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Ursula Grussercornehls - One of the best experts on this subject based on the ideXlab platform.
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dependence of parvalbumin expression on purkinje cell input in the Deep Cerebellar Nuclei
The Journal of Comparative Neurology, 1998Co-Authors: Jorg Baurle, Muna Hoshi, Ursula GrussercornehlsAbstract:A complete loss of Purkinje cell (PC) input leads to an increase in expression of the calcium-binding protein parvalbumin (Parv) in neurons of the Deep Cerebellar Nuclei (DCN) of PC degeneration (pcd) mutants. To verify this apparent dependence of Parv expression on PC input in the DCN, the patterns of expression in five other Cerebellar mutants (weaver, staggerer, leaner, nervous, and lurcher) with differing grades and chronologies of PC loss were compared. Degree and time course of PC loss and the subsequent denervation of DCN neurons were monitored by using Calbindin D-28k (Calb) immunocytochemistry. Similar to pcd mice, somatal Parv in lurcher mutants increased massively throughout the Cerebellar Nuclei. In nervous and leaner mutants, somatal Parv was restricted to almost completely denervated nuclear areas, whereas areas with appreciable remnants of PC input were spared. The first appearance of Parv+ somata was closely correlated with the time course of PC degeneration—postnatal day 19 in lurcher mutants and postnatal day 23 in nervous mutants. In staggerer mice, neurons immunopositive for Parv as well as for Calb were present in outer DCN areas, likely representing ectopic PCs rather than DCN neurons. No Parv+ DCN somata were found in weaver mutants at any time. In conclusion, increased expression of somatal Parv in DCN neurons is not restricted to the specific histopathology in pcd mutants but is a common mechanism that is dependent on the topography and severeness of PC-input loss. The functional significance of the Parv increase and its possible contribution to the degree of motor disability among the different mutants are discussed. J. Comp. Neurol. 392:499–514, 1998. © 1998 Wiley-Liss, Inc.
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differential number of glycine and gaba immunopositive neurons and terminals in the Deep Cerebellar Nuclei of normal and purkinje cell degeneration mutant mice
The Journal of Comparative Neurology, 1997Co-Authors: Jorg Baurle, Ursula GrussercornehlsAbstract:The total number of glycine-immunopositive (Gly+) neurons in the Deep Cerebellar Nuclei (DCN) was quantified under normal conditions in wild-types (B6C3Fe) and compared with the Purkinje cell-deprived situation in Purkinje cell degeneration (PCD)-mutants by using an unbiased stereological method, the disector. In addition, the size and density of Gly+ terminals, the number of gamma-aminobutyric acid immunopositive (GABA+) somata and the somatal colocalization of Gly and GABA were determined. In both wild-types and PCD mutants, Gly+ somata are distributed relatively homogeneously among the different subdivisions of the DCN. However, in the complete volume of the DCN, which is reduced in PCD mutants by 52%, 8,582 Gly+ neuronal somata are present in wild-types and 14,637 in PCD mutants, which corresponds to an increase of 70.5% in the mutant. In contrast, the total number of GABA+ somata is almost the same in wild-types (16,713) and in PCD mutants (15,339). The number of neurons that colocalize both Gly and GABA is again almost identical in wild-types (3,976) and PCD mutants (3,861). Moreover, the size and number of Gly+ terminals contacting DCN neurons of PCD mutants are increased significantly compared to the wild-types. These data define for the first time the normal distribution of glycine and its somatal colocalization with GABA in the DCN of the mouse. In addition, it is shown that the Purkinje cell loss in PCD mutants leads to a significant increase in Gly+ somata and to a larger size and number of Gly+ boutons in the DCN. This suggests that the respective neurons are capable of exerting an enhanced inhibitory synaptic activity on their target neurons, substituting, at least in part, for the lost Purkinje cell (PC) inhibition. Probable correlations of these findings with the mildness of the motor disturbances found in PCD mutants are discussed.
Shogo Endo - One of the best experts on this subject based on the ideXlab platform.
