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PubMed1978

The action of phenytoin on a composite electrical-chemical synapse in the lamprey spinal cord.

The effect of phenytoin (PTN), 20 microgram per milliliter, was tested on the composite electrical-chemical synapse between pairs of giant interneurons in the isolated spinal cords of river lampreys (Ichthimyzon unicuspis). The main observations were that: (1) PTN reversibly reduced the chemical component of the excitatory postsynaptic potential by up to 70%; (2) PTN greatly reduced or eliminated posttetanic potentiation (PTP) of the chemical component; (3) PTN produced little or no decrease in the size of the electrical component; and (4) PTN did not cause blockage of the electrical component during high-frequency stimulation of the presynaptic neuron. Since the electrical component reflects the presynaptic spike, the suppression of PTP cannot be explained by blockage of this spike during the tetanus. These four observations are consistent with a current hypothesis concerning the anticonvulsant effect of PTN--that the drug inhibits calcium entry into stimulated presynaptic terminals. This would block PTP by reducing the accumulation of calcium in the terminal during repetitive stimulation.

Animals↗
PubMed1981

A unifying hypothesis for the cause of amyotrophic lateral sclerosis, parkinsonism, and Alzheimer disease.

The causes of amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer disease are unknown. Furthermore, treatment for two of these conditions is almost totally lacking. The thesis is presented that each of these disorders is due to lack of a disorder-specific neurotrophic hormone. The hormone would be elaborated or stored in the target of the affected neurons. It would be released by the postsynaptic cell and then exert its effects in a retrograde fashion after being taken up by the presynaptic terminal. In the lower motor neuron syndromes of amyotrophic lateral sclerosis, failure of muscle cells to release the appropriate motor neurotrophic hormone would result in impaired function of anterior horn cells. In Parkinson disease, the neurotrophic failure would be characterized by inability of striatal cells to provide the required dopamine neurotrophic hormone with resulting impairment of substantia nigra cells. In Alzheimer disease, the abnormalities would lie in failure of the hippocampus and cortical cells to supply the relevant cholinergic neurotrophic hormone with resulting impairment of medial septal and nucleus basalis neurons. Central nervous system tissue culture provides a convenient system in which to assay these neurotrophic hormones and should permit a test of the hypothesis.

Alzheimer Disease↗
PubMed1996

Genetic studies in Alzheimer's disease with an NACP/alpha-synuclein polymorphism.

The non-Abeta component of Alzheimer's disease amyloid (NAC) is copurified with amyloid from the brain tissue of Alzheimer's disease victims and is immunohistochemically localized to amyloid fibrils. NAC is a hydrophobic peptide fragment from the NAC precursor protein (NACP/alpha-synuclein) that is localized to presynaptic terminals. We used a polymorphic dinucleotide repeat sequence in a genomic clone of NACP for genetic association and linkage studies. Screening of Alzheimer's disease families failed to establish linkage between NACP and Alzheimer's disease. Nevertheless, one of the NACP polymorphisms (NACP allele 2) was shown to have significant association with healthy elderly control individuals with apolipoprotein E risk. This may indicate a possible protective function of the allele.

Aged↗
PubMed1981

An ultrastructural morphometric study of developing rat substantia gelatinosa.

A morphometric analysis has been done on developing rat substantia gelatinosa of the lower cervical and upper thoracic levels of the spinal cord starting on the 15th day of gestation. The following parameters were measured: cell body diameter, cytoplasmic/nuclear areas, synaptic density, synaptic type and vesicle morphology of the presynaptic terminal in axodendritic synapses. Cell body size and cytoplasmic/nuclear areas of gelatinosal cells increase until the 15th day postnatally and then decrease somewhat to the adult values. The first synapses are seen on gestation day 17. Synaptic density increases linearly until the third day postnatally. Axodendritic synapses are most common throughout development and in the adult, while the proportion of axoaxonic synapses increases and axosomatic synapses decreases during development. Most of the terminals in axodendritic synapses contain clear-spherical vesicles but the occurrence of clear-flat vesicles and dense-cored vesicles in the terminals increases during development. It appears that these morphological parameters provide a stable index of development in the substantia gelatinosa which can be correlated with functional devleopment of the area. Hopefully, they will provide a means to asses subtle anomalies induced by nonteratogenic drugs or other environmental changes.

Animals↗
PubMed2006

The 11-mer repeats of human alpha-synuclein in vesicle interactions and lipid composition discrimination: a cooperative role.

alpha-Synuclein is a protein abundant in presynaptic terminals in the brain. The N-terminal region of the sequence contains an imperfect 11-residue periodicity also found in A-class apolipoproteins and able to fold into an amphipathic helix. Here, the ability of three fragments of the protein, which include one, two, and all repeats, respectively, to bind to vesicles of different phospholipid composition is described. The results suggest a cooperative action of the repeats in selecting target membranes for interaction based on their lipid composition. This deduction is possibly related to the physiological role of the protein, which is still poorly understood.

Amino Acid Sequence↗
PubMed2001

Gamma synuclein: subcellular localization in neuronal and non-neuronal cells and effect on signal transduction.

