1,721,300 research outputs found
The problem of a true consensual light reflex in birds
No full textThe problem of the consensual light reflex in birds has been studied with the aid of 2 techniques which have recently been introduced into ocular physiology: examination under infrared light and photocoagulation of the optic papilla. It was, therefore, concluded that in the owl a true consensual light reflex exists. There is also the possibility of a "pseudo-consensual" light reflex due to the light which crosses the interocular bony septum; but the contribution of this "pseudo-consensual-reflex," when present, is quantitatively negligible when compared with the true consensual reflex. ((c) 1997 APA/PsycINFO, all rights reserved
Presynaptic modulation by group III metabotropic glutamate receptors (mGluRs) of the excitatory postsynaptic potential mediated by mGluR1 in rat cerebellar Purkinje cells.
No full textPurkinje neurons were recorded from rat cerebellar slices. Parallel fibres stimulation elicited a fast excitatory postsynaptic potential (EPSP) mediated by ionotropic glutamate (iGluR) alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors followed by the inhibitory gamma-aminobutyric acid(A) (GABA(A))-dependent postsynaptic potential. In the presence of antagonists for iGluRs and for GABA(A) receptors, brief tetanic activation evoked a slow metabotropic glutamate receptor (mGluR)-dependent EPSP (mGluR-EPSP). This mGluR-EPSP was blocked by the selective mGluR1 antagonists LY367385 and CPCCOEt, but not by the mGluR5 antagonist MPEP. Group II agonists affected neither iGluR-EPSP nor mGluR-EPSP. Conversely, L-AP4 and L-SOP, group III mGluR agonists, inhibited both iGluR- and mGluR-EPSPs. The depolarisations evoked by both AMPA and group I agonists were unaffected, indicating a presynaptic action of group III mGluRs. These data suggest that glutamate released by parallel fibres activates group III mGluR autoreceptors, depressing both iGluR- and mGluR1-mediated EPSPs. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved
Structural plasticity of climbing fibers and the growth-associated protein GAP-43
No full textStructural plasticity occurs physiologically or after brain damage to adapt or re-establish proper synaptic connections. This capacity depends on several intrinsic and extrinsic determinants that differ between neuron types. We reviewed the significant endogenous regenerative potential of the neurons of the inferior olive in the adult rodent brain and the structural remodeling of the terminal arbor of their axons the climbing fiber under various experimental conditions, focusing on the growth-associated protein GAP-43. Climbing fibers undergo remarkable collateral sprouting in the presence of denervated Purkinje cells that are available for new innervation. In addition, severed olivo-cerebellar axons regenerate across the white matter through a graft of embryonic Schwann cells. In contrast, climbing fibers undergo a regressive modification when their target is deleted. In vivo knockdown of GAP-43 in olivary neurons, leads to the atrophy of their climbing fibers and a reduction in the ability to sprout toward surrounding denervated Purkinje cells. These findings demonstrate that GAP-43 is essential for promoting denervation-induced sprouting and maintaining normal climbing fiber architecture
Spontaneous saccades and gaze holding ability in the pigmented rat: I. Effects of inferior olive lesion.
No full textWe have studied the effects of lesion of the inferior olive on the spontaneous eye movements performed both in the light and dark in head restrained pigmented rats. The inferior olive lesion was made at least 1 month before study with 3-acetylpyridine and eye movements were recorded through a phase detection search coil apparatus. Following lesion, the spontaneous saccades performed in the dark present a postsaccadic drift which is made up of two components characterized by their different time courses, the first one being fast and the second one slow. The latter component is due to the leakage of the neural integrator and the former is mainly the consequence of a mismatch between the phasic and the tonic component of the ocular movement. In the light only the first component is present and then the eye maintains a steady position. After the lesion the saccades in the dark present a time constant of the slow component of the postsaccadic drift which is significantly reduced to approximately 600 - 900 ms from a value of 1600 - 4000 ms of the intact rats. This means that the integrity of the inferior olive is necessary to keep the time constant of the neural integrator within the physiological range. In the light, the amplitude of the postsaccadic drift depends on two factors. First, there is a mismatch between the phasic and the tonic components of the ocular movement, which are due to the pulse and the step of innervation of the extraocular muscles respectively. Different types of analysis have shown that the gain of the pulse to step transformation is about 0.77 at all saccadic amplitudes and eccentricities. Second, there is an increased leakiness of the neural integrator. Such a contribution increases linearly as a function of the eccentricity with a slope of 0.21. The main sequence of the saccades is not appreciably affected by the olivary lesion. Thus, the consequence of the inferior olive lesion may be interpreted as a general disruption of the integration process which, in physiological conditions, generates a proper and sustained oculomotor signal. More generally, it may be viewed as a loss of coordination between phasic and tonic motor commands
Effects of ethanol and imidazobenzodiazepine Ro 15-4513 on spontaneous saccades of the pigmented rat
No full textThe present study was aimed at investigating the alterations of the spontaneous saccadic eye movements of pigmented rats following ethanol administration. In addition we have studied the efficacy of the imidazobenzodiazepine Ro 15-4513 in reversing the effects of alcohol on saccades. The horizontal component of spontaneous eye movements was recorded by means of the magnetic field search coil technique on 11 head-restrained, pigmented rats. After the intraperitoneal injection of ethanol (1 g/kg) spontaneous saccades showed: i) a backward post-saccadic drift, with an exponential-like time course (time constant 100-150 ms); ii) a remarkable reduction of mean saccadic amplitude, up to 37% of control; iii) a significant decrease of peak velocity, which was reduced to about 80% of control. All these effects appeared and developed within a few minutes after the administration and were still present one hour later. When Ro 15-4513 (5 mg/kg) was injected i.p., 15 min after ethanol, the post-saccadic drift amplitude was immediately reduced and the drift was completely abolished within about 30 min. Mean saccadic amplitude returned to control values within a few minutes and was then steadily maintained for the following period examined (30 min). On the contrary, peak velocity showed only a slight tendency to recover which never was significant. When the same dose of Ro 15-4513 was injected alone there was no post-saccadic drift. However, mean saccadic amplitude increased, almost immediately, up to 160% of control. Its value showed a slight constant decrease in the following 30 min. Peak velocity was only slightly increased (up to 106% of control), but never was significantly different from control. Our results show that ethanol induces a remarkable impairment in the performance of spontaneous saccades. The imidazobenzodiazepine Ro 15-4513 is able to reverse completely only some of the alcohol-induced alterations, i.e. the post-saccadic drift and the reduction of saccadic amplitude, while it fails to counter efficiently the reduction of peak velocity. Ro 15-4513 exerts an intrinsic action, which is opposite to that of ethanol, on some of the saccadic parameters we have examined
Spontaneous saccades and gaze holding ability in the pigmented rat: II. Effects of localized cerebellar lesions.
No full textWe have studied the effects of the ablation of the cerebellar vermal area corresponding to lobules VI - VIII and of the flocculus - paraflocculus of both sides on the spontaneous eye movements performed in the light and in the dark in head-restrained pigmented rats. These effects have been compared with those already described for the inferior olive lesion. The cerebellar lesions were performed 1 week to 6 months in advance. Eye movements were recorded through a phase detection search coil apparatus. Following vermal topectomy, the main characteristics of the spontaneous saccades are unmodified. Following the ablation of the flocculus - paraflocculus there is no change in the saccadic main sequence. However, the spontaneous saccades in the dark present a postsaccadic drift made up of two components with different time courses, the first one being fast and the second one slow. The former is due in part to a mismatch between the phasic (the pulse) and the tonic (the step) components of the eye movements; the latter to the leakage of the neural integrator. In light only the first component is present and the eye maintains a steady position. The time constant of the neural integrator is considerably reduced to approximately 600 - 900 ms from a value of approximately 1600 - 4000 ms in the intact rats. The amplitude of the postsaccadic drift in the light depends on both the mismatch between the pulse and the step of innervation of the extraocular muscles and the increased leakiness of the neural integrator. The gain of the pulse to step transformation is reduced to approximately 0.79 at all saccadic amplitudes and eccentricities and such a reduction is due to a decreased step amplitude, while the pulse amplitude remains unchanged. The contribution of the leakage of the neural integrator to the postsaccadic drift in the light is a function of the eccentricity with a slope of 0.23. The deficits described after flocculus - paraflocculus ablation are also very similar to those described following inferior olive lesion from a quantitative point of view. The possible mechanisms of the visually activated olivocerebellar system in the control of saccadic performance and in maintaining its calibration are discussed
Postsynaptic current mediated by metabotropic glutamate receptors in cerebellar Purkinje cells
No full textIn rat cerebellar slices, repetitive parallel fiber stimulation evokes an inward, postsynaptic current in Purkinje cells with a fast component mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors and a slower component mediated by metabotropic glutamate receptors (mGluR). The mGluR-mediated excitatory postsynaptic current (mGluR-EPSC) is evoked selectively by parallel fiber stimulation; climbing fiber stimulation is ineffective. The mGluR-EPSC is elicited most effectively with increasing frequencies of parallel fiber stimulation, from a threshold of 10 Hz to a maximum response at ~ 100 Hz. The amplitude of the mGluR-EPSC is a linear function of the number of stimulus pulses without any apparent saturation, even with > 10 pulses. Thus mGluRs at the parallel fiber-Purkinje cell synapse can function as linear detectors of the number of spikes in a burst of activity in parallel fibers. The mGluR-EPSC is present from postnatal day 15 and persists into adulthood. It is inhibited by the generic mGluR antagonist (RS)-a-methyl-4-carboxyphenylglycine and by the group I mGluR antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid at a concentration selective for mGluR1. Although the intracellular transduction pathway involves a G protein, the putative mediators of mGluR1 (phospholipase C and protein kinase C) are not directly involved, indicating that the mGluR- EPSC studied here is mediated by a different and still unidentified second- messenger pathway. Heparin, a nonselective antagonist of inositol- trisphosphate (IP3) receptors, has no significant effect on the mGluR-EPSC, suggesting that also IP3 might be not required for the response. Buffering intracellular Ca2+ with a high concentration of bis-(o-aminophenoxy)- N,N,N',N'-tetraacetic acid partially inhibits the mGluR-EPSC, indicating that Ca2+ is not directly responsible for the response but that resting Ca2+ levels exert a tonic potentiating effect on the mGluR-EPSC
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