Activity In Primary Visual Cortex Research Articles

Visual cortical area contributions to the transient, multifocal and steady-state VEP: A forward model-informed analysis

Abstract Central to our understanding of how visual-evoked potentials (VEPs) contribute to visual processing is the question of where their anatomical sources are. Three well-established measures of low-level visual cortical activity are widely used: the first component (“C1”) of the transient and multifocal VEP, and the steady-state VEP (SSVEP). Although primary visual cortex (V1) activity has often been implicated in the generation of all three signals, their dominant sources remain uncertain due to the limited resolution and methodological heterogeneity of source modelling. Here, we provide the first characterisation of all three signals in one analytic framework centred on the “cruciform model”, which describes how scalp topographies of V1 activity vary with stimulus location due to the retinotopy and unique folding pattern of V1. We measured the transient C1, multifocal C1, and SSVEPs driven by an 18.75 Hz and 7.5 Hz flicker, and regressed them against forward models of areas V1, V2, and V3 generated from the Benson-2014 retinotopy atlas. The topographic variations of all four VEP signals across the visual field were better captured by V1 models, explaining between 2 and 6 times more variance than V2/V3. Models with all three visual areas improved fit further, but complementary analyses of temporal dynamics across all three signals indicated that the bulk of extrastriate contributions occur considerably later than V1. Overall, our data support the use of peak C1 amplitude and SSVEPs to probe V1 activity, although the SSVEP contains stronger extrastriate contributions. Moreover, we provide elaborated heuristics to distinguish visual areas in VEP data based on signal lateralisation as well as polarity inversion.

Are we aware of neural activity in primary visual cortex? A neuropsychological case study.

According to a seminal hypothesis stated by Crick and Koch in 1995, one is not aware of neural activity in primary visual cortex (V1) because this region lacks reciprocal connections with prefrontal cortex (PFC). We provide here a neuropsychological illustration of this hypothesis in a patient with a very rare form of cortical blindness: ventral and dorsal cortical pathways were lesioned bilaterally while V1 areas were partially preserved. Visual stimuli escaped conscious perception but still activated V1 regions that were functionally disconnected from PFC. These results are consistent with the hypothesis of a causal role of PFC in visual awareness.

Retinal neurodegeneration induced by sodium iodate administration and visual cortex activity

Aims/Purpose: Recently investigations have shown that using sodium iodate (NaIO3) provides a promising animal model of retinal neurodegeneration. The aim of this research is to characterize the effects of this compound in the visual pathway.Methods: First, a single dose of NaIO3 (65 mg/kg) was administered intraperitoneally to mice (C57BL/6J strain) with a knock‐out mutation for the Opn4 gene (Opn4−/−). Then, behavioural tests (light avoidance assay, optomotor test, pupillary light reflex) were performed until Day 28. Electrophysiological tests (electroretinogram, ERG; visual evoked potentials, VEP), were performed weekly until Day 42. Finally, the retina was analysed histologically by immunohistochemical methods on day 57th.Results: First, the results of the behavioural test in the experimental group (NaIO3) reflected a progressive decrease in light sensitivity after 28 days, and a decrease in visual acuity and as well as a completely loss of the pupillary light reflex after 7 days since the administration. Second, the electrophysiological activity of retina and primary visual cortex (ERG, VEP) was significantly reduced in the treated group (NaIO3) with respect to the control group. Finally, histological analysis of the retina showed structural alterations in the outer segments of the photoreceptors of the treated animals (NaIO3).Conclusions: This research demonstrates the appearance of alterations in the outer retina and a decrease in the response at the level of the visual cortex after NaIO3 administration, as expected. This confirms that NaIO3‐induced retinal neurodegeneration is effective in obtaining a promising experimental model that could be used in the study of diseases associated with the visual system and in the development of novel therapeutic strategies.

Spontaneous and Visual Stimulation Evoked Firing Sequences Are Distinct Under Desflurane Anesthesia.

Recurring spike sequences are thought to underlie cortical computations and may be essential for information processing in the conscious state. How anesthesia at graded levels may influence spontaneous and stimulus-related spike sequences in visual cortex has not been fully elucidated. We recorded extracellular single-unit activity in the rat primary visual cortex in vivo during wakefulness and three levels of anesthesia produced by desflurane. The latencies of spike sequences within 0-200ms from the onset of spontaneous UP states and visual flash-evoked responses were compared. During wakefulness, spike latency patterns linked to the local field potential theta cycle were similar to stimulus-evoked patterns. Under desflurane anesthesia, spontaneous UP state sequences differed from flash-evoked sequences due to the recruitment of low-firing excitatory neurons to the UP state. Flash-evoked spike sequences showed higher reliability and longer latency when stimuli were applied during DOWN states compared to UP states. At deeper levels, desflurane altered both UP state and flash-evoked spike sequences by selectively suppressing inhibitory neuron firing. The results reveal desflurane-induced complex changes in cortical firing sequences that may influence visual information processing.

