The olivocerebellar system. II. Some ultrastructural correlates of inferior olive destruction in the rat

Desclin, Jean; Colin, Fabienne

doi:10.1016/0006-8993(80)90492-8

Cited by 76 publications

(16 citation statements)

References 39 publications

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“…Second, the increased irregularity of Purkinje cell firing in tg contributes to the occurrence of high frequency bursts of simple spikes [9]. Increased simple spike firing frequencies have been shown to affect the formation of vacuoles, mitochondria, smooth endoplasmatic reticulum, and cause the formation of whorled bodies, e.g., in response to lesions of the inferior olive [22,36,37]. Although the changes in simple spike firing in tg are not as profound as seen in wild-type animals after lesioning the inferior olive, the effects in tg are chronic and could therefore amount to a similar effect on Purkinje cell terminals.…”

Section: Discussionmentioning

confidence: 98%

Purkinje Cell Input to Cerebellar Nuclei in Tottering: Ultrastructure and Physiology

et al. 2008

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Homozygous tottering mice are spontaneous ataxic mutants, which carry a mutation in the gene encoding the ion pore of the P/Q-type voltage-gated calcium channels. P/Q-type calcium channels are prominently expressed in Purkinje cell terminals, but it is unknown to what extent these inhibitory terminals in tottering mice are affected at the morphological and electrophysiological level. Here, we investigated the distribution and ultrastructure of their Purkinje cell terminals in the cerebellar nuclei as well as the activities of their target neurons. The densities of Purkinje cell terminals and their synapses were not significantly affected in the mutants. However, the Purkinje cell terminals were enlarged and had an increased number of vacuoles, whorled bodies, and mitochondria. These differences started to occur between 3 and 5 weeks of age and persisted throughout adulthood. Stimulation of Purkinje cells in adult tottering mice resulted in inhibition at normal latencies, but the activities of their postsynaptic neurons in the cerebellar nuclei were abnormal in that the frequency and irregularity of their spiking patterns were enhanced. Thus, although the number of their terminals and their synaptic contacts appear quantitatively intact, Purkinje cells in tottering mice show several signs of axonal damage that may contribute to altered postsynaptic activities in the cerebellar nuclei.

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Section: Discussionmentioning

confidence: 98%

Purkinje Cell Input to Cerebellar Nuclei in Tottering: Ultrastructure and Physiology

et al. 2008

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“…Because IO projection neurons are not thought to give rise to excitatory local collaterals (Desclin and Colin, 1980;Foster and Peterson, 1986; De Zeeuw et al, 1998), we stimulated EPSCs by placing pairs of glass pipettes into the neuropil of the dPO. For experiments involving agonist application, pairs of EPSCs were evoked with an interstimulus interval of 20 ms at 0.1 Hz.…”

Section: Methodsmentioning

confidence: 99%

Serotonin Evokes Endocannabinoid Release and Retrogradely Suppresses Excitatory Synapses

Best

Regehr²

2008

Journal of Neuroscience

101

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5-HT 2 -type serotonin receptors (5-HT 2 Rs) are widely expressed throughout the brain and mediate many of the modulatory effects of serotonin. It has been thought that postsynaptic 5-HT 2 Rs act primarily by depolarizing neurons and thereby increasing their excitability. However, it is also known that 5-HT 2 Rs are coupled to G q/11 -type G-proteins and that some other types of G q/11 -coupled receptors can regulate synapses by evoking endocannabinoid release and activating presynaptic cannabinoid-type 1 receptors (CB 1 Rs). Here, we examine whether activation of 5-HT 2 Rs can regulate synapses through such a mechanism by studying excitatory synapses onto cells in the inferior olive (IO). These cells express 5-HT 2 Rs on their soma and dendrites, and the IO receives extensive serotonergic input. We find that the excitatory synaptic inputs onto IO cells are strongly suppressed by serotonin receptor agonists as well as release of endogenous serotonin. Both 5-HT 2 Rs and 5-HT 1B Rs contribute to this modulation by decreasing the probability of glutamate release from presynaptic boutons. The suppression by 5-HT 2 Rs is of particular interest because it is prevented by CB 1 R antagonists, and 5-HT 2 Rs are thought to be located only postsynaptically on IO cells. Our results indicate that serotonin activates 5-HT 2 Rs on IO neurons, thereby releasing endocannabinoids that act retrogradely to suppress glutamate release by activating presynaptic CB 1 Rs. These findings establish a link between serotonin signaling and endocannabinoid signaling. Based on the extensive distribution of 5-HT 2 Rs and CB 1 Rs, it seems likely that this mechanism could mediate many of the actions of 5-HT 2 Rs throughout the brain.

