Contralateral Visual Cortex Research Articles

Bilateral connections from the amygdala to extrastriate visual cortex in the marmoset monkey.

It is known that the primate amygdala forms projections to many areas of the ipsilateral cortex, but the extent to which it forms connections with the contralateral visual cortex remains less understood. Based on retrograde tracer injections in marmoset monkeys, we report that the amygdala forms widespread projections to the ipsilateral extrastriate cortex, including V1 and areas in both the dorsal (MT, V4T, V3a, 19M, and PG/PFG) and the ventral (VLP and TEO) streams. In addition, contralateral projections were found to target each of the extrastriate areas, but not V1. In both hemispheres, the tracer-labeled neurons were exclusively located in the basolateral nuclear complex. The number of labeled neurons in the contralateral amygdala was small relative to the ipsilateral connection (1.2% to 5.8%). The percentage of contralateral connections increased progressively with hierarchical level. An injection in the corpus callosum demonstrated that at least some of the amygdalo-cortical connections cross through this fiber tract, in addition to the previously documented path through the anterior commissure. Our results expand knowledge of the amygdalofugal projections to the extrastriate cortex, while also revealing pathways through which visual stimuli conveying affective content can directly influence early stages of neural processing in the contralateral visual field.

A novel interface for cortical columnar neuromodulation with multipoint infrared neural stimulation

Cutting edge advances in electrical visual cortical prosthetics have evoked perception of shapes, motion, and letters in the blind. Here, we present an alternative optical approach using pulsed infrared neural stimulation. To interface with dense arrays of cortical columns with submillimeter spatial precision, both linear array and 100-fiber bundle array optical fiber interfaces were devised. We deliver infrared stimulation through these arrays in anesthetized cat visual cortex and monitor effects by optical imaging in contralateral visual cortex. Infrared neural stimulation modulation of response to ongoing visual oriented gratings produce enhanced responses in orientation-matched domains and suppressed responses in non-matched domains, consistent with a known higher order integration mediated by callosal inputs. Controls include dynamically applied speeds, directions and patterns of multipoint stimulation. This provides groundwork for a distinct type of prosthetic targeted to maps of visual cortical columns.

Combined therapy of bilateral transcranial direct current stimulation and ocular occlusion improves visual function in adults with amblyopia, a randomized pilot study.

Amblyopia is the interocular visual acuity difference of two lines or more with the best correction in both eyes. It is treated with ocular occlusion therapy, but its success depends on neuroplasticity, and thus is effective in children but not adults. Transcranial Direct Current Stimulation (tDCS) is suggested to increase neuroplasticity. To determine if combined intervention of bilateral tDCS and ocular occlusion improves visual function in adults with amblyopia. A double-blind randomized, controlled pilot trial was conducted in 10 volunteers with amblyopia. While applying ocular occlusion and performing a reading task, participants received bilateral tDCS (n = 5) or sham stimulation (n = 5), with the anodal tDCS electrode in the contralateral visual cortex and the cathodal in the ipsilateral visual cortex in relation to the amblyopic eye. Visual function (through visual acuity, stereopsis, and contrast sensitivity tests) and visual evoked potential (with checkerboard pattern stimuli presentation) were evaluated immediately after. A total of 30 min after treatment with bilateral tDCS, visual acuity improved by 0.16 (± 0.025) LogMAR in the treatment group compared with no improvement (-0.02 ± 0.02) in five controls (p = 0.0079), along with a significant increase in the amplitude of visual evoked potentials of the amblyopic eye response (p = 0.0286). No significant changes were observed in stereopsis and contrast sensitivity. No volunteer reported any harm derived from the intervention. Our study is the first to combine anodal and cathodal tDCS for the treatment of amblyopia, showing transient improved visual acuity in amblyopic adults.