Individual alpha frequency appears unrelated to the latency of early visual responses.

A large body of work has linked neural oscillations in the alpha-band (8-13 Hz) to visual perceptual outcomes. In particular, studies have found that alpha phase prior to stimulus onset predicts stimulus detection, and sensory responses and that the frequency of alpha can predict temporal properties of perception. These findings have bolstered the idea that alpha-band oscillations reflect rhythmic sampling of visual information, however the mechanisms of this are unclear. Recently two contrasting hypotheses have been proposed. According to the rhythmic perception account, alpha oscillations impose phasic inhibition on perceptual processing and primarily modulate the amplitude or strength of visual responses and thus the likelihood of stimulus detection. On the other hand, the discrete perception account proposes that alpha activity discretizes perceptual inputs thereby reorganizing the timing (not only the strength) of perceptual and neural processes. In this paper, we sought neural evidence for the discrete perception account by assessing the correlation between individual alpha frequencies (IAF) and the latency of early visual evoked event-related potential (ERP) components. If alpha cycles were responsible for shifting neural events in time, then we may expect higher alpha frequencies to be associated with earlier afferent visual ERPs. Participants viewed large checkerboard stimuli presented to either the upper or lower visual field that were designed to elicit a large C1 ERP response (thought to index feedforward primary visual cortex activation). We found no reliable correlation between IAF and the C1 latency, or subsequent ERP component latencies, suggesting that the timing of these visual-evoked potentials was not modulated by alpha frequency. Our results thus fail to find evidence for discrete perception at the level of early visual responses but leave open the possibility of rhythmic perception.

Enhanced Visual Cortex Activation in People With Narcolepsy Type 1 During Active Sleep Resistance: An fMRI-EEG Study.

The brain activation patterns related to sleep resistance remain to be discovered in health and disease. The maintenance of wakefulness test (MWT) is an objective neuropsychological assessment often used to assess an individual’s ability to resist sleep. It is frequently used in narcolepsy type 1, a disorder characterized by impaired sleep-wake control and the inability to resist daytime sleep. We investigated the neural correlates of active sleep resistance in 12 drug-free people with narcolepsy type 1 and 12 healthy controls. Simultaneous fMRI-EEG measurements were recorded during five cycles of two alternating conditions of active sleep resistance and waking rest. Cleaned EEG signals were used to verify wakefulness and task adherence. Pooling both subject groups, significantly higher fMRI activation when actively resisting sleep was seen in the brainstem, superior cerebellum, bilateral thalamus and visual cortices. In controls the activation clusters were generally smaller compared to patients and no significant activation was seen in the brainstem. Formal comparison between groups only found a significantly higher left primary visual cortex activation in patients during active sleep resistance. The active sleep resistance paradigm is a feasible fMRI task to study sleep resistance and induces evident arousal- and visual-related activity. Significantly higher left primary visual cortical activation in patients could be caused by an enhanced need of visual focus to resist sleep, or reflecting a more rapid descent in their level of alertness when resting.

Novel stimuli evoke excess activity in the mouse primary visual cortex

To explore how neural circuits represent novel versus familiar inputs, we presented mice with repeated sets of images with novel images sparsely substituted. Using two-photon calcium imaging to record from layer 2/3 neurons in the mouse primary visual cortex, we found that novel images evoked excess activity in the majority of neurons. This novelty response rapidly emerged, arising with a time constant of 2.6 ± 0.9 s. When a new image set was repeatedly presented, a majority of neurons had similarly elevated activity for the first few presentations, which decayed to steady state with a time constant of 1.4 ± 0.4 s. When we increased the number of images in the set, the novelty response's amplitude decreased, defining a capacity to store ∼15 familiar images under our conditions. These results could be explained quantitatively using an adaptive subunit model in which presynaptic neurons have individual tuning and gain control. This result shows that local neural circuits can create different representations for novel versus familiar inputs using generic, widely available mechanisms.

