An attempt has been made to discriminate synaptic diversity in the neostriatum of the cat with emphasis on the characteristic structures of axon terminals and postsynaptic profiles. The differentiation of the axon terminals was based on the size and shape of synaptic vesicles in the axoplasm. Three types of axon terminals could be differentiated: Type I, the terminals contained small round (45 nm in diameter) vesicles; type II, the terminals with large pleomorphic (50 nm) vesicles; and type III, the terminals contained flattened (45 x 25 nm) vesicles. The type I terminals were making asymmetrical or symmetrical synapses in contact with the somata, dendrites and dendritic spines of neurons in the neostriatum, and a few type I terminals making asymmetrical or symmetrical contact with axons were also observed. The type II and III terminals were making symmetrical contact with the somata and dendrites of neostriatal neurons. A few type II terminals formed at the node of Ranvier of myelinated nerve fibers were making symmetrical contact with large dendrites. Additionally, dendro-dendritic and serial syanpses were rarely found in the neostriatum. In the serial synapses composed of axo-dendritic and dendro-dendritic synapses, the type I terminals making asymmetrical contact and the type II making symmetrical contact were identified.
Animals ; Axons ; Cats* ; Dendrites ; Dendritic Spines ; Neostriatum* ; Nerve Fibers, Myelinated ; Neurons ; Presynaptic Terminals ; Synapses ; Synaptic Vesicles

Synaptic adhesion molecules mediate synapse formation, maturation and maintenance. These proteins are localized at synaptic sites in neuronal axons and dendrites. These proteins function as a bridge of synaptic cleft via interaction with another synaptic adhesion molecules in the opposite side. They can interact with scaffold proteins via intracellular domain and recruit many synaptic proteins, signaling proteins and synaptic vesicles. Scaffold proteins function as a platform in dendritic spines or axonal terminals. Recently, many genetic studies have revealed that synaptic adhesion molecules and scaffold proteins are important in neurodevelopmental disorders, psychotic disorders, mood disorders and anxiety disorders. In this review, fundamental mechanisms of synapse formation and maturation related with synaptic adhesion molecules and scaffold proteins are introduced and their psychiatric implications addressed.
Anxiety Disorders ; Axons ; Child ; Autism Spectrum Disorder ; Dendrites ; Dendritic Spines ; Mood Disorders ; Neurons ; Proteins ; Psychotic Disorders ; Synapses ; Synaptic Vesicles

To analyze the synaptic characteristics of axon terminals originated from tooth pulp in the trigeminal principal sensory nucleus, and find morphological evidence that p-endings on these terminals use GABA as neurotransmitter, labeling of tooth pulp afferents with wheat -germ agglutinin conjugated horseradish peroxidase, postembedding immunocytochemistry and morphometric analysis were performed. The results obtained were as follows. The labeled boutons contained clear and round synaptic vesicles, and the mean number of synaptic contacts was 4.21 +/- 2.58. The postsynaptic profiles were usually middle or distal dendrites and dendritic spines rather than soma or proximal dendrites. The mean number of synaptic contacts with p -endings was 2.62 +/- 2.01. The volume of labeled bouton was 4.39 +/- 3.08 micro meter 3 and highly correlated (P<.01) with surface area (r = 0.96), total apposed surface area (r = 0.84), total active zone area (r = 0.84), mitochondrial volume (r = 0.95), the number of synaptic vesicles (r = 0.92), the number of synaptic profiles (r = 0.76) and the number of synaptic p -endings (r = 0.67). The p -endings contained pleomorphic synaptic vesicles. The volume of p -ending was 0.91 +/- 0.47 micro meter 3 and highly correlated (P<.01) with surface area (r = 0.94), total apposed surface area (r = 0.76), total active zone area (r = 0.62), mitochondrial volume (r = 0.70) and the number of synaptic vesicles (r = 0.94). P -endings were GABA immunoreactive. These results suggest that tooth pulp afferent terminals in trigeminal principal sensory nucleus may be related to complex processing of sensory information and presynaptic p -endings using GABA as neurotransmitter, are important in this sensory processing. The "size principle" of Pierce and Mendel (1993) is also applicable to tooth pulp afferent terminals and presynaptic p -endings.
Carisoprodol ; Dendrites ; Dendritic Spines ; gamma-Aminobutyric Acid ; Horseradish Peroxidase ; Immunohistochemistry ; Mitochondrial Size ; Neurotransmitter Agents ; Presynaptic Terminals ; Synaptic Vesicles ; Tooth* ; Triticum