Visual-cortical enhancement by acoustic distractors: The effects of endogenous spatial attention and visual working memory load

Past work has shown that when a peripheral sound captures our attention, it activates the contralateral visual cortex as revealed by an event-related potential component labelled the auditory-evoked contralateral occipital positivity (ACOP). This cross-modal activation of the visual cortex has been observed even when the sounds were not relevant to the ongoing task (visual or auditory), suggesting that peripheral sounds automatically activate the visual cortex. However, it is unclear whether top-down factors such as visual working memory (VWM) load and endogenous attention, which modulate the impact of task-irrelevant information, may modulate this spatially-specific component. Here, we asked participants to perform a lateralized VWM task (change detection), whose performance is supported by both endogenous spatial attention and VWM storage. A peripheral sound that was unrelated to the ongoing task was delivered during the retention interval. The amplitude of sound-elicited ACOP was analyzed as a function of the spatial correspondence with the cued hemifield, and of the memory array set-size. The typical ACOP modulation was observed over parieto-occipital sites in the 280–500 ms time window after sound onset. Its amplitude was not affected by VWM load but was modulated when the location of the sound did not correspond to the hemifield (right or left) that was cued for the change detection task. Our results suggest that sound-elicited activation of visual cortices, as reflected in the ACOP modulation, is unaffected by visual working memory load. However, endogenous spatial attention affects the ACOP, challenging the hypothesis that it reflects an automatic process.

Inefficient white matter activity in Schizophrenia evoked during intra and inter-hemispheric communication

Intensive cognitive tasks induce inefficient regional and network responses in schizophrenia (SCZ). fMRI-based studies have naturally focused on gray matter, but appropriately titrated visuo-motor integration tasks reliably activate inter- and intra-hemispheric white matter pathways. Such tasks can assess network inefficiency without demanding intensive cognitive effort. Here, we provide the first application of this framework to the study of white matter functional responses in SCZ. Event-related fMRI data were acquired from 28 patients (nine females, mean age 43.3, ±11.7) and 28 age- and gender-comparable controls (nine females, mean age 42.1 ± 10.1), using the Poffenberger paradigm, a rapid visual detection task used to induce intra- (ipsi-lateral visual and motor cortex) or inter-hemispheric (contra-lateral visual and motor cortex) transfer. fMRI data were pre- and post-processed to reliably isolate activations in white matter, using probabilistic tractography-based white matter tracts. For intra- and inter-hemispheric transfer conditions, SCZ evinced hyper-activations in longitudinal and transverse white matter tracts, with hyper-activation in sub-regions of the corpus callosum primarily observed during inter-hemispheric transfer. Evidence for the functional inefficiency of white matter was observed in conjunction with small (~50 ms) but significant increases in response times. Functional inefficiencies in SCZ are (1) observable in white matter, with the degree of inefficiency contextually related to task-conditions, and (2) are evoked by simple detection tasks without intense cognitive processing. These cumulative results while expanding our understanding of this dys-connection syndrome, also extend the search of biomarkers beyond the traditional realm of fMRI studies of gray matter.

Isolating the Neural Substrates of Visually Guided Attention Orienting in Humans.

The neural processes that enable healthy humans to orient attention to sudden visual events are poorly understood because they are tightly intertwined with purely sensory processes. Here we isolated visually guided orienting activity from sensory activity using event-related potentials (ERPs). By recording ERPs to a lateral stimulus and comparing waveforms obtained under conditions of attention and inattention, we identified an early positive deflection over the ipsilateral visual cortex that was associated with the covert orienting of visual attention to the stimulus. Across five experiments with male and female adult participants, this ipsilateral visual orienting activity (VOA) could be distinguished from purely sensory-evoked activity and from other top-down spatial attention effects. The VOA was linked with behavioral measures of orienting, being significantly larger when the stimulus was detected rapidly than when it was detected more slowly, and its presence was independent of saccadic eye movements toward the targets. The VOA appears to be a specific neural index of the visually guided orienting of attention to a stimulus that appears abruptly in an otherwise uncluttered visual field.SIGNIFICANCE STATEMENT The study of visual attention orienting has been an important impetus for the field of cognitive neuroscience. Seminal reaction-time studies demonstrated that a suddenly appearing visual stimulus attracts attention involuntarily, but the neural processes associated with visually guided attention orienting have been difficult to isolate because they are intertwined with sensory processes that trigger the orienting. Here, we disentangled orienting activity from sensory activity using scalp recordings of event-related electrical activity in the human brain. A specific neural index of visually guided attention orienting was identified. Surprisingly, whereas peripheral sensory stimulation is processed initially and predominantly by the contralateral visual cortex, this electrophysiological index of visual orienting was recorded over the cerebral hemisphere that was ipsilateral to the attention-capturing stimulus.

NGF Eye Administration Recovers the TrkB and Glutamate/GABA Marker Deficit in the Adult Visual Cortex Following Optic Nerve Crush.