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Deep Cerebellar Nuclei play an important role in two tone discrimination on delay eyeblink conditioning in c57bl 6 mice
PLOS ONE, 2013Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:Previous studies have shown that Deep Cerebellar Nuclei (DCN)-lesioned mice develop conditioned responses (CR) on delay eyeblink conditioning when a salient tone conditioned stimulus (CS) is used, which suggests that the cerebellum potentially plays a role in more complicated cognitive functions. In the present study, we examined the role of DCN in tone frequency discrimination in the delay eyeblink-conditioning paradigm. In the first experiment, DCN-lesioned and sham-operated mice were subjected to standard simple eyeblink conditioning under low-frequency tone CS (LCS: 1 kHz, 80 dB) or high-frequency tone CS (HCS: 10 kHz, 70 dB) conditions. DCN-lesioned mice developed CR in both CS conditions as well as sham-operated mice. In the second experiment, DCN-lesioned and sham-operated mice were subjected to two-tone discrimination tasks, with LCS+ (or HCS+) paired with unconditioned stimulus (US), and HCS− (or LCS−) without US. CR% in sham-operated mice increased in LCS+ (or HCS+) trials, regardless of tone frequency of CS, but not in HCS− (or LCS−) trials. The results indicate that sham-operated mice can discriminate between LCS+ and HCS− (or HCS+ and LCS−). In contrast, DCN-lesioned mice showed high CR% in not only LCS+ (or HCS+) trials but also HCS− (or LCS−) trials. The results indicate that DCN lesions impair the discrimination between tone frequency in eyeblink conditioning. Our results suggest that the cerebellum plays a pivotal role in the discrimination of tone frequency.
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amygdala Deep Cerebellar Nuclei and red nucleus contribute to delay eyeblink conditioning in c57bl 6 mice
European Journal of Neuroscience, 2010Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:That the cerebellum plays an essential role in delay eyeblink conditioning is well established in the rabbit, but not in the mouse. To elucidate the critical brain structures involved in delay eyeblink conditioning in mice, we examined the roles of the Deep Cerebellar Nuclei (DCN), the amygdala and the red nucleus (RN) through the use of electrolytic lesions and reversible inactivation. All mice received eyeblink training of 50 trials during a daily session in the higher-intensity conditioned stimulus (CS) condition (10 kHz, 70 dB). DCN lesions caused severe ataxia; nonetheless, the mice acquired conditioned responses (CRs). Reversible inactivation of DCN, by muscimol (MSC) injection, led to a severe CR impairment in the early sessions of conditioning; however, in later sessions, the mice acquired CRs. Amygdala lesions impaired the acquisition of CRs, which did not reach the level of sham-operated mice, even after prolonged training sessions. MSC injections into the lateral amygdala severely impaired CRs, which began to recover after the removal of MSC. RN inactivation with MSC completely abolished CRs, and removal of MSC immediately restored CRs to the level of control mice. The results indicate that: (i) the DCN are important, but not essential, at least for the late acquisition in mouse eyeblink conditioning; (ii) the amygdala plays an important role in the acquisition and expression of CRs; and (iii) the RN is essential for the expression of CRs. Our findings reveal the various brain areas critically involved in mouse eyeblink conditioning, which include the cerebellum, amygdala and RN.
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gabaa receptors in Deep Cerebellar Nuclei play important roles in mouse eyeblink conditioning
Brain Research, 2008Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:Abstract The neural circuitry of eyeblink conditioning in rabbits has been studied in detail, however, the basic knowledge of eyeblink conditioning in mice remains limited. In the present study, we examined the role of the Deep Cerebellar Nuclei (DCN) in mice in delay eyeblink conditioning and rotor rod test performance by using the γ-aminobutyric acidA (GABAA) receptor agonist muscimol (MSC) and the GABAA receptor antagonist picrotoxin (PTX). Bilateral injections of MSC and PTX into the DCN significantly impaired motor coordination in the rotor rod test, however the performance recovered within 24 h after the injections. Bilateral injection of MSC and PTX significantly impaired learned eyeblink responses (LER) during the acquisition test. MSC-injected mice could not acquire LER, however, PTX-injected mice acquired LER latently, suggesting the distinctive effect of these drugs in DCN. Bilateral injection of MSC and PTX also impaired the retention of acquired LER during a 7-day performance test. Furthermore, ipsilateral injections of MSC and PTX impaired the acquired LER as much as bilateral injection of them. Contralateral MSC injections also impaired the expression of LER, but contralateral PTX injections only partially impaired eyeblink conditioning. These results suggest that GABAA receptors in bilateral DCN play important roles in both the acquisition and the expression of mouse eyeblink conditioning, and that GABAA receptors not only in ipsilateral but also in contralateral DCN are critical for the expression of LER.
