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Harriott, A.

Publications and source records attributed to Harriott, A..

2 recordsLinked to original sources

Olfactory Bulb Pinprick Induction of Cortical Spreading Depolarizations

Cortical spreading depolarization (CSD) is a wave of cellular depolarization followed by prolonged depression of neuronal activity and is associated with a broad array of neurological diseases, including migraine with aura, traumatic brain injury, and stroke. Traditional CSD induction methods for animal studies have included pinprick, concentrated potassium chloride (KCl) application, and electrical stimulation. These methods are invasive and can cause injury to the cortex. Recently, a non-invasive approach using optogenetics has become available, but requires the use of transgenic mice or transfection of an optogene, which limits its wide adoption. Here, we describe a novel approach using olfactory bulb needle insertion in rodents to induce CSD. We also included KCl-induced CSDs as a comparator in the same mice. Olfactory bulb pinprick resulted in CSDs on every attempt (n = 18/18) as confirmed with optical intrinsic signal imaging. Histological analysis revealed that needle disruption in the caudal olfactory bulb, which is continuous with the cerebral cortex, may account for the propagation of CSD from the olfactory bulb to the cortex. Olfactory bulb pinprick reliably induces CSD and is non-invasive with respect to cortex. The approach may prove to be useful in rodent studies where maintenance of cortical integrity is important.

neuroscience↗

Subarachnoid hemorrhage leads to early and persistent functional connectivity and behavioral changes in mice

Aneurysmal subarachnoid hemorrhage (SAH) leads to significant long-term cognitive deficits. Studies in survivors of SAH show an association between persistent cognitive deficits and alterations in resting state functional connectivity (RSFC). However, modalities commonly used to assess RSFC in humans, such as fMRI, have practical limitations in small animals. Therefore, we used non-invasive functional optical intrinsic signal imaging to determine the effect of SAH on measures of RSFC in mice at early (day 4), intermediate (1 month), and late (3 months) time points after prechiasmatic arterial blood injection. We assessed Morris water maze, open field test, Y-maze, and rotarod performance from approximately 2 weeks to 3 months after SAH induction. We found qualitative and quantitative differences in seed-based connectivity maps between sham and SAH mice. SAH reduced motor, retrosplenial and visual seed-based connectivity indices, which persisted in retrosplenial and visual cortex seeds at 3 months. Seed-to-seed connectivity analysis confirmed attenuation of correlation coefficients in SAH mice, which persisted in predominantly posterior network connections at later time points. Seed-independent global and interhemispheric indices of connectivity revealed decreased correlations following SAH for at least 1 month. SAH led to Morris water maze hidden platform and open field deficits at 2 weeks, and Y-maze deficits for at least 3 months, without altering rotarod performance. In conclusion, experimental SAH leads to early and persistent alterations both in hemodynamically-derived measures of RSFC and in cognitive performance.

neuroscience↗