The role of glycine as an inhibitory neurotransmitter is well established, and glycinergic neurons appear to play an important role in the mammalian retinae[Ikeda & Sheardown, 1983 ; Bolz et al., 1985]. Though it has been reported that certain conventional and displaced amacrine cells and a few of bipolar cells are consistently labeled with anti-glycine antiserum in the mammalian retinae so far[W ssle et al., 1986 ; Pourcho & Goebel, 1987 ; Davanger et al., 1991 ; Yoo & Chung, 1992], little has been studied on the synaptic circuitry of glycinergic neurons to clarify mechanism of its action in the visual processing of the mammalian retinae. This study was conducted to localize glycinergic neurons and to define their synaptic circuitry in the rat retina by immunocytochemical method using anti -glycine antiserum. The results were as follows : 1. Glycinergic neurons of the rat retina were conventional and displaced amacrine cells, interstitial cells and bipolar cells. 2. Glycinergic amacrine cells could be subdivided into two types, that is, A II amacrine cells and other amacrine cells, according to their ultrastructures. Glycinergic A II amacrine and other amacrine cell processes comprised postsynaptic dyad at the ribbon synapse of rod bipolar axon terminals in the sublamina b of the inner plexiform layer of the retina. Glycinprgic A II amacrine cell processes made gap junctions with axon terminals of unlabeled invaginating cone bipolar cells in the sublamina b, and made chemical synapses onto axon terminals of unlabeled flat cone bipolar cells and onto dendrites of ganglion cells in the sublamina a of the inner plexiform layer. In the sublamina b of the inner plexiform layer, g1ycinergic amacrine cell processes were postsynaptic to axon terminals of unlabeled invaginating cone bipolar cells, and made chemical output synapses onto axon terminals of unlabeled invaginating cone bipolar and rod bipolar cells and onto the dendrites of ganglion cells. Such cases that pre- and post-synaptic processes of glycinergic amacrine cell processes were non- glycinergic amacrine cell processes were frequently observed throughout the inner plexiform layer. In some cases, glycinergic amacrine cell processes receiving synaptic inputs from other glycinergic amacrine cell process made synaptic outputs onto the non-glycinergic or glycinergic amacrine cell processes. 3. Glycinergic bipolar cells could be subdivided into invaginating and flat cone bipolar cells. Postsynaptic dyads of cone bipolar cells at the ribbon synapses were non-glycinergic amacrine and amacrine cell processes, glycinergic amacrine and amacrine cell processes, glycinergic amacrine and non-glycinergic amacrine cell processes, and dendrite and dendrite of ganglion cells. These results demonstrate that [1] glycinergic A II amacrine cell receiving synaptic input from rod bipolar cells inhibit flat cone bipolar cells and OFF ganglion cells via chemical synapse, and excite ON cone bipolar cells via electrical synapse ; thereby visual information in the darkness can be transmitted to ON ganglion cells via ON cone bipolar cells, and [2] glycine released from glycinergic neurons inhibits directly ON and OFF ganglion cells or indirectly ON and OFF ganglion cells via non-glycinergic amacrine or bipolar cells.
Amacrine Cells ; Animals ; Darkness ; Dendrites ; Electrical Synapses ; Ganglion Cysts ; Gap Junctions ; Glycine ; Neurons* ; Neurotransmitter Agents ; Presynaptic Terminals ; Rats* ; Retina* ; Synapses