Toshiro Sakamoto - One of the best experts on this subject based on the ideXlab platform.
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Deep Cerebellar Nuclei play an important role in two tone discrimination on delay eyeblink conditioning in c57bl 6 mice
PLOS ONE, 2013Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:Previous studies have shown that Deep Cerebellar Nuclei (DCN)-lesioned mice develop conditioned responses (CR) on delay eyeblink conditioning when a salient tone conditioned stimulus (CS) is used, which suggests that the cerebellum potentially plays a role in more complicated cognitive functions. In the present study, we examined the role of DCN in tone frequency discrimination in the delay eyeblink-conditioning paradigm. In the first experiment, DCN-lesioned and sham-operated mice were subjected to standard simple eyeblink conditioning under low-frequency tone CS (LCS: 1 kHz, 80 dB) or high-frequency tone CS (HCS: 10 kHz, 70 dB) conditions. DCN-lesioned mice developed CR in both CS conditions as well as sham-operated mice. In the second experiment, DCN-lesioned and sham-operated mice were subjected to two-tone discrimination tasks, with LCS+ (or HCS+) paired with unconditioned stimulus (US), and HCS− (or LCS−) without US. CR% in sham-operated mice increased in LCS+ (or HCS+) trials, regardless of tone frequency of CS, but not in HCS− (or LCS−) trials. The results indicate that sham-operated mice can discriminate between LCS+ and HCS− (or HCS+ and LCS−). In contrast, DCN-lesioned mice showed high CR% in not only LCS+ (or HCS+) trials but also HCS− (or LCS−) trials. The results indicate that DCN lesions impair the discrimination between tone frequency in eyeblink conditioning. Our results suggest that the cerebellum plays a pivotal role in the discrimination of tone frequency.
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amygdala Deep Cerebellar Nuclei and red nucleus contribute to delay eyeblink conditioning in c57bl 6 mice
European Journal of Neuroscience, 2010Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:That the cerebellum plays an essential role in delay eyeblink conditioning is well established in the rabbit, but not in the mouse. To elucidate the critical brain structures involved in delay eyeblink conditioning in mice, we examined the roles of the Deep Cerebellar Nuclei (DCN), the amygdala and the red nucleus (RN) through the use of electrolytic lesions and reversible inactivation. All mice received eyeblink training of 50 trials during a daily session in the higher-intensity conditioned stimulus (CS) condition (10 kHz, 70 dB). DCN lesions caused severe ataxia; nonetheless, the mice acquired conditioned responses (CRs). Reversible inactivation of DCN, by muscimol (MSC) injection, led to a severe CR impairment in the early sessions of conditioning; however, in later sessions, the mice acquired CRs. Amygdala lesions impaired the acquisition of CRs, which did not reach the level of sham-operated mice, even after prolonged training sessions. MSC injections into the lateral amygdala severely impaired CRs, which began to recover after the removal of MSC. RN inactivation with MSC completely abolished CRs, and removal of MSC immediately restored CRs to the level of control mice. The results indicate that: (i) the DCN are important, but not essential, at least for the late acquisition in mouse eyeblink conditioning; (ii) the amygdala plays an important role in the acquisition and expression of CRs; and (iii) the RN is essential for the expression of CRs. Our findings reveal the various brain areas critically involved in mouse eyeblink conditioning, which include the cerebellum, amygdala and RN.