Eye-drop recombinant human nerve growth factor (ed-rhNGF) has proved to recover the retina and optic nerve damage in animal models, including the unilateral optic nerve crush (ONC), and to improve visual acuity in humans. These data, associated with evidence that ed-rhNGF stimulates the brain derived neurotrophic factor (BDNF) in retina and cortex, suggests that NGF might exert retino-fugal effects by affecting BDNF and its receptor TrkB. To address these questions, their expression and relationship with the GABAergic and glutamatergic transmission markers, GAD65 and GAD67, vesicular inhibitory amino acid transporter (VGAT), and vesicular glutamate transporters 1 and 2 (VGLUT-1 and VGLUT-2) were investigated in adult ONC rats contralateral and ipsilateral visual cortex (VCx). Ed-rhNGF recovers the ONC-induced alteration of GABAergic and glutamatergic markers in contralateral VCx, induces an upregulation of TrkB, which is positively correlated with BDNF precursor (proBDNF) decrease in both VCx sides, and strongly enhances TrkB+ cell soma and neuronal endings surrounded by GAD65 immuno-reactive afferents. These findings contribute to enlarging the knowledge on the mechanism of actions and cellular targets of exogenously administrated NGF, and suggest that ed-rhNGF might act by potentiating the activity-dependent TrkB expression in GAD+ cells in VCx following retina damage and/or ONC.

Sensory Recruitment Revisited: Ipsilateral V1 Involved in Visual Working Memory.

The "sensory recruitment hypothesis" posits an essential role of sensory cortices in working memory, beyond the well-accepted frontoparietal areas. Yet, this hypothesis has recently been challenged. In the present study, participants performed a delayed orientation recall task while high-spatial-resolution 3T functional magnetic resonance imaging (fMRI) signals were measured in posterior cortices. A multivariate inverted encoding model approach was used to decode remembered orientations based on blood oxygen level-dependent fMRI signals from visual cortices during the delay period. We found that not only did activity in the contralateral primary visual cortex (V1) retain high-fidelity representations of the visual stimuli, but activity in the ipsilateral V1 also contained such orientation tuning. Moreover, although the encoded tuning was faded in the contralateral V1 during the late delay period, tuning information in the ipsilateral V1 remained sustained. Furthermore, the ipsilateral representation was presented in secondary visual cortex (V2) as well, but not in other higher-level visual areas. These results thus supported the sensory recruitment hypothesis and extended it to the ipsilateral sensory areas, which indicated the distributed involvement of visual areas in visual working memory.

Aberrant visual population receptive fields in human albinism.

Retinotopic organization is a fundamental feature of visual cortex thought to play a vital role in encoding spatial information. One important aspect of normal retinotopy is the representation of the right and left hemifields in contralateral visual cortex. However, in human albinism, many temporal retinal afferents decussate aberrantly at the optic chiasm resulting in partially superimposed representations of opposite hemifields in each hemisphere of visual cortex. Previous functional magnetic resonance imaging (fMRI) studies in human albinism suggest that the right and left hemifield representations are superimposed in a mirror-symmetric manner. This should produce imaging voxels which respond to two separate locations mirrored across the vertical meridian. However, it is not yet clear how retino-cortical miswiring in albinism manifests at the level of single voxel population receptive fields (pRFs). Here, we used pRF modeling to fit both single and dual pRF models to the visual responses of voxels in visual areas V1 to V3 of five subjects with albinism. We found that subjects with albinism (but not controls) have sizable clusters of voxels with unequivocal dual pRFs consistently corresponding to, but not fully coextensive with, regions of hemifield overlap. These dual pRFs were typically positioned at locations roughly mirrored across the vertical meridian and were uniquely clustered within a portion of the visual field for each subject.

Experience-dependent structural plasticity in the adult brain: How the learning brain grows

Volumetric magnetic resonance imaging studies have shown that intense learning can be associated with grey matter volume increases in the adult brain. The underlying mechanisms are poorly understood. Here we used monocular deprivation in rats to analyze the mechanisms underlying use-dependent grey matter increases. Optometry for quantification of visual acuity was combined with volumetric magnetic resonance imaging and microscopic techniques in longitudinal and cross-sectional studies. We found an increased spatial vision of the open eye which was associated with a transient increase in the volumes of the contralateral visual and lateral entorhinal cortex. In these brain areas dendrites of neurons elongated, and there was a strong increase in the number of spines, the targets of synapses, which was followed by spine maturation and partial pruning. Astrocytes displayed a transient pronounced swelling and underwent a reorganization of their processes. The use-dependent increase in grey matter corresponded predominantly to the swelling of the astrocytes. Experience-dependent increase in brain grey matter volume indicates a gain of structure plasticity with both synaptic and astrocyte remodeling.