To analyze the synaptic characteristics of axon terminals originated from the tooth pulp in the trigeminal nucleus oralis, labeling of tooth pulp afferents with wheat-germ agglutinin conjugated horseradish peroxidase and morphometric analysis with electron microscopic photographs were performed. The results obtained from 23 labeled endings were as follows. All of the labeled boutons contained clear and round synaptic vesicles (dia. 45~55 nm). 3 (13.64%) out of 23 labeled endings have 20~105 dense cored vesicles and do not make synaptic contacts with p-endings. But remaining 20 labeled endings (86.36%) almost do not have dense cored vesicles and 12 of them make synaptic contacts with p-endings. The mean number of synaptic contacts was 2.61+/-2.06 and the postsynaptic profiles were usually middle or distal dendrite and dendritic spine (1.74+/-1.36) rather than soma or proximal dendrite. The mean number of synaptic contacts with pendings was 0.87+/-1.01. And the frequency of the synaptic triads were 0.39+/-0.58. The vesicle density was 993.23+/-267.41/mum(2). The volume of labeled bouton was 3.54+/-2.20 mum(3) and highly correlated (P < 0.01) with surface area (11.78+/-4.92 mum(2), r = 0.95), total apposed surface area (2.90+/-1.56 mum(2), r=0.72), total active zone area (0.61+/-0.37 mum(2), r = 0.82), mitochondrial volume (0.75+/-0.53 mum(3), r = 0.94), the number of synaptic vesicles (2621.30+/-1473.61, r= 0.91) and the number of synaptic contacts (r = 0.76). These results suggest that there are two groups of tooth pulp afferent terminals according to the presence of dense cored vesicles in the trigeminal nucleus oralis. And the sensory processing mechanism of each groups may be different. And the "size principle" of Pierce & Mendell (1993) is also applicable to these terminals.
Carisoprodol ; Dendrites ; Dendritic Spines ; Horseradish Peroxidase ; Mitochondrial Size ; Mouth* ; Presynaptic Terminals ; Synapses ; Synaptic Vesicles ; Tooth ; Trigeminal Nuclei*

No abstract available.
Dendrites* ; Hippocampus* ; Interneurons*

In this study, change of optical properties and microstructure of an Ag-Pd-In alloy according to Ag content was investigated. For this purpose, specimen alloys were prepared by adding 0–100 wt.% of Ag to the 50Pd-50In (wt.%) alloy. When the content of Ag was more than 40 wt.%, the color difference with pure gold specimen was increased(p < 0.001). L* value increased as the Ag content of the specimen increased, but a* and b* value increased until the addition of 20 wt.% Ag, and then decreased with increasing Ag content(p < 0.001). Ag-free specimen was single phase in the as-cast state, but when the content of Ag was more than 20 wt.%, the phase separation occurred and two phases of matrix and dendrite or granular structure were confirmed. The dendrite or granular structure was composed of the InPd phase, and the matrix was composed of the Ag-rich phase. From these results, it can be concluded that the specimens with Ag content of 20–70 wt.% have the Ag-rich matrix which has a high L* value and low a* and b* value, and have the dendrite structure which has a low L* value and high a* and b* value. As the content of Ag increased, the color changed from light yellow to silver white due to the increase in the ratio of the matrix to the dendrite or granular structure.
Alloys ; Dendrites ; Silver

Voltage dependent calcium channels (VDCC) participate in regulation of neuronal Ca2+. The Rolling mouse Nagoya (Cacna1a(tg-rol) ) is a spontaneous P/Q type VDCC mutant, which has been suggested as an animal model for some human neurological diseases such as autosomal dominant cerebellar ataxia (SCA6), familial hemiplegic migraine and episodic ataxia type-2. Morphology of Purkinje cell (PC) dendritic spine is suggested to be regulated by signal molecules such as Ca2+ and by interactions with afferent inputs. The amplitude of excitatory postsynaptic current was decreased in parallel fiber (PF) to PC synapses, whereas apparently increased in climbing fiber (CF) to PC synapses in rolling mice Nagoya. We have studied synaptic morphology changes in cerebella of this mutant strain. We previously found altered synapses between PF varicosity and PC dendritic spines. To study dendritic spine plasticity of PC in the condition of insufficient P/Q type VDCC function, we used high voltage electron microscopy (HVEM). We measured the density and length of PC dendritic spines at tertiary braches. We observed statistically a significant decrease in spine density as well as shorter spine length in rolling mice compared to wild type mice at tertiary dendritic braches. In proximal PC dendrites, however, there were more numerous dendritic spines in rolling mice Nagoya. The differential regulation of rolling PC spines at tertiary and proximal dendrites in rolling mice Nagoya suggests that two major excitatory afferent systems may be regulated reciprocally in the cerebellum of rolling mouse Nagoya.
Animals ; Ataxia ; Calcium ; Calcium Channels ; Cerebellar Ataxia ; Cerebellum ; Dendrites ; Dendritic Spines ; Excitatory Postsynaptic Potentials ; Humans ; Mice ; Microscopy, Electron ; Migraine with Aura ; Models, Animal ; Neurons ; Plastics ; Spine ; Sprains and Strains ; Synapses