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gabaa receptors in Deep Cerebellar Nuclei play important roles in mouse eyeblink conditioning
Brain Research, 2008Co-Authors: Toshiro Sakamoto, Shogo EndoAbstract:Abstract The neural circuitry of eyeblink conditioning in rabbits has been studied in detail, however, the basic knowledge of eyeblink conditioning in mice remains limited. In the present study, we examined the role of the Deep Cerebellar Nuclei (DCN) in mice in delay eyeblink conditioning and rotor rod test performance by using the γ-aminobutyric acidA (GABAA) receptor agonist muscimol (MSC) and the GABAA receptor antagonist picrotoxin (PTX). Bilateral injections of MSC and PTX into the DCN significantly impaired motor coordination in the rotor rod test, however the performance recovered within 24 h after the injections. Bilateral injection of MSC and PTX significantly impaired learned eyeblink responses (LER) during the acquisition test. MSC-injected mice could not acquire LER, however, PTX-injected mice acquired LER latently, suggesting the distinctive effect of these drugs in DCN. Bilateral injection of MSC and PTX also impaired the retention of acquired LER during a 7-day performance test. Furthermore, ipsilateral injections of MSC and PTX impaired the acquired LER as much as bilateral injection of them. Contralateral MSC injections also impaired the expression of LER, but contralateral PTX injections only partially impaired eyeblink conditioning. These results suggest that GABAA receptors in bilateral DCN play important roles in both the acquisition and the expression of mouse eyeblink conditioning, and that GABAA receptors not only in ipsilateral but also in contralateral DCN are critical for the expression of LER.
J. Caston - One of the best experts on this subject based on the ideXlab platform.
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Differential Roles of Cerebellar Cortex and Deep Cerebellar Nuclei in Learning and Retention of a Spatial Task: Studies in Intact and Cerebellectomized Lurcher Mutant Mice
Behavior Genetics, 1998Co-Authors: P. Hilber, F. Jouen, N. Delhaye-bouchaud, J. Mariani, J. CastonAbstract:Lurcher mutant mice (+/Lc) exhibit a massive loss of neurons in the Cerebellar cortex and the inferior olivary nucleus, while Deep Cerebellar Nuclei are essentially intact. To discriminate the relative participation of the Cerebellar cortex and Deep structures in learning and memory, 3 to 6-month-old +/Lc mice were subjected to a spatial learning task derived from the Morris water escape. They were able to learn to escape as well as their strain-matched controls (+/+). Seven days later, their scores showed that they had memorized the spatial environment but not as accurately as +/+ mice. Cerebellectomy before training did not significantly alter the escape learning capabilities of either group, whereas cerebellectomy performed after learning completely abolished retention in +/+, as well as in +/Lc, mice. These results suggest that the cerebellum, although not necessary for learning a spatial task, plays a crucial role in its retention, and that the storing structure of spatial information differs in +/+ and +/Lc mice.
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delayed spontaneous alternation in intact and cerebellectomized control and lurcher mutant mice differential role of Cerebellar cortex and Deep Cerebellar Nuclei
Behavioral Neuroscience, 1997Co-Authors: J. Caston, F Vasseur, Nicole Delhayebouchaud, J. MarianiAbstract:Lurcher mutant (+/Lc) mice exhibit a massive loss of neurons in the Cerebellar cortex and in the inferior olivary nucleus while Deep Cerebellar Nuclei are essentially intact. To discriminate the respective participation of the Cerebellar cortex and Deep structures in learning and memory, the authors subjected 3- to 6-month-old +/Lc mice to a delayed spontaneous alternation task to test their working and long-term spatial memories. Results show that wild type (+/+) mice alternated above chance even after a 1-hr delay between the forced and choice trials, whereas in +/Lc mice, long-term memory was impaired. Cerebellectomized +/+ mice behave as +/Lc mice (working memory was preserved but long-term memory was not), whereas in the cerebellectomized +/Lc mice, both working and long-term memories were altered. These results are discussed in terms of relationships between the cerebellum and the hippocampus.
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Differential roles of Cerebellar cortex and Deep Cerebellar Nuclei in the learning of the equilibrium behavior: studies in intact and cerebellectomized lurcher mutant mice.
