No abstract

The lateral and interposed cerebellar nuclei may have different functions in the control of movement. Efferent fibres from both nuclei project predominantly to areas of the thalamus, which in turn project to the motor cortex. In this study, single and double anterograde-tracing techniques have been used to examine and compare the pathways from the lateral and interposed nuclei to the thalamus in the rat by using both light and electron microscopy to look for evidence of organisational or structural features that may underlie the proposed functional differences between these nuclei. Terminals from the lateral nucleus were found to be located most medially in the thalamus, predominantly in the ventral lateral nucleus and the rostral pole of the posterior nuclear group. Terminals from the posterior interposed nucleus were located slightly rostral and lateral to those from the lateral nucleus, mainly around the border between the ventral lateral nucleus and the ventral posterior medial nucleus. Terminals from the anterior interposed nucleus were located slightly rostral and lateral to those from the posterior interposed nucleus, predominantly in the rostral pole of the ventral posterior lateral nucleus. Terminals from the lateral and interposed nuclei were also found in double anterograde-tracing experiments to be nonoverlapping in the regions between these main areas of termination. The structure of terminals from the lateral and interposed nuclei, however, as well as their synaptic relationship with thalamic neurones, were found to be similar. The terminals are large and form synapses with proximal dendrites of thalamic neurones. They contained round vesicles and formed multiple synaptic contacts with dendritic shafts, as well as dendritic spines. The findings indicate that information from the lateral and interposed nuclei is processed in separate regions of the thalamus but that the mode of synaptic transfer to thalamic neurones is likely to be similar for the two projections.

Fragile X associated tremor/ataxia (FXTAS) affects older males carrying premutation, that is, expansions of the CGG repeat (in the 55-200 range), in the FMR1 gene. The neurological changes are linked to the excessive FMR1 mRNA, becoming toxic through a 'gain-of-function'. Since elevated levels of this mRNA are also found in carriers of the smaller expansion (grey zone) alleles, ranging from 40 to 54 CGGs, we tested for a possible role of these alleles in the origin of movement disorders associated with tremor.We screened 228 Australian males affected with idiopathic Parkinson's disease and other causes of parkinsonism recruited from Victoria and Tasmania, for premutation and grey zone alleles. The frequencies of either of these alleles were compared with the frequencies in a population-based sample of 578 Guthrie spots from consecutive Tasmanian male newborns (controls). There was a significant excess of premutation carriers (Fisher's exact test P =.006). There was also a more than 2-fold increase in grey zone carriers in the combined sample of the Victorian and Tasmanian cases, with odds ratio (OR)=2.36, and 95% confidence intervals (CI):1.20-4.63, as well as in Tasmanian cases only (OR=2.33, 95% CI:1.06-5.13), compared with controls. The results suggest

Failed storage capacity, leading to pulsatile delivery of dopamine (DA) in the striatum, is used to explain the emergence of 'wearing off' and dyskinaesia in Parkinson's disease. In this study, we show that surviving DA neurons in 6-OHDA lesioned rats sprout to re-innervate the striatum, and maintain terminal density until approximately 60% of neurons are lost. We demonstrate that DA terminal density correlates with baseline striatal DA concentration ([DA]). Electrochemical and synaptosome studies in 6-OHDA lesioned rats and primates suggest that impaired striatal DA re-uptake and increased DA release from medial forebrain bundle fibres contribute to maintaining striatal DA levels. In lesioned rats where terminal density fell by 60% or more, L-DOPA administration increased striatal DA levels markedly. The striatal [DA] produced by L-DOPA directly correlated with the extent of dyskinaesia, suggesting that dyskinaesia was related to high striatal [DA]. While sprouting and decreased dopamine uptake transporter function would be expected to contribute to the marked increase in L-DOPA induced [DA], the increased [DA] was most marked when DAergic fibres were >60% denervated, suggesting that other release sites, such as serotonergic fibres might be contributing. In conclusion, the extent of dyskinaesia was directly proportional to the extent of DA terminal denervation and levels of extra-synaptic striatal DA. We propose that sprouting of DA terminals and decreased dopamine uptake transporter function prevent the appearance of Parkinsonian symptoms until about 60% loss of nigral neurons, but also contribute to dysregulated striatal DA release that is responsible for the emergence of dyskinaesia and 'wearing off'.

The entopeduncular nucleus (EP) is a major outflow nucleus of the basal ganglia and innervates the lateral habenula, parafascicular, pedunculopontine, ventrolateral (VL), ventromedial (VM), and mediodorsal thalamic nuclei. This study investigated the morphology of single axons of entopeduncular neurons projecting to the motor thalamus by placing small injections of dextran biotin into the EP and reconstructing drawings of single axons from serial sections. There were two populations of entopeduncular-thalamic projection axons: those that projected only to the motor thalamus (VL and VM) and those that projected to both the motor thalamus and other nuclei (e.g., the habenula). The neurochemistry of EP neurons projecting to the thalamus was investigated by injecting the retrograde tracer FluoroGold into the VL and VM thalamic nuclei to retrogradely fill entopeduncular projection neurons. These were subsequently immunohistochemically labeled for choline acetyl transferase, gamma-aminobutyric acid (GABA), and glutamate. Consistent with previous studies, significant proportions of these neurons were GABA immunoreactive. In addition, approximately half of the entopeduncular-thalamic projecting neurons were found to be cholinergic. This excitatory input is most likely derived from axons that branch as they pass through the motor thalamus to the lateral habenula.

No abstract

A review on the geographical distribution, host range, diagnosis, pathogenesis, genetic characteristics, control, treatment and epizootiology of Enteric Redmouth Disease (ERM) in fishes caused by Yersinia ruckeri was presented.

The impetus behind this review is the question of whether the dopamine (DA) phenotype of neurons in the substantia nigra pars compacta (SNc) is activity-dependent. SNc DA neurons control movement through their projections to, and DA signaling in the dorsal striatum (the nigrostriatal pathway). Abnormal reduction of nigrostriatal DA signaling causes the motor symptoms of Parkinson's disease (PD), and abnormal DA signaling originating from the ventral midbrain generally (i.e. the nigrostriatal and mesocorticolimbic pathways) is thought to underlie symptoms of schizophrenia, drug addiction, and depression. The possibility that the DA phenotype of SNc neurons is activity-dependent is therefore intriguing from the viewpoints of neurobiology, behavior, and neurological disorders.Gene expression in neurons is activity-and Ca 2+ -dependent. More specifically, gene expression is sensitive to