Microanatomical localization of dopamine receptor protein immunoreactivity in the rat cerebellar cortex
ABSTRACT Dopamine (DA) receptor subtype localization was investigated in rat cerebellar cortex using immunohistochemical techniques with antibodies raised against D1–D5 receptor protein. A faint D1 receptor protein immunoreactivity was developed in molecular and Purkinje neurons layers. D2 receptor protein immunoreactivity was found primarily in cerebellar white matter followed by molecular and granular layers and Purkinje neurons. Antibodies against D2S receptor protein were localized in molecular layer and to a lesser extent, in granular layer. A few Purkinje neurons displayed a faint D2S receptor protein immunoreactivity. D3 receptor protein immunoreactivity was observed primarily in molecular and in Purkinje neurons layers of lobules 9 and 10. A faint D3 receptor protein immunoreactivity was also localized in Purkinje neurons and to a lesser extent, in molecular and granular layers of cerebellar lobules 1–8. D4 receptor protein immunoreactivity was found in cerebellar white matter. A pale immunostaining was also visualized in molecular layer. D5 receptor protein immunoreactivity was localized primarily in molecular and Purkinje neurons layers and to a lesser extent, in granular layer and in white matter. The above results indicate that rat cerebellar cortex expresses the DA receptor subtypes so far identified. Purkinje neurons, which are the only efferent neurons of cerebellum, are richest in DA receptor protein immunoreactivity. This suggests that dopaminergic neurotransmission may modulate efferent inputs from cerebellum. The localization of the majority of D2 and D4 and of a faint D5 protein receptor immunoreactivity in cerebellar white matter suggests that these receptors may be presynaptic and transported axonally.
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ABSTRACT: The senescence-accelerated mouse (SAM) was developed by selective breeding of the AKR/J strain, based on a graded score for senescence, which led to the development of both senescence-accelerated prone (SAMP), and senescence-accelerated resistant (SAMR) strains. Among the SAMP strains, SAMP6 is well characterized as a model of senile osteoporosis, but its brain and neuronal functions have not been well studied. We therefore decided to characterize the central nervous system of SAMP6, in combination with different behavioral tests and analysis of its biochemical and pharmacological properties. Multiple behavioral tests revealed higher motor activity, reduced anxiety, anti-depressant activity, motor coordination deficits, and enhanced learning and memory in SAMP6 compared with SAMR1. Biochemical and pharmacological analyses revealed several alterations in the dopamine and serotonin systems, and in long-term potentiation (LTP)-related molecules. In this review, we discuss the possibility of using SAMP6 as a model of brain function.Experimental Animals 01/2014; 63(1):1-9. · 1.46 Impact Factor
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ABSTRACT: Missing data are a common problem in most epidemiological and medical studies, including surveys and clinical trials. Imputation, or filling in the missing values, is an intuitive and flexible way to handle the incomplete data sets that arise because of such missing data. Here, in addition to imputation, including multiple imputation (MI), we discuss several other strategies and their theoretical background, as well as present some examples and advice on computation. Our focus is on MI, which is a statistically valid strategy for handling missing data, although we review other less sound methods, as well as direct maximum likelihood and Bayesian methods for estimating parameters, which are also valid approaches. The analysis of a multiply-imputed data set is now relatively standard using readily available statistical software. The creation of multiply-imputed data sets is more challenging than their analysis but still straightforward relative to other valid methods of handling missing data, and we discuss available software for doing so. Ad hoc methods, including using singly-imputed data sets, almost always lead to invalid inferences and should be eschewed, especially when the focus is on valid interval estimation or testing hypotheses.Handbook of Statistics 01/2007; 27:569-601.
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ABSTRACT: Plasticity at the cerebellar parallel fiber to Purkinje cell synapse may underlie information processing and motor learning. In vivo, parallel fibers appear to fire in short high frequency bursts likely to activate sparsely distributed synapses over the Purkinje cell dendritic tree. Here, we report that short parallel fiber tetanic stimulation evokes a ∼7-15% depression which develops over 2 min and lasts for at least 20 min. In contrast to the concomitantly evoked short-term endocannabinoid-mediated depression, this persistent posttetanic depression (PTD) does not exhibit a dependency on the spatial pattern of synapse activation and is not caused by any detectable change in presynaptic calcium signaling. This persistent PTD is however associated with increased paired-pulse facilitation and coefficient of variation of synaptic responses, suggesting that its expression is presynaptic. The chelation of postsynaptic calcium prevents its induction, suggesting that post- to presynaptic (retrograde) signaling is required. We rule out endocannabinoid signaling since the inhibition of type 1 cannabinoid receptors, monoacylglycerol lipase or vanilloid receptor 1, or incubation with anandamide had no detectable effect. The persistent PTD is maximal in pre-adolescent mice, abolished by adrenergic and dopaminergic receptors block, but unaffected by adrenergic and dopaminergic agonists. Our data unveils a novel form of plasticity at parallel fiber synapses: a persistent PTD induced by physiologically relevant input patterns, age-dependent, and strongly modulated by the monoaminergic system. We further provide evidence supporting that the plasticity mechanism involves retrograde signaling and presynaptic diacylglycerol.PLoS ONE 01/2013; 8(7):e70277. · 3.53 Impact Factor