Expression of actin- and oxidative phosphorylation-related transcripts across the cortical visuospatial working memory network in unaffected comparison and schizophrenia subjects.

Visuospatial working memory (vsWM), which is impaired in schizophrenia (SZ), is mediated by a distributed cortical network. In one node of this network, the dorsolateral prefrontal cortex (DLPFC), altered expression of transcripts for actin assembly and mitochondrial oxidative phosphorylation (OXPHOS) have been reported in SZ. To understand the relationship between these processes, and the extent to which similar alterations are present in other regions of vsWM network in SZ, a subset of actin- (CDC42, BAIAP2, ARPC3, and ARPC4) and OXPHOS-related (ATP5H, COX4I1, COX7B, and NDUFB3) transcripts were quantified in DLPFC by RNA sequencing in 139 SZ and unaffected comparison (UC) subjects, and in DLPFC and three other regions of the cortical vsWM network by qPCR in 20 pairs of SZ and UC subjects. By RNA sequencing, levels of actin- and OXPHOS-related transcripts were significantly altered in SZ, and robustly correlated in both UC and SZ subject groups. By qPCR, cross-regional expression patterns of these transcripts in UC subjects were consistent with greater actin assembly in DLPFC and higher OXPHOS activity in primary visual cortex (V1). In SZ, CDC42 and ARPC4 levels were lower in all regions, BAIAP2 levels higher only in V1, and ARPC3 levels unaltered across regions. All OXPHOS-related transcript levels were lower in SZ, with the disease effect decreasing from posterior to anterior regions. The differential alterations in markers of actin assembly and energy production across regions of the cortical vsWM network in SZ suggest that each region may make specific contributions to vsWM impairments in the illness.

MRI Evaluation of the Relationship Between Abnormalities in Vision-Related Brain Networks and Quality of Life in Patients with Migraine without Aura.

ObjectiveTo evaluate whether migraine without aura (MwoA) can be partly attributed to abnormalities of vision-related brain networks (VBN) and whether these specific regional abnormalities affect the patients’ quality of life (QoL).MethodsA total of 40 participants, including 20 MwoA patients and 20 healthy control volunteers, were enrolled. There were no significant differences in sex, age, educational qualifications and dominant hand between the two groups. Headache intensity and QoL were assessed by the Pain Number Evaluation Scale (NRS) and the Migraine-Specific Quality of Life Questionnaire (MSQ 2.1), respectively. Resting state functional magnetic resonance imaging (rs-fMRI) and independent component analysis (ICA) were performed to determine and evaluate the VBN.ResultsThree components were identified as consistent with the VBN in the template and recorded as N1, N2 and N3, respectively. The functional activity of the left primary visual cortex (N1), left culmen of cerebellum (N1), left lingual gyrus (N2), superior frontal gyrus (N2) and left posterior lateral prefrontal cortex (N3) in the MwoA group enhanced compared with the healthy control group. However, the functional activity of right middle occipital gyrus, left fusiform gyrus, right lingual gyrus, and right primary motor cortex in the N3 network weakened. Pearson correlation analysis showed that decline of attention to work and life (MSQ5) was positively associated with the functional activity of left primary visual cortex and left lingual gyrus. Canceling from work and daily life (MSQ8) was inversely associated with the functional activity of right primary motor cortex. The burden of feeling like others (MSQ13) and the overall decrease in QoL were both positively associated with the functional activity of right lingual gyrus.ConclusionMwoA patients showed abnormal VBN function, which was moderately correlated with decreased QoL. This study provides evidence for the precise prevention and treatment of migraine by neural regulation.

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.

Cortical mechanisms of visual hypersensitivity in women at risk for chronic pelvic pain.

Increased sensory sensitivity across non-nociceptive modalities is a common symptom of chronic pain conditions and is associated with chronic pain development. Providing a better understanding of the brain-behavior relationships that underlie multimodal hypersensitivity (MMH) may clarify the role of MMH in the development of chronic pain. We studied sensory hypersensitivity in a cohort of women (n = 147) who had diary confirmation of menstrual status and were enriched with risk factors for chronic pelvic pain, such as dysmenorrhea and increased bladder sensitivity. We administered 2 experimental tasks to evaluate the cross-modal relationship between visual and visceral sensitivity. Visual sensitivity was probed by presenting participants with a periodic pattern-reversal checkerboard stimulus presented across 5 brightness intensities during electroencephalography recording. Self-reported visual unpleasantness ratings for each brightness intensity were simultaneously assessed. Visceral sensitivity was evaluated with an experimental bladder-filling task associated with early clinical symptoms of chronic pelvic pain. Visually evoked cortical activity increased with brightness intensity across the entire scalp, especially at occipital electrode sites. Visual stimulation-induced unpleasantness was associated with provoked bladder pain and evoked primary visual cortex activity. However, the relationship between unpleasantness and cortical activity was moderated by provoked bladder pain. These results demonstrate that activity in the primary visual cortex is not greater in individuals with greater visceral sensitivity. We hypothesize that downstream interpretation or integration of this signal is amplified in individuals with visceral hypersensitivity. Future studies aimed at reducing MMH in chronic pain conditions should prioritize targeting of cortical mechanisms responsible for aberrant downstream sensory integration.

Attention reduces the burstiness of V1 neurons involved in attended target enhancement.

Attention-dependent reduction in the tendency for neurons to fire bursts (burstiness) is widely observed in the visual cortex. However, the underlying mechanism and the functional role of this phenomenon remain unclear. We recorded well-isolated single-unit activities in primary visual cortex (V1) from two primates (Macaca mulatta) while they performed a detection task engaging spatial attention with two levels of difficulty (hard/easy). We found that attention modulated burstiness of V1 neurons in a cell-type specific manner. For neurons whose net response enhanced with the increase of task difficulty (difficulty-enhanced neuron), representing their involvement in boosting the signal of the attended stimulus, attention led to a reduction in burstiness during hard task but not during easy task. In contrast, regardless of the level of task difficulty, attention-dependent reduction in burstiness was not observed in neurons that showed a net suppression in firing rate with the increase of task difficulty (difficulty-suppressed neuron), indicating their commitment in filtering out the interference of distractor. This differentiation in the effects of attentional modulation on burstiness among the cells with distinct functional roles in attention suggests that the reduction in burstiness by attention is linked to target enhancement and is not associated with distractor suppression.

Gamma rhythms and visual information in mouse V1 specifically modulated by somatostatin+ neurons in reticular thalamus.

Visual perception in natural environments depends on the ability to focus on salient stimuli while ignoring distractions. This kind of selective visual attention is associated with gamma activity in the visual cortex. While the nucleus reticularis thalami (nRT) has been implicated in selective attention, its role in modulating gamma activity in the visual cortex remains unknown. Here, we show that somatostatin- (SST) but not parvalbumin-expressing (PV) neurons in the visual sector of the nRT preferentially project to the dorsal lateral geniculate nucleus (dLGN), and modulate visual information transmission and gamma activity in primary visual cortex (V1). These findings pinpoint the SST neurons in nRT as powerful modulators of the visual information encoding accuracy in V1 and represent a novel circuit through which the nRT can influence representation of visual information.

Spontaneous Activity in Primary Visual Cortex Relates to Visual Creativity.

Cognitive and neural processes underlying visual creativity have attracted substantial attention. The current research uses a critical time point analysis (CTPA) to examine how spontaneous activity in the primary visual area (PVA) is related to visual creativity. We acquired the functional magnetic resonance imaging (fMRI) data of 16 participants at the resting state and during performing a visual creative synthesis task. According to the CTPA, we then classified spontaneous activity in the PVA into critical time points (CTPs), which reflect the most useful and important functional meaning of the entire resting-state condition, and the remaining time points (RTPs). We constructed functional brain networks based on the brain activity at two different time points and then subsequently based on the brain activity at the task state in a separate manner. We explore the relationship between resting-state and task-fMRI (T-fMRI) functional brain networks. Our results found that: (1) the pattern of spontaneous activity in the PVA may associate with mental imagery, which plays an important role in visual creativity; (2) in comparison with the RTPs-based brain network, the CTP-network showed an increase in global efficiency and a decrease in local efficiency; (3) the regional integrated properties of the CTP-network could predict the integrated properties of the creative-network while the RTP-network could not. Thus, our findings indicated that spontaneous activity in the PVA at CTPs was associated with a visual creative task-evoked brain response. Our findings may provide an insight into how the visual cortex is related to visual creativity.