Synucleins are small, highly conserved proteins in vertebrates, especially abundant in neurons and typically enriched in presynaptic terminals. alpha-Synuclein protein and a fragment of it, called NAC, have been found in association with pathological lesions of neurodegenerative diseases. Recently, mutations in a alpha-synuclein gene have been reported in families susceptible to an inherited form of Parkinson's diseases. In addition, alpha-synuclein has been implicated in the pathophysiology of other neurodegenerative diseases, including Alzheimer's disease and multiple system atrophy. Far less is known about other members of the synuclein family, beta- and gamma-synucleins. gamma-synuclein is up-regulated in several types of cancer and may affect the integrity of the neurofilament network, while its bovine ortholog, synoretin, activates the Elk-1 signal transduction pathway. In this paper, we present data about the localization and properties of human and bovine gamma-synuclein in several neuronal and non-neuronal cell cultures derived from ocular tissues. We show that gamma-synuclein is present in the perinuclear area and is localized to centrosomes in several types of human interphase cells and in bovine retinal pigment epithelium. In mitotic cells, gamma-synuclein staining is localized to the poles of the spindle. Further, overexpression of synoretin in retinoblastoma cells up-regulates MAPK and Elk-1. These results support the view that gamma-synuclein is a centrosome protein that may be involved in signal transduction pathways.

Animals↗
PubMed2002

Intact sorting, targeting, and clustering of gamma-aminobutyric acid A receptor subtypes in hippocampal neurons in vitro.

The cellular and subcellular distribution of four GABA(A) receptor subtypes, identified by the presence of the alpha1, alpha2, alpha3, or alpha5 subunit, was investigated immunocytochemically in dissociated cultures of hippocampal neurons. We addressed the questions whether (1) cell-type specific expression, (2) axonal/somatodendritic targeting, and (3) synaptic/extrasynaptic clustering of GABA(A) receptor subtypes was retained in vitro. For comparison, the in vivo distribution pattern was assessed in sections from adult rat brain. The differential expression of GABA(A) receptor subunits allowed to identify five morphologically distinct cell types in culture: the alpha1 subunit was observed in glutamic acid decarboxylase-positive interneurons, the alpha2 and alpha5 subunits marked pyramidal-like cells, and the alpha3 subunit labeled three additional cell types, including presumptive hilar cells. All subunits were found in the somatodendritic compartment. In addition, appropriate axonal targeting was evidenced by the intense alpha2, and sometimes alpha3 subunit labeling of axon-initial segments (AIS) of pyramidal cells and hilar cells, respectively. Accordingly, both receptor subtypes were targeted to AIS in vivo, as well. Synaptic receptors were identified by colocalization with gephyrin, a postsynaptic clustering protein, and apposition to presynaptic terminals labeled with synapsin I. In vitro and in vivo, alpha1- and alpha2-receptor subtypes formed numerous synaptic clusters, alpha3-GABA(A) receptors were located either synaptically or extrasynaptically depending on the cell type, whereas alpha5-GABA(A) receptors were extrasynaptic. We conclude that receptor targeting to broad subcellular locations does not require specific GABAergic innervation patterns, which are disturbed in vitro, but depends on protein-protein interactions in the postsynaptic cell that are both subunit- and neuron-specific.

Animals↗
PubMed2003

"Dormant basket cell" hypothesis revisited: relative vulnerabilities of dentate gyrus mossy cells and inhibitory interneurons after hippocampal status epilepticus in the rat.

The "dormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results from the loss of vulnerable neurons that normally excite insult-resistant inhibitory basket cells. We have reexamined the experimental basis of this hypothesis in light of reports that excitatory hilar mossy cells are not consistently vulnerable and inhibitory basket cells are not consistently seizure resistant. Prolonged afferent stimulation that reliably evoked granule cell discharges always produced extensive hilar neuron degeneration and immediate granule cell disinhibition. Conversely, kainic acid-induced status epilepticus in chronically implanted animals produced similarly extensive hilar cell loss and immediate granule cell disinhibition, but only when granule cells discharged continuously during status epilepticus. In both preparations, electron microscopy revealed degeneration of presynaptic terminals forming asymmetrical synapses in the mossy cell target zone, including some terminating on gamma-aminobutyric acid-immunoreactive elements, but no evidence of axosomatic or axoaxonic degeneration in the adjacent granule cell layer. Although parvalbumin immunocytochemistry and in situ hybridization revealed decreased staining, this apparently was due to altered parvalbumin expression rather than basket cell death, because substance P receptor-positive interneurons, some of which contained residual parvalbumin immunoreactivity, survived. These results confirm the inherent vulnerability of dendritically projecting hilar mossy cells and interneurons and the relative resistance of dentate inhibitory basket and chandelier cells that target granule cell somata. The variability of hippocampal cell loss after status epilepticus suggests that altered hippocampal structure and function cannot be assumed to cause the spontaneous seizures that develop in these animals and highlights the importance of confirming hippocampal pathology and pathophysiology in vivo in each case.