Excitation of the Pre-frontal and Primary Visual Cortex in Response to Transcorneal Electrical Stimulation in Retinal Degeneration Mice

Retinal degeneration (rd) is one of the leading causes of blindness in the modern world today. Various strategies including electrical stimulation are being researched for the restoration of partial or complete vision. Previous studies have demonstrated that the effectiveness of electrical stimulation in somatosensory, frontal and visual cortices is dependent on stimulation parameters including stimulation frequency and brain states. The aim of the study is to investigate the effect of applying a prolonged electrical stimulation on the eye of rd mice with various stimulation frequencies, in awake and anesthetized brain states. We recorded spontaneous electrocorticogram (ECoG) neural activity in prefrontal cortex and primary visual cortex in a mouse model of retinitis pigmentosa (RP) after prolonged (5-day) transcorneal electrical stimulation (pTES) at various frequencies (2, 10, and 20 Hz). We evaluated the absolute power and coherence of spontaneous ECoG neural activities in contralateral primary visual cortex (contra Vcx) and contralateral pre-frontal cortex (contra PFx). Under the awake state, the absolute power of theta, alpha and beta oscillations in contra Vcx, at 10 Hz stimulation, was higher than in the sham group. Under the anesthetized state, the absolute power of medium-, high-, and ultra-high gamma oscillations in the contra PFx, at 2 Hz stimulation, was higher than in the sham group. We also observed that the ultra-high gamma band coherence in contra Vcx-contra PFx was higher than in the sham group, with both 10 and 20 Hz stimulation frequencies. Our results showed that pTES modulates rd brain oscillations in a frequency and brain state-dependent manner. These findings suggest that non-invasive electrical stimulation of retina changes patterns of neural oscillations in the brain circuitry. This also provides a starting point for investigating the sustained effect of electrical stimulation of the retina to brain activities.

The contribution of phonological information to visual word recognition: Evidence from Chinese phonetic radicals

Lateralization is a critical characteristic of language production and also plays a role in visual word recognition. However, the neural mechanisms underlying the interactions between visual input and spoken word representations are still unclear. We investigated the contribution of sub-lexical phonological information in visual word processing by exploiting the fact that Chinese characters can contain phonetic radicals in either the left or right half of the character. FMRI data were collected while 39 Chinese participants read words in search of target color words. On the basis of whole-brain analysis and three laterality analyses of regions of interest, we argue that visual information from centrally presented Chinese characters is split in the fovea and projected to the contralateral visual cortex, from which phonological information can be extracted rapidly if the character contains a phonetic radical. Extra activation, suggestive of more effortful processing, is observed when the phonetic radical is situated in the left half of the character and therefore initially sent to the visual cortex in the right hemisphere that is less specialized for language processing. Our results are in line with the proposal that phonological information helps written word processing by means of top-down feedback.

Polysialylated – neural cell adhesion molecule (PSA-NCAM) promotes recovery of vision after the critical period

Vision loss has long since been considered irreversible after a critical period; however, there is potential to restore limited vision, even in adulthood. This phenomenon is particularly pronounced following complete loss of vision in the dominant eye. Adult neural cell adhesion molecule (NCAM) knockout mice have an age-related impairment of visual acuity. The underlying cause of early deterioration in visual function remains unknown. Polysialylated (PSA) NCAM is involved in different forms of neural plasticity in the adult brain, raising the possibility that NCAM plays a role in the plasticity of the visual cortex, and therefore, in visual ability. Here, we examined whether PSA-NCAM is required for visual cortical plasticity in adult C57Bl/6J mice following deafferentation and long-term monocular deprivation. Our results show that elevated PSA in the contralateral visual cortex of the reopened eye is accompanied by changes in other markers of neural plasticity: increased brain-derived neurotrophic factor (BDNF) levels and degradation of perineuronal nets (PNNs). The removal of PSA-NCAM in the visual cortex of these mice reduced BDNF expression, decreased PNN degradation, and resulted in impaired recovery of visual acuity after optic nerve transection and chronic monocular deprivation. Collectively, our results demonstrate that PSA-NCAM is necessary for the reactivation of visual cortical plasticity and recovery of visual function in adult mice. It also offers a potential molecular target for the therapeutic treatment of cortically based visual impairments.

