), and was obvious when the adapting orientation was at an appropriate location relative to the original preferred orientation. Moreover, when the V1 was inactivated, the response at the adapting orientation was also decreased but the preferred orientation did not show a systematic shift after orientation adaptation in LGN. This result indicates that cortical feedback contributes to the effect of orientation adaptation on LGN neurons, which have a high OB. These data provide an example of how the corticothalamic loop modulates the processing of visual information, and suggest that the LGN is not only a simply passive relay but also a modulator of visual information.

Selective potentiation of crossed vs. uncrossed inputs from lateral geniculate nucleus to visual cortex by the basal forebrain: Potential facilitation of rodent binocularity

Cholinergic projections originating in the basal forebrain (BF) play important roles in the heterosynaptic facilitation of synaptic strength in various sensory cortices, including the primary visual cortex (V1). Here, using urethane-anesthetized rats, we find that pairing burst stimulation of the BF with single pulse stimulation of the lateral geniculate nucleus (LGN) does not consistently increase field postsynaptic potentials (fPSPs) in V1 elicited by ipsilateral LGN stimulation. However, longer latency fPSPs recorded in V1 in response to stimulation of the contralateral LGN, reflecting crossed, polysynaptic inputs, show significant potentiation when paired with preceding BF stimulation. This synaptic enhancement requires relatively short time intervals between paired BF burst and LGN pulse stimulation (40 ms) and is abolished by systemic or local V1 muscarinic receptor blockade (scopolamine), while systemic nicotinic receptor blockade (mecamylamine) is ineffective. Together, these data provide evidence for a differential capacity for cholinergic/muscarinic-dependent plasticity induction among different signals in V1, with inputs reaching V1 from the contralateral LGN exhibiting potentiation in the face of stable strength in ipsilateral LGN-V1 projections. This preferential readiness for potentiation in crossed fiber systems could serve to amplify binocular responses in V1 elicited by synchronized excitation of ipsi- and contralateral LGN neurons.