Animals↗
PubMed2005

Distribution of proteins associated with synaptic vesicle endocytosis in the mouse and goldfish retina.

Current models of synaptic transmission require retrieval of membrane from the presynaptic terminal following neurotransmitter exocytosis. Dynamin, a GTPase, is thought to be critical for this retrieval process. At ribbon synapses of retinal bipolar neurons, however, compensatory endocytosis does not require GTP hydrolysis, suggesting that endocytosis mechanisms may differ among synapses. To understand better the synaptic vesicle recycling at conventional and ribbon synapses, the distributions of dynamin and two associated proteins, amphiphysin and clathrin, were examined in the retinas of goldfish and mouse by using immunocytochemical methods. Labeling for dynamin, clathrin, and amphiphysin was distributed differentially among conventional and ribbon synapses in retinas of both species. Ribbon synapses of photoreceptors and most bipolar cells labeled only weakly for dynamin relative to conventional synapses. Amphyiphysin labeling was strong at many ribbon synapses, and labeling in rod terminals was stronger than in cone terminals in the mouse retina. Clathrin labeling was heterogeneous among ribbon synapses. Similarly to the case with amphiphysin, mouse rod terminals showed stronger clathrin labeling than cone terminals. Among conventional synapses, there was heterogeneous labeling for all three endocytic proteins. Some labeling for each protein might have been associated with postsynaptic terminals. The differential distribution of labeling for these proteins among identified synapses in the retina suggests considerable heterogeneity in the molecular mechanisms underlying synaptic membrane retrieval, even among synapses with similar active zone ultrastructure. Thus, as with exocytosis, mechanisms of synaptic membrane retrieval may be tuned by the precise complement of proteins expressed within the synaptic terminal.

Animals↗
PubMed2005

Postnatal changes of vesicular glutamate transporter (VGluT)1 and VGluT2 immunoreactivities and their colocalization in the mouse forebrain.

Vesicular glutamate transporter 1 (VGluT1) and VGluT2 accumulate neurotransmitter glutamate into synaptic vesicles at presynaptic terminals, and their antibodies are thus considered to be a good marker for glutamatergic axon terminals. In the present study, we investigated the postnatal development and maturation of glutamatergic neuronal systems by single- and double-immunolabelings for VGluT1 and VGluT2 in mouse forebrain including the telencephalon and diencephalon. VGluT2 immunoreactivity was widely distributed in the forebrain, particularly in the diencephalon, from postnatal day 0 (P0) to adulthood, suggesting relatively early maturation of VGluT2-loaded glutamatergic axons. In contrast, VGluT1 immunoreactivity was intense only in the limbic regions at P0, and drastically increased in the other telencephalic and diencephalic regions during three postnatal weeks. Interestingly, VGluT1 immunoreactivity was frequently colocalized with VGluT2 immunoreactivity at single axon terminal-like profiles in layer IV of the primary somatosensory area from P5 to P10 and in the ventral posteromedial thalamic nucleus from P0 to P14. This was in sharp contrast to the finding that almost no colocalization was found in glomeruli of the olfactory bulb, patchy regions of the caudate-putamen, and the ventral posterolateral thalamic nucleus, where moderate to intense immunoreactivities for VGluT1 and VGluT2 were intermingled with each other in neuropil during postnatal development. The present results indicate that VGluT2-loaded glutamatergic axons maturate earlier than VGluT1-laden axons in the mouse telencephalic and diencephalic regions, and suggest that VGluT1 plays a transient developmental role in some glutamatergic systems that mainly use VGluT2 in the adulthood.

Animals↗
PubMed2006

Structure and autonomic innervation of the swim bladder in the zebrafish (Danio rerio).

Many teleosts actively regulate buoyancy by using a gas-filled swim bladder, which is thought to be under autonomic control. Here we investigated the swim bladder in the zebrafish to determine possible mechanisms of gas-content regulation. Fluorescently labelled phalloidin revealed myocytes that appeared to form a possible sphincter at the junction of the pneumatic duct and esophagus. Myocytes also formed thick bands along the ventral surface of the anterior chamber and bilaterally along the posterior chamber. Thinner layers of myocytes were located elsewhere. Staining of peroxidase within erythrocytes revealed a putative rete and smaller blood vessels in muscle bands and elsewhere. The antibodies zn-12, a general neuronal marker, and SV2, a synaptic vesicle marker labelling presynaptic terminals, revealed widespread innervation of the swim bladder system. Widespread innervation of the swim bladder was also indicated by acetylcholinesterase histochemistry, but choline acetyltransferase-immunoreactive (-IR) somata and fibers were limited to the junction of the pneumatic duct and esophagus. In contrast, varicose tyrosine hydroxylase-IR fibers innervated muscles and blood vessels throughout the system. Neuropeptide Y-IR somata were located near the junction of the duct and esophagus and varicose fibers innervated muscles and vasculature of the posterior chamber and duct. Vasoactive intestinal polypeptide immunoreactivity was abundant throughout the anterior chamber but sparsely distributed elsewhere. