For the apparent discrepancy. First and most importantly, UVD results in

For the apparent discrepancy. First and most importantly, UVD results in an imbalance in the vestibulo-ocular (VOR) and AG-221 manufacturer vestibulo-spinal reflexes (VSR), causing symptoms such as spontaneous ocular nystagmus (SN, with quick phase toward the intact side) and postural asymmetry toward the lesioned side (see [29] for a review). These symptoms, which are a result of an imbalance between the left and right central vestibular systems, are so severe initially, that animals such as rats and guinea pigs have difficulty standing immediately after recovery from anaesthesia. Gradually, over a period of 2? days, the SN and postural asymmetry decrease in severity in a process known as `vestibular compensation’ (see [29] for a review). If a UVD is then performed on the contralateral side after compensation has occurred for the first UVD, this generates SN and postural asymmetry in the opposite direction to the original symptoms, in a phenomenon known as Bechterew’s syndrome (see [29] for a review). Following BVD, in which one labyrinth is lesioned afterGlutamate Receptors after Vestibular Damagethe other under anaesthesia, SN and postural asymmetry do not occur, because there is no imbalance in activity between the two labyrinths following recovery from the anaesthetic. Rather, BVD results in a complete loss of the VORs and VSRs. Therefore, the behavioural symptoms which follow UVD or two UVD procedures in sequence, are quite different from those that follow a simultaneous BVD under anaesthesia. The most likely BU-4061T web explanation for the difference between our results for the NR1, NR2A and NR2B subunits of the NMDA receptor and Besnard et al.’s [8] results for the NMDA receptor, is the different temporal sequence of the lesions. However, another important difference is that Besnard et al. [8] used Sprague Dawley rats, whereas we used Wistar rats. It must also be considered that whereas we used surgical lesions of the labyrinth, Besnard et al. [8] used intratympanic injections of the ototoxin, sodium arsanilate. The sodium arsanilate method has been demonstrated to destroy the vestibular hair cells in the vestibular labyrinth without damaging the VIIIth nerve dendrites, axons or primary afferent neurons in Scarpa’s ganglion [45]. By contrast, surgical lesions of the rat labyrinth have been reported destroy the vestibular hair cells as well as damage some VIIIth nerve dendrites [46]. Both models induce severe spatial memory deficits that should lead to similar consequences in terms of receptor changes. However, we do not know if remaining ectopic vestibular inputs might be generated by the vestibular system via the intact vestibular nerve with the chemical model, therefore explaining the long-term difference in glutamate receptor expression observed in the two models. Besnard et al. [8] also conducted their analyses of the whole hippocampus at 2 months after the second lesion, whereas we analysed 3 separate hippocampal subregions at 24 h, 72 h, 1 week, 1 month and 6 months post-BVD. Finally, we used western blotting to analyse NMDA receptor subunit expression, whereas Besnard et al. [8] used receptor autoradiography to measure the NMDA receptor number and affinity. Whereas quantitative receptor autoradiography, using beta-imaging, allows for quantification of membrane receptor density, i.e. functional receptors, with a resolution of approximately 150 to 200 mm, western blotting is a semiquantitative method that quantifies both intra-cytoplasmic and membrane rec.For the apparent discrepancy. First and most importantly, UVD results in an imbalance in the vestibulo-ocular (VOR) and vestibulo-spinal reflexes (VSR), causing symptoms such as spontaneous ocular nystagmus (SN, with quick phase toward the intact side) and postural asymmetry toward the lesioned side (see [29] for a review). These symptoms, which are a result of an imbalance between the left and right central vestibular systems, are so severe initially, that animals such as rats and guinea pigs have difficulty standing immediately after recovery from anaesthesia. Gradually, over a period of 2? days, the SN and postural asymmetry decrease in severity in a process known as `vestibular compensation’ (see [29] for a review). If a UVD is then performed on the contralateral side after compensation has occurred for the first UVD, this generates SN and postural asymmetry in the opposite direction to the original symptoms, in a phenomenon known as Bechterew’s syndrome (see [29] for a review). Following BVD, in which one labyrinth is lesioned afterGlutamate Receptors after Vestibular Damagethe other under anaesthesia, SN and postural asymmetry do not occur, because there is no imbalance in activity between the two labyrinths following recovery from the anaesthetic. Rather, BVD results in a complete loss of the VORs and VSRs. Therefore, the behavioural symptoms which follow UVD or two UVD procedures in sequence, are quite different from those that follow a simultaneous BVD under anaesthesia. The most likely explanation for the difference between our results for the NR1, NR2A and NR2B subunits of the NMDA receptor and Besnard et al.’s [8] results for the NMDA receptor, is the different temporal sequence of the lesions. However, another important difference is that Besnard et al. [8] used Sprague Dawley rats, whereas we used Wistar rats. It must also be considered that whereas we used surgical lesions of the labyrinth, Besnard et al. [8] used intratympanic injections of the ototoxin, sodium arsanilate. The sodium arsanilate method has been demonstrated to destroy the vestibular hair cells in the vestibular labyrinth without damaging the VIIIth nerve dendrites, axons or primary afferent neurons in Scarpa’s ganglion [45]. By contrast, surgical lesions of the rat labyrinth have been reported destroy the vestibular hair cells as well as damage some VIIIth nerve dendrites [46]. Both models induce severe spatial memory deficits that should lead to similar consequences in terms of receptor changes. However, we do not know if remaining ectopic vestibular inputs might be generated by the vestibular system via the intact vestibular nerve with the chemical model, therefore explaining the long-term difference in glutamate receptor expression observed in the two models. Besnard et al. [8] also conducted their analyses of the whole hippocampus at 2 months after the second lesion, whereas we analysed 3 separate hippocampal subregions at 24 h, 72 h, 1 week, 1 month and 6 months post-BVD. Finally, we used western blotting to analyse NMDA receptor subunit expression, whereas Besnard et al. [8] used receptor autoradiography to measure the NMDA receptor number and affinity. Whereas quantitative receptor autoradiography, using beta-imaging, allows for quantification of membrane receptor density, i.e. functional receptors, with a resolution of approximately 150 to 200 mm, western blotting is a semiquantitative method that quantifies both intra-cytoplasmic and membrane rec.