Experience dependent plasticity of higher visual cortical areas in the mouse.

Experience dependent plasticity in the visual cortex is a key paradigm for the study of mechanisms underpinning learning and memory. Despite this, studies involving manipulating visual experience have largely been limited to the primary visual cortex, V1, across various species. Here we investigated the effects of monocular deprivation (MD) on the ocular dominance (OD) and orientation selectivity of neurons in four visual cortical areas in the mouse: the binocular zone of V1 (V1b), the putative "ventral stream" area LM and the putative "dorsal stream" areas AL and PM. We employed two-photon calcium imaging to record neuronal responses in young adult mice before MD, immediately after MD, and following binocular recovery. OD shifts following MD were greatest in LM and smallest in AL and PM; in LM and AL, these shifts were mediated primarily through a reduction of deprived-eye responses, in V1b and LM through an increase in response through the non-deprived eye. The OD index recovered to pre-MD levels within 2 weeks in V1 only. MD caused a reduction in orientation selectivity of deprived-eye responses in V1b and LM only. Our results suggest that changes in OD in higher visual areas are not uniformly inherited from V1.

Evaluation of the impact of assistive artificial intelligence on ultrasound scanning for regional anaesthesia.

BACKGROUND: Ultrasound-guided regional anaesthesia relies on the visualisation of key landmark, target, and safety structures on ultrasound. However, this can be challenging, particularly for inexperienced practitioners. Artificial intelligence (AI) is increasingly being applied to medical image interpretation, including ultrasound. In this exploratory study, we evaluated ultrasound scanning performance by non-experts in ultrasound-guided regional anaesthesia, with and without the use of an assistive AI device. METHODS: Twenty-one anaesthetists, all non-experts in ultrasound-guided regional anaesthesia, underwent a standardised teaching session in ultrasound scanning for six peripheral nerve blocks. All then performed a scan for each block; half of the scans were performed with AI assistance and half without. Experts assessed acquisition of the correct block view and correct identification of sono-anatomical structures on each view. Participants reported scan confidence, experts provided a global rating score of scan performance, and scans were timed. RESULTS: Experts assessed 126 ultrasound scans. Participants acquired the correct block view in 56/62 (90.3%) scans with the device compared with 47/62 (75.1%) without (P=0.031, two data points lost). Correct identification of sono-anatomical structures on the view was 188/212 (88.8%) with the device compared with 161/208 (77.4%) without (P=0.002). There was no significant overall difference in participant confidence, expert global performance score, or scan time. CONCLUSIONS: Use of an assistive AI device was associated with improved ultrasound image acquisition and interpretation. Such technology holds potential to augment performance of ultrasound scanning for regional anaesthesia by non-experts, potentially expanding patient access to these techniques. CLINICAL TRIAL REGISTRATION: NCT05156099.

Assistive artificial intelligence for ultrasound image interpretation in regional anaesthesia: an external validation study.

BACKGROUND: Ultrasonound is used to identify anatomical structures during regional anaesthesia and to guide needle insertion and injection of local anaesthetic. ScanNav Anatomy Peripheral Nerve Block (Intelligent Ultrasound, Cardiff, UK) is an artificial intelligence-based device that produces a colour overlay on real-time B-mode ultrasound to highlight anatomical structures of interest. We evaluated the accuracy of the artificial-intelligence colour overlay and its perceived influence on risk of adverse events or block failure. METHODS: Ultrasound-guided regional anaesthesia experts acquired 720 videos from 40 volunteers (across nine anatomical regions) without using the device. The artificial-intelligence colour overlay was subsequently applied. Three more experts independently reviewed each video (with the original unmodified video) to assess accuracy of the colour overlay in relation to key anatomical structures (true positive/negative and false positive/negative) and the potential for highlighting to modify perceived risk of adverse events (needle trauma to nerves, arteries, pleura, and peritoneum) or block failure. RESULTS: The artificial-intelligence models identified the structure of interest in 93.5% of cases (1519/1624), with a false-negative rate of 3.0% (48/1624) and a false-positive rate of 3.5% (57/1624). Highlighting was judged to reduce the risk of unwanted needle trauma to nerves, arteries, pleura, and peritoneum in 62.9-86.4% of cases (302/480 to 345/400), and to increase the risk in 0.0-1.7% (0/160 to 8/480). Risk of block failure was reported to be reduced in 81.3% of scans (585/720) and to be increased in 1.8% (13/720). CONCLUSIONS: Artificial intelligence-based devices can potentially aid image acquisition and interpretation in ultrasound-guided regional anaesthesia. Further studies are necessary to demonstrate their effectiveness in supporting training and clinical practice. CLINICAL TRIAL REGISTRATION: NCT04906018.