Brain functional MRI responses to blue light stimulation in Leber’s hereditary optic neuropathy

Melanopsin retinal ganglion cells (mRGCs) are intrinsically photosensitive photoreceptors contributing both to image and non-image-forming (NIF) functions of the eye. They convey light signal to the brain to modulate circadian entrainment, sleep, alertness, cognition, brightness perception and coarse vision. Given that rods and cones also contribute to all these impacts of light, isolating mRGC visual and NIF roles in humans is challenging so that mRGC functions remains to be fully characterized. Here, we evaluated light-driven visual and cognitive brain responses in Leber’s Hereditary Optic Neuropathy (LHON), an inherited optic neuropathy that is characterized by a selective relative sparing of the melanopsin-expressing retinal ganglion cells (mRGCs). Twelve patients and twelve matched healthy controls (HC) were enrolled in a functional brain magnetic resonance imaging (fMRI) protocol including visual and visual-cognitive paradigms under blue (480 nm) and red (620 nm) light exposures. Primary visual cortex activation was detected in LHON patients; in particular higher occipital activation was found in response to sustained blue vs. red stimulation in LHON vs. HC. Similarly, brain responses to the executive task were larger under blue vs. red light in LHON over lateral prefrontal cortex. These findings are in line with the relative mRGC sparing demonstrated in LHON and support the mRGC contribution to both non-visual and visual brain functions, with potential implication for visual rehabilitation in hereditary optic neuropathy patients.

Abstract PD6-11: Altered regional cerebral blood flow in adjuvant-treated breast cancer survivors after chemo- and endocrine therapy

Abstract Objectives: In the first published observation of altered brain metabolism in patients exposed to chemotherapy (Breast Cancer Res Treat. 2007; 103:303-311), we described diminished metabolism in prefrontal cortex in proportion to magnitude of diminishment of short-term memory performance, 5-10 years following patients’ last chemotherapy dose. Subsequently, at least 7 other groups of investigators have independently demonstrated altered cerebral metabolism of frontal cortex as assessed by FDG-PET (J Nucl Med. 2019; 60:16821690). We now offer the first report of regional cerebral blood flow (rCBF) changes assessed by [O-15]water PET in prospectively recruited subjects with newly diagnosed breast cancer, longitudinally followed from time of initial therapy for one year. Methods: A total of 204 brain [O-15]water PET scans were obtained of 17 right-handed female subjects newly diagnosed with breast cancer, with near-equal portions of 10 chemo-exposed (C) and 7 unexposed (U) subjects undergoing endocrine therapy in the ensuing year (5/10, 3/7). For each subject, 12 scans were obtained – 6 during short-term memory, long-term memory, and control tasks presented in counterbalanced order soon after completion of any adjuvant chemotherapy but prior to initiation of any endocrine therapy (baseline), and repeating one year later. PET data were assessed through paired t statistical tests at the voxel level, after Family Wise Error (FWE)-based corrections for multiple comparisons. Results: Across all subjects, scans at baseline during short-term recall revealed most marked activation of bilateral temporal-occipital cortex (peak voxel t=7.20; size 4,649 voxels, p<.0005 FWEcorr.) and similar activation occurred during long-term recall (t=6.48; 6,446 voxels, p<.0005 FWEcorr.). One year later, left prefrontal cortex, including Broca’s area, activated during short-term recall (t=5.74; 227 voxels, p=.02 FWEcorr), as did bilateral medial occipital cortex (t=5.45; 908 voxels, p<.0005 FWEcorr.); during long-term recall, prefrontal cortex activated with greater bilaterality, but with an extent in left frontal lobe (1031 voxels, p=.008 FWEcorr.) about double the size of right (452 voxels), and with less occipital activation. In therapy-stratified analyses, baseline short-term recall of left prefrontal cortex, including Broca’s area, activated more extensively (3253 voxels, p<.0005 FWEcorr.) in U, while C showed more extensive activation in medial occipital cortex (5670 voxels, p<.0005 FWEcorr.vs. 423 voxels, p=.001). One year later, short-term recall in U continued to activate left prefrontal cortex including Broca’s area (4035 voxels, p<.0005 FWEcorr.), while C still primarily activated medial occipital cortex (976 voxels, p=.008 FWEcorr.), though demonstrating a shift of activation away from this region relative to one year prior, with more voxels of activation tending to appear in left prefrontal cortex over that interval. Similar, though less striking, differences were observed during long-term recall. Conclusions: Activation of rCBF during recall of verbal associative memories was diminished in left prefrontal brain areas critical to verbal memory performance in C relative to U. Concomitantly, C demonstrated apparent compensatory activation of primary visual cortex, involved in perceiving the visually presented verbal memory cues, in lieu of specific activation of the prefrontal cortical regions in the dominant hemisphere involved in processing language information. The strengths of these therapy-associated differences were generally diminished one year later, consistent with partial interim recovery in C of cerebral processing by language-specialized areas. Citation Format: Claire L Vandenberg, Patricia A Ganz, Stephen S Liu, Daniel HS Silverman. Altered regional cerebral blood flow in adjuvant-treated breast cancer survivors after chemo- and endocrine therapy [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PD6-11.