MicroRNAs (miRNAs) are critical for both development and function of the central nervous system. Significant evidence suggests that abnormal expression of miRNAs is associated with neurodevelopmental disorders. MeCP2 protein is an epigenetic regulator repressing or activating gene transcription by binding to methylated DNA. Both loss-of-function and gain-of-function mutations in the MECP2 gene lead to neurodevelopmental disorders such as Rett syndrome, autism and MECP2 duplication syndrome. In this study, we demonstrate that miR-130a inhibits neurite outgrowth and reduces dendritic spine density as well as dendritic complexity. Bioinformatics analyses, cell cultures and biochemical experiments indicate that miR-130a targets MECP2 and down-regulates MeCP2 protein expression. Furthermore, expression of the wild-type MeCP2, but not a loss-of-function mutant, rescues the miR-130a-induced phenotype. Our study uncovers the MECP2 gene as a previous unknown target for miR-130a, supporting that miR-130a may play a role in neurodevelopment by regulating MeCP2. Together with data from other groups, our work suggests that a feedback regulatory mechanism involving both miR-130a and MeCP2 may serve to ensure their appropriate expression and function in neural development.
Animals ; Dendrites ; genetics ; metabolism ; Dendritic Spines ; genetics ; metabolism ; Down-Regulation ; physiology ; Methyl-CpG-Binding Protein 2 ; biosynthesis ; genetics ; MicroRNAs ; genetics ; metabolism ; Rats

No abstract available.
Child* ; Dendrites* ; Epilepsy* ; Humans ; Interneurons*

The tottering (tg/tg) is neurologic mutant mouse exhibiting three neurological disorders: ataxia, petit mal-like absence seizures and myoclonic intermittent movement disorder. The tottering mouse carries an autosomal recessive single gene mutation on chromosome 8. The leaner (tgla) and Nagoya rolling (tgrol) are another two alleles of the tottering (tg). The combination of two mutant (tottering and leaner) produces compound heterozygous, tottering/leaner (tg/tgla) mouse. The genetic etilogy of the tottering and leaner was identified to be a mutation in voltage-dependent calcium channel a1A subunit. It made us link these animal model to human neurologic disease such as autosomal dominant cerebellar ataxia (SCA6), familial hemiplegic migraine and episodic ataxia type-2. The different onset and severity of neurological symptom of these three mutants (tg/tg, tg/tgla, tgla/tgla) offer good scale to analysis of pathophysiolgy of the neurologic disorder. Altered synapase between parallel fiber varicosity and dendritic spines of Purkinje cell was observed in adult tottering and leaner mice. Through the electron microscopic observation and anticalbindin-28 kd immunohistochemistry, we anaylzed not only the relationship between neurologic symptoms and synaptic plasticity around the ataxic onset of tottering, leaner and tottering leaner double mutation but also Purkinje cell morphology affected by voltage-sensitive calcium channel a1A subunit mutation in totterring mouse. Purkinje cell dendritic spines from proximal dendrites and axonal swellings of Purkine cell were observed frequently in wild type mice. The first apperance point of altered synapse based on semi-quantitative analysis was postnatal 15 days in leaner, postnatal 18 days in totering/leaner double mutation, and 30 days in tottering. These data suggest that altered synapse is associated with ataxia in tottering and leaner mice. Further study is needed to determine whether altered synapse is primary cause of ataxia.
Adult ; Alleles ; Animals ; Ataxia ; Axons ; Calcium Channels ; Cerebellar Ataxia ; Cerebellum* ; Chromosomes, Human, Pair 8 ; Dendrites ; Dendritic Spines* ; Epilepsy, Absence ; Humans ; Immunohistochemistry ; Mice* ; Mice, Neurologic Mutants ; Migraine with Aura ; Models, Animal ; Movement Disorders ; Nervous System Diseases ; Neurologic Manifestations ; Plastics* ; Synapses*