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“…The extreme ataxia and atypical gait exhibited by 3-AP-treated rats in this study were characteristic of ION destruction (Llinas et al, 1975;Desclin and Colin, 1980). The severe loss of motor control as a result of damage to the motor centers made feeding difficult and was most likely responsible for the decrease in body weight observed in 3-AP-lesioned rats.…”

Section: Discussionmentioning

confidence: 52%

“…For example, cervical vagotomy and nodose ganglionectomy decrease Ang I1 binding sites in the nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMV) (Diz et al, 1986;Lewis et al, 1986;Speth et al, 1987b). Intraperitoneal administration of the niacinamide antagonist, 3-acetylpyndine (3-AP), is reported to lesion neuronal penkarya preferentially in the ION (Desclin and Escubi, 1974;Llinas et al, 1975) while sparing afferent inputs to this nucleus (Desclin and Colin, 1980). In the present study, adult rats were treated with 3-AP a n d the binding of 1251sarcosinel, isoleucine' angiotensin I1 ('"I-SI Ang II), a n Ang I1 antagonist which binds with high affinity to Ang I1 receptors (Khosla et al, 1972), was then examined.…”

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confidence: 99%

Neuronal Localization of Specific Angiotensin II Binding Sites in the Rat Inferior Olivary Nucleus

Walters

Speth

1988

Journal of Neurochemistry

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Adult male Sprague-Dawley rats were treated with 3-acetylpyridine, a neurotoxin selective for the inferior olivary nucleus. Following treatment, the rats exhibited deficits in locomotor behavior indicative of destruction in the inferior olivary nucleus. The rats were sacrificed 3 weeks later, and the binding of 125I-sarcosine, isoleucine angiotensin II to brain homogenates and slide-mounted sections of brainstem was determined. Treatment with 3-acetylpyridine significantly decreased specific 125I-sarcosine, isoleucine angiotensin II binding in homogenates of posteroventral brainstem (containing the inferior olivary nucleus) by approximately 50%. Homogenates of dorsal brainstem and hypothalamus-thalamus-midbrain showed no significant changes in specific binding. Treatment with 3-acetylpyridine did not significantly alter the radioligand binding affinity which was determined in the hypothalamus-thalamus-midbrain. Autoradiographic analysis of 125I-sarcosine, isoleucine angiotensin II binding in the brainstem sections indicated that specific angiotensin II binding sites in the inferior olivary nucleus were virtually eliminated by the 3-acetylpyridine treatment. In addition, a comparatively small, but significant, decrease in specific 125I-sarcosine, isoleucine angiotensin II binding occurred in the solitary tract nucleus/dorsal vagal motor nucleus complex. These results indicate that specific angiotensin II binding sites in the inferior olivary nucleus occur exclusively on neuronal perikarya and/or dendrites.

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The olivocerebellar system. II. Some ultrastructural correlates of inferior olive destruction in the rat

Cited by 76 publications

References 39 publications

Purkinje Cell Input to Cerebellar Nuclei in Tottering: Ultrastructure and Physiology

Purkinje Cell Input to Cerebellar Nuclei in Tottering: Ultrastructure and Physiology

Serotonin Evokes Endocannabinoid Release and Retrogradely Suppresses Excitatory Synapses

Neuronal Localization of Specific Angiotensin II Binding Sites in the Rat Inferior Olivary Nucleus

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