Brain research. Developmental brain research, 1995Co-Authors: J. Caston, T. Stelz, N. Delhaye-bouchaud, F Vasseur, C Chianale, J. MarianiAbstract:Three- to 6-month-old lurcher mutant mice (+/lc), which exhibit a massive loss of neurons in the Cerebellar cortex and in the inferior olivary nucleus but whose Deep Cerebellar Nuclei are essentially intact, were trained daily, for 9 days, to maintain their equilibrium upon a rota rod rotating at 20 or 30 revolutions per minute (rpm). Their scores were measured and their behavior upon the rotating rod quantified in comparison to those of matched control (+/+) mice. Lurcher mice were able to learn to maintain their equilibrium efficiently when rotated at 20 rpm but were not when rotated at 30 rpm. After cerebellectomy, the equilibrium capabilities of the animals were much altered, especially in +/lc. These results show that the Deep Cerebellar Nuclei are sufficient for motor learning, provided the task is not too difficult (20 rpm), but that the Cerebellar cortex is required when the task is more difficult (30 rpm). Therefore, it can be concluded that the adaptive motor capabilities of lurcher mice are less developed than those of control animals.
Guy Cheron - One of the best experts on this subject based on the ideXlab platform.
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beta gamma burst stimulations of the inferior olive induce high frequency oscillations in the Deep Cerebellar Nuclei
European Journal of Neuroscience, 2018Co-Authors: Julian Cheron, Guy CheronAbstract:The cerebellum displays various sorts of rhythmic activities covering both low- and high-frequency oscillations. These Cerebellar high-frequency oscillations were observed in the Cerebellar cortex. Here, we hypothesised that not only is the Cerebellar cortex a generator of high-frequency oscillations but also that the Deep Cerebellar Nuclei may also play a similar role. Thus, we analysed local field potentials and single-unit activities in the Deep Cerebellar Nuclei before, during and after electric stimulation in the inferior olive of awake mice. A high-frequency oscillation of 350 Hz triggered by the stimulation of the inferior olive, within the beta-gamma range, was observed in the Deep Cerebellar Nuclei. The amplitude and frequency of the oscillation were independent of the frequency of stimulation. This oscillation emerged during the period of stimulation and persisted after the end of the stimulation. The oscillation coincided with the inhibition of Deep Cerebellar neurons. As the inhibition of the Deep Cerebellar Nuclei is related to inhibitory inputs from Purkinje cells, we speculate that the oscillation represents the unmasking of the synchronous activation of another subtype of Deep Cerebellar neuronal subtype, devoid of GABA receptors and under the direct control of the climbing fibres from the inferior olive. Still, the mechanism sustaining this oscillation remains to be deciphered. Our study sheds new light on the role of the olivo-Cerebellar loop as the final output control of the interCerebellar circuitry.
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purkinje cell bkchannel ablation induces abnormal rhythm in Deep Cerebellar Nuclei and prevents ltd
Scientific Reports, 2018Co-Authors: Guy Cheron, Julian Cheron, Javier Marquezruiz, Cynthia Prigogine, Claudia Ammann, Robert Lukowski, Peter Ruth, Bernard DanAbstract:Purkinje cells (PC) control Deep Cerebellar Nuclei (DCN), which in turn inhibit inferior olive nucleus, closing a positive feedback loop via climbing fibers. PC highly express potassium BK channels but their contribution to the olivo-Cerebellar loop is not clear. Using multiple-unit recordings in alert mice we found in that selective deletion of BK channels in PC induces a decrease in their simple spike firing with a beta-range bursting pattern and fast intraburst frequency (~200 Hz). To determine the impact of this abnormal rhythm on the olivo-Cerebellar loop we analyzed simultaneous rhythmicity in different Cerebellar structures. We found that this abnormal PC rhythmicity is transmitted to DCN neurons with no effect on their mean firing frequency. Long term depression at the parallel-PC synapses was altered and the intra-burst complex spike spikelets frequency was increased without modification of the mean complex spike frequency in BK-PC−/− mice. We argue that the ataxia present in these conditional knockout mice could be explained by rhythmic disruptions transmitted from mutant PC to DCN but not by rate code modification only. This suggests a neuronal mechanism for ataxia with possible implications for human disease.