Spatially congruent negative BOLD responses to different stimuli do not summate in visual cortex

The negative BOLD response (NBR) is a prevalent feature of brain activity during sensory and cognitive tasks. It is thought to reflect suppression or deactivation of cortical areas unrequired for task performance, but much remains to be understood regarding its response properties and generative pathways. Here we study a unique property of sensory cortex NBR that most distinguishes it from positive BOLD responses (PBR), its appearance in a single location due to different stimuli. We investigate whether such NBR are additive, as a means of studying whether stimulus driven NBR arise via a single or multiple pathways.During fMRI, subject’s passively viewed separate checkerboard stimulation of the foveal and middle-eccentricity areas of the left visual field and a third condition that stimulated both areas concurrently. PBR was observed in the contralateral primary visual cortex and NBR was seen throughout the ipsilateral cortex as well as in contralateral regions superior and anterior to the PBR. Strong spatial overlap of NBRs to all three conditions was observed.We found that neither PBR nor NBR were additive. NBR amplitudes to combined stimuli were equal to those of the strongest (foveal) stimulus alone, despite the mid-eccentricity stimulus inducing substantial NBR on its own. The lack of summation of NBRs, both in the same and opposite hemispheres to the PBR, suggests that they arise from a single pathway. Our findings suggest that although individual stimuli each exert a separate inhibitory effect on non-stimulated regions, once in combination these effects operate as a binary system. Deactivation of a given visual area is driven by a single signal, representing only the largest of the contributing sources.

Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice.

PurposeTo determine how visual cortex plasticity changes after monocular deprivation (MD) in mice and whether conventional protein kinase C gamma (cPKCγ) plays a role in visual cortex plasticity.MethodscPKCγ membrane translocation levels were quantified by using immunoblotting to explore the effects of MD on cPKCγ activation. Electrophysiology was used to record field excitatory postsynaptic potential (fEPSP) amplitude with the goal of observing changes in visual cortex plasticity after MD. Immunoblotting was also used to determine the phosphorylation levels of GluR1 at Ser831. Light transmission was analyzed using electroretinography to examine the effects of MD and cPKCγ on mouse retinal function.ResultsMembrane translocation levels of cPKCγ significantly increased in the contralateral visual cortex of MD mice compared to wild-type (WT) mice (P < 0.001). In the contralateral visual cortex, long-term potentiation (LTP) and the phosphorylation levels of GluR1 at Ser 831 were increased in cPKCγ+/+ mice after MD. Interestingly, these levels could be downregulated by cPKCγ knockout compared to cPKCγ+/++MD mice (P < 0.001). Compared to the right eyes of WT mice, the amplitudes of a-waves and b-waves declined in deprived right eyes of mice after MD (P < 0.001). There were no significant differences when comparing cPKCγ+/+ and cPKCγ−/− mice with MD.ConclusionscPKCγ participates in the plasticity of the visual cortex after MD, which is characterized by increased LTP in the contralateral visual cortex, which may be a result of cPKCγ-mediated phosphorylation of GluR1 at Ser 831.

Peripheral sounds elicit stronger activity in contralateral occipital cortex in blind than sighted individuals

Previous research has shown that peripheral, task-irrelevant sounds elicit activity in contralateral visual cortex of sighted people, as revealed by a sustained positive deflection in the event-related potential (ERP) over the occipital scalp contralateral to the sound’s location. This Auditory-evoked Contralateral Occipital Positivity (ACOP) appears between 200–450 ms after sound onset, and is present even when the task is entirely auditory and no visual stimuli are presented at all. Here, we investigate whether this cross-modal activation of contralateral visual cortex is influenced by visual experience. To this end, ERPs were recorded in 12 sighted and 12 blind subjects during a unimodal auditory task. Participants listened to a stream of sounds and pressed a button every time they heard a central target tone, while ignoring the peripheral noise bursts. It was found that task-irrelevant noise bursts elicited a larger ACOP in blind compared to sighted participants, indicating for the first time that peripheral sounds can enhance neural activity in visual cortex in a spatially lateralized manner even in visually deprived individuals. Overall, these results suggest that the cross-modal activation of contralateral visual cortex triggered by peripheral sounds does not require any visual input to develop, and is rather enhanced by visual deprivation.

P2-11-03. TMS over the contralateral primary visual cortex induces cortico-cortical inhibition in the primary motor cortex

P2-11-03. TMS over the contralateral primary visual cortex induces cortico-cortical inhibition in the primary motor cortex

Neural correlates of attentional capture by stimuli previously associated with social reward

ABSTRACTOur attention is strongly influenced by reward learning. Stimuli previously associated with monetary reward have been shown to automatically capture attention in both behavioral and neurophysiological studies. Stimuli previously associated with positive social feedback similarly capture attention; however, it is unknown whether such social facilitation of attention relies on similar or dissociable neural systems. Here, we used the value-driven attentional capture paradigm in an fMRI study to identify the neural correlates of attention to stimuli previously associated with social reward. The results reveal learning-dependent priority signals in the contralateral visual cortex, posterior parietal cortex, and caudate tail, similar to studies using monetary reward. An additional priority signal was consistently evident in the right middle frontal gyrus (MFG). Our findings support the notion of a common neural mechanism for directing attention on the basis of selection history that generalizes across different types of reward.

Desynchronizing to be faster? Perceptual- and attentional-modulation of brain rhythms at the sub-millisecond scale

Neural oscillatory signals has been associated with many high-level functions (e.g. attention and working memory), because they reflect correlated behaviors of neural population that would facilitate the information transfer in the brain. On the other hand, a decreased power of oscillation (event-related desynchronization, ERD) has been associated with an irregular state in which many neurons behave in an uncorrelated manner. In contrast to this view, here we show that the human ERD is linked to the increased regularity of oscillatory signals. Using magnetoencephalography, we found that presenting a visual stimulus not only induced a decrease in power of alpha (8–12 Hz) to beta (13–30 Hz) rhythms in the contralateral visual cortex but also reduced the mean and variance of their inter-peak intervals (IPIs). This indicates that the suppressed alpha/beta rhythms became faster (reduced mean) and more regular (reduced variance) during visual stimulation. The same changes in IPIs, especially those of beta rhythm, were observed when subjects allocated their attention to a contralateral visual field. Those results revealed a new role of the event-related decrease in alpha/beta power and further suggested that our brain regulates and accelerates a clock for neural computations by actively suppressing the oscillation amplitude in task-relevant regions.

5-HTR2A and 5-HTR3A but not 5-HTR1A antagonism impairs the cross-modal reactivation of deprived visual cortex in adulthood

Visual cortical areas show enhanced tactile responses in blind individuals, resulting in improved behavioral performance. Induction of unilateral vision loss in adult mice, by monocular enucleation (ME), is a validated model for such cross-modal brain plasticity. A delayed whisker-driven take-over of the medial monocular zone of the visual cortex is preceded by so-called unimodal plasticity, involving the potentiation of the spared-eye inputs in the binocular cortical territory. Full reactivation of the sensory-deprived contralateral visual cortex is accomplished by 7 weeks post-injury. Serotonin (5-HT) is known to modulate sensory information processing and integration, but its impact on cortical reorganization after sensory loss, remains largely unexplored. To address this issue, we assessed the involvement of 5-HT in ME-induced cross-modal plasticity and the 5-HT receptor (5-HTR) subtype used. We first focused on establishing the impact of ME on the total 5-HT concentration measured in the visual cortex and in the somatosensory barrel field. Next, the changes in expression as a function of post-ME recovery time of the monoamine transporter 2 (vMAT2), which loads 5-HT into presynaptic vesicles, and of the 5-HTR1A and 5-HTR3A were assessed, in order to link these temporal expression profiles to the different types of cortical plasticity induced by ME. In order to accurately pinpoint which 5-HTR exactly mediates ME-induced cross-modal plasticity, we pharmacologically antagonized the 5-HTR1A, 5-HTR2A and 5-HTR3A subtypes. This study reveals brain region-specific alterations in total 5-HT concentration, time-dependent modulations in vMAT2, 5-HTR1A and 5-HTR3A protein expression and 5-HTR antagonist-specific effects on the post-ME plasticity phenomena. Together, our results confirm a role for 5-HTR1A in the early phase of binocular visual cortex plasticity and suggest an involvement of 5-HTR2A and 5-HTR3A but not 5-HTR1A during the late cross-modal recruitment of the medial monocular visual cortex. These insights contribute to the general understanding of 5-HT function in cortical plasticity and may encourage the search for improved rehabilitation strategies to compensate for sensory loss.