Stable Encoding of Visual Cues in the Mouse Retrosplenial Cortex.

The rodent retrosplenial cortex (RSC) functions as an integrative hub for sensory and motor signals, serving roles in both navigation and memory. While RSC is reciprocally connected with the sensory cortex, the form in which sensory information is represented in the RSC and how it interacts with motor feedback is unclear and likely to be critical to computations involved in navigation such as path integration. Here, we used 2-photon cellular imaging of neural activity of putative excitatory (CaMKII expressing) and inhibitory (parvalbumin expressing) neurons to measure visual and locomotion evoked activity in RSC and compare it to primary visual cortex (V1). We observed stimulus position and orientation tuning, and a retinotopic organization. Locomotion modulation of activity of single neurons, both in darkness and light, was more pronounced in RSC than V1, and while locomotion modulation was strongest in RSC parvalbumin-positive neurons, visual-locomotion integration was found to be more supralinear in CaMKII neurons. Longitudinal measurements showed that response properties were stably maintained over many weeks. These data provide evidence for stable representations of visual cues in RSC that are spatially selective. These may provide sensory data to contribute to the formation of memories of spatial information.

Plasticity in Adult Mouse Visual Cortex Following Optic Nerve Injury.

Optic nerve (ON) injury is an established model of axonal injury which results in retrograde degeneration and death of retinal ganglion cells as well anterograde loss of transmission and Wallerian degeneration of the injured axons. While the local impact of ON crush has been extensively documented we know comparatively little about the functional changes that occur in higher visual structures such as primary visual cortex (V1). We explored the extent of adult cortical plasticity using ON crush in aged mice. V1 function of the contralateral hemisphere was assessed longitudinally by intrinsic signal imaging and 2-photon calcium imaging before and after ON crush. Functional imaging demonstrated an immediate shift in V1 ocular dominance towards the ipsilateral, intact eye, due to the expected almost complete loss of responses to contralateral eye stimulation. Surprisingly, within 2 weeks we observed a delayed increase in ipsilateral eye responses. Additionally, spontaneous activity in V1 was reduced, similar to the lesion projection zone after retinal lesions. The observed changes in V1 activity indicate that severe ON injury in adulthood evokes cortical plasticity not only cross-modally but also within the visual cortex; this plasticity may be best compared with that seen after retinal lesions.

Midget retinal ganglion cell dendritic and mitochondrial degeneration is an early feature of human glaucoma.

Glaucoma is characterized by the progressive dysfunction and loss of retinal ganglion cells. However, the earliest degenerative events that occur in human glaucoma are relatively unknown. Work in animal models has demonstrated that retinal ganglion cell dendrites remodel and atrophy prior to the loss of the cell soma. Whether this occurs in human glaucoma has yet to be elucidated. Serial block face scanning electron microscopy is well established as a method to determine neuronal connectivity at high resolution but so far has only been performed in normal retina from animal models. To assess the structure-function relationship of early human glaucomatous neurodegeneration, regions of inner retina assessed to have none-to-moderate loss of retinal ganglion cell number were processed using serial block face scanning electron microscopy (n = 4 normal retinas, n = 4 glaucoma retinas). This allowed detailed 3D reconstruction of retinal ganglion cells and their intracellular components at a nanometre scale. In our datasets, retinal ganglion cell dendrites degenerate early in human glaucoma, with remodelling and redistribution of the mitochondria. We assessed the relationship between visual sensitivity and retinal ganglion cell density and discovered that this only partially conformed to predicted models of structure-function relationships, which may be affected by these early neurodegenerative changes. In this study, human glaucomatous retinal ganglion cells demonstrate compartmentalized degenerative changes as observed in animal models. Importantly, in these models, many of these changes have been demonstrated to be reversible, increasing the likelihood of translation to viable therapies for human glaucoma.

Enhancement of visual cortex plasticity by dark exposure.

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory-inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.