The purpose of this study was to investigate the distribution of neuropeptide Y (NPY) in the cat spinal trigeminal subnucleus caudalis following pulpectomy of mandibular premolars and molar by means of an immunohistochemical and immunoelectron microscopic study. The animals were divided into normal and experimental group which were sacrificed at 14 days after pulpectomy. The results were as follows; 1. On the light microscopic observation of the spinal trigeminal subnucleus caudalis in normal group, NPY-immunoreactivity (IR) was weak within lamina I and lamina II outer. In pulpectomy group, NPY-IR was strong and appeared to extend into lamina I and lamina II inner at 14 days. 2. On the immunoelectron microscopic observation of the spinal trigeminal subnucleus caudalis in normal group, NPY-IR was revealed in axon terminals, dendrites, myelinated axons and unmyelinated axons. NPY-IR was associated with membrane structures within microtubules, synaptic vesicles, outer membrane of mitochondria and inner surface of the axolemma. In NPY-immunoreactive structure, there was a small amount of DAB precipita-tions. 3. On the immunoelectron microscopic observation of the spinal trigeminal subnucleus caudalis at 14 days in pulpectomy group, the number of NPY-immunoreactive axon terminals, dendrites, myelinated axons and unmyelinated axons was increased than normal group. DAB precipitations in NPY-immunoreactive structure was increased than normal group. Some NPY-immunoreactive axon terminal formed synaptic glomerulus and axoaxonic synapse. 4. The results indicate that NPY-IR was increased in the spinal trigeminal subnucleus caudalis after pulpectomy, and it is speculated that the increased NPY by injury of peripheral nerve may participate in the processing of nociception.
Animals ; Axons ; Bicuspid ; Cats* ; Dendrites ; Immunohistochemistry ; Membranes ; Microtubules ; Mitochondria ; Molar ; Myelin Sheath ; Neuropeptide Y* ; Neuropeptides* ; Nociception ; Peripheral Nerves ; Presynaptic Terminals ; Pulpectomy* ; Synapses ; Synaptic Vesicles

No abstract available.
Synapses

The vertebrate neuromuscular junction (NMJ) is considered as a “tripartite synapse” consisting of a motor axon terminal, a muscle endplate, and terminal Schwann cells that envelope the motor axon terminal. The neuregulin 1 (NRG1)-ErbB2 signaling pathway plays an important role in the development of the NMJ. We previously showed that Grb2-associated binder 1 (Gab1), a scaffolding mediator of receptor tyrosine kinase signaling, is required for NRG1-induced peripheral nerve myelination. Here, we determined the role of Gab1 in the development of the NMJ using muscle-specific conditional Gab1 knockout mice. The mutant mice showed delayed postnatal maturation of the NMJ. Furthermore, the selective loss of the gab1 gene in terminal Schwann cells produced delayed synaptic elimination with abnormal morphology of the motor endplate, suggesting that Gab1 in both muscles and terminal Schwann cells is required for proper NMJ development. Gab1 in terminal Schwann cells appeared to regulate the number and process elongation of terminal Schwann cells during synaptic elimination. However, Gab2 knockout mice did not show any defects in the development of the NMJ. Considering the role of Gab1 in postnatal peripheral nerve myelination, our findings suggest that Gab1 is a pleiotropic and important component of NRG1 signals during postnatal development of the peripheral neuromuscular system.
Animals ; Mice ; Mice, Knockout ; Motor Endplate ; Muscle, Skeletal* ; Muscles ; Myelin Sheath ; Neuregulin-1 ; Neuromuscular Junction ; Peripheral Nerves ; Presynaptic Terminals ; Protein-Tyrosine Kinases ; Schwann Cells* ; Synapses* ; Vertebrates

Although the distribution of locus ceruleus terminals has been demonstrated in the fundus striati[nucleus accumbens septi] by light microscopy[Jones & Moore, 1977 ; Mason & Fibiger, 1979 ; Streit or et al., 1979 ; Groenewegen et al., 1980], the synaptic organization of its terminals was not clarified. The purpose of the present investigation was to demonstrate the direct monosynaptic connection of the locus ceruleus terminals to the neuronal elements of the fundus stirati, and to clarify the synaptic structures of its terminals by electron microscopy two days after unilateral electric coagulation of the locus ceruleus. In the ipsilateral fundus striati, many axon terminals undergone dark degeneration were observed. These degenerating terminals containing small clear vesicles have asymmetric synaptic contacts with dendritic spines. Already two days after locus ceruleus lesion, distinct features of terminal degenerations appeared in the fundus striati ; enlarged axon terminals with altered synaptic vesicles, decrease of synaptic vesicles detached from the synaptic site, multiplication of dense bodies and infiltration of floccular material. At the same time, a regressive change occurred in which astrocytic processes encircled totally degenerated synapses spiraled around the synaptic remnants. These observations indicate that monosynaptic noradrenertic afferent connections to the fungus striati are confirmed, and the locus ceruleus terminals characterized by small round vesicles might be formed asymmetrical axo-spinous synapses with spiny neurons in the fundus striati.
Animals ; Cats* ; Dendritic Spines ; Fungi ; Locus Coeruleus* ; Microscopy, Electron ; Neurons ; Presynaptic Terminals ; Synapses ; Synaptic Vesicles

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

Early postnatal period is considered as the critical period for formation and maturation of the synapses. And cerebellum has the major role in the development of equilibrium and somatic motor function, especially in the early postnatal age. So, I performed this study to investigate the morphological changes of the synapses in the rat cerebellar cortex. Sprague-Dawley rats were used as experimental animals. The ultrastructure of Synapses was observed in six groups ; 3-day, 1-week, 2-week, 3-week, 4-week, 5-week. The results are as followes. 1. After birth, the synaptic density was increased gradually by the forth week. 2. The length of postsynaptic densities was increased significantly in the period between first and second week. 3. There was significant correlation between the length of postsynaptic densities and the area of synaptic vesicle clusters. 4. The frequency of asymmetric and/or frown synapses was increased dramatically with advancing ages. According to the above results, the synaptogenesis in the rat cerebellum is very active in their early postnatal periods. And asymmetric and/or active frown synapses were the major type of synapses with advancing ages.
Animals ; Cerebellar Cortex* ; Cerebellum ; Critical Period (Psychology) ; Parturition ; Post-Synaptic Density ; Rats* ; Rats, Sprague-Dawley ; Synapses* ; Synaptic Vesicles

Neurotransmission begins with neurotransmitter being released from synaptic vesicles. To achieve this function, synaptic vesicles endure the dynamic "release-recycle" process to maintain the function and structure of presynaptic terminal. Synaptic transmission starts with a single action potential that depolarizes axonal bouton, followed by an increase in the cytosolic calcium concentration that triggers the synaptic vesicle membrane fusion with presynaptic membrane to release neurotransmitter; then the vesicle membrane can be endocytosed for reusing afterwards. This process requires delicate regulation, intermediate steps and dynamic balances. Accumulating evidence showed that the release ability and mobility of synapses varies under different stimulations. Synaptic vesicle heterogeneity has been studied at molecular and cellular levels, hopefully leading to the identification of the relationships between structure and function and understanding how vesicle regulation affects synaptic transmission and plasticity. People are beginning to realize that different types of synapses show diverse presynaptic activities. The steady advances of technology studying synaptic vesicle recycling promote people's understanding of this field. In this review, we discuss the following three aspects of the research progresses on synaptic vesicle recycling: 1) presynaptic vesicle pools and recycling; 2) research progresses on the differences of glutamatergic and GABAergic presynaptic vesicle recycling mechanism and 3) comparison of the technologies used in studying presyanptic vesicle recycling and the latest progress in the technology development in this field.
Action Potentials ; Axons ; physiology ; Calcium ; physiology ; Endocytosis ; Humans ; Presynaptic Terminals ; physiology ; Synapses ; physiology ; Synaptic Transmission ; Synaptic Vesicles ; physiology

Parkinson disease (PD) is the second most prevalent neurodegenerative disorder after Alzheimer disease. The loss of specific brain area, the substantia nigra pars compacta is known as a major etiology, however it is not fully understood how this neurodegeneration is initiated and what precisely causes this disease. As one aspect of pathophysiology for PD, synaptic dysfunction (synaptopathy) is thought to be an earlier appearance for neurodegeneration. In addition, some of the familial factors cumulatively exhibit that these factors such as α-synuclein, leucine-rich repeat kinase 2, parkin, PTEN-induced kinase 1, and DJ-1 are involved in the regulation of synaptic function and missense mutants of familial factors found in PD-patient show dysregulation of synaptic functions. In this review, we have discussed the physiological function of these genetic factors in presynaptic terminal and how dysregulation of presynaptic function by genetic factors might be related to the pathogenesis of Parkinson disease.
Alzheimer Disease ; Brain ; Neurodegenerative Diseases ; Parkinson Disease* ; Pars Compacta ; Phosphotransferases ; Presynaptic Terminals ; Synapses ; Synaptic Transmission ; Synaptic Vesicles

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*