Irreversible Primary Visual Cortex Impairment in a Mouse Model of High-Risk Schizophrenia.

PurposeAlthough visual deficits can be observed at any stage of schizophrenia, few studies have focused on visual cortex alterations in individuals at high risk of schizophrenia. This study aimed to investigate the pathological changes of the primary visual cortex in a prenatal mouse model of MK801-induced high-risk schizophrenia.MethodsThe high-risk schizophrenia model was generated by MK801 injection into pregnant mice. The male offspring without schizophrenia-like behaviors in early adulthood were defined as the high-risk mouse model of schizophrenia (HRMMS) and divided into two groups. One HRMMS group received the antipsychotic agent risperidone beginning at postnatal week 4 and another group did not receive any treatment. After treatment for 4 weeks, in vivo two-photon calcium imaging was performed to characterize the primary visual cortex activity. The novel object recognition test and the prepulse inhibition apparatus test were also implemented to assess the cognitive and behavioral performance, respectively.ResultsBoth groups of HRMMS mice, with or without antipsychotic treatment, had decreased neuronal calcium activity, demonstrating primary visual cortex impairment. More notably, antipsychotic treatment did not normalize the impaired neuronal activities in the primary visual cortex. Correspondingly, the treatment did not improve the cognitive or behavioral impairment.ConclusionVisual cortex impairment might be a prominent feature of individuals at high risk of schizophrenia that cannot be normalized by early treatment with antipsychotic medication, indicating the presence of independent regulatory pathways for visual perception disturbance in schizophrenia. Thus, visual system impairment in schizophrenic patients must be further studied.

Decoding Mouse Behavior from neural activity in primary visual cortex

Background and Hypothesis: 
 Brain-machine interfaces (BMIs) aim to restore motor control to patients. To develop effective BMIs, it is imperative that we build highly accurate models relating cortical neural activity with natural movements. Neurons in the visual cortex of the brain respond strongly to visual signals, but are also modulated by fluctuating internal states such as alertness, which closely correlates pupil size. We thus hypothesized that an animal’s pupil size can be decoded directly from the activity of a population of neurons in mouse primary visual cortex. 
 
 Project Methods: 
 We used an open-access dataset from the Allen Institute for Brain Science, which consisted of in-vivo 2 photon calcium imaging data of 128 neurons recorded from primary visual cortex of an awake mouse viewing a video screen. Video imaging was used to track the mouse’s pupil size. 
 
 To relate neural activity with pupil size, we used linear regression, first smoothing the data with a Savitzky Gall filter. The model was fit on the first 80% of the data, and tested on the remaining 20%, using the computed coefficients to predict pupil size from neural activity. A Pearson correlation coefficient between the true and predicted data was computed. All analyses were performed in Python. 
 
 Results: 
 We found that there was a strong linear relationship between neural activity and pupil size, as the correlation coefficient between the true and predicted data was 0.376. Therefore, we have shown quantitatively that pupil size can be modeled based on neuronal activity within the visual cortex with a high level of accuracy. 
 
 Conclusion and Potential Impact: 
 This experiment demonstrates the feasibility of linear regression for modeling neuronal behavior in the visual system, particularly related to pupil size. Results suggest opportunities for further experimental analysis of the relationship between neural activity and other physiological markers, such as running speed.

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.

Head Movements Control the Activity of Primary Visual Cortex in a Luminance-Dependent Manner

The vestibular system broadcasts head-movement-related signals to sensory areas throughout the brain, including visual cortex. These signals are crucial for the brain's ability to assess whether motion of the visual scene results from the animal's head movements. However, how head movements affect visual cortical circuits remains poorly understood. Here, we discover that ambient luminance profoundly transforms how mouse primary visual cortex (V1) processes head movements. While in darkness, head movements result in overall suppression of neuronal activity; in ambient light, the same head movements trigger excitation across all cortical layers. This light-dependent switch in how V1 processes head movements is controlled by somatostatin-expressing (SOM) inhibitory neurons, which are excited by head movements in dark, but not in light. This study thus reveals a light-dependent switch in the response of V1 to head movements and identifies a circuit in which SOM cells are key integrators of vestibular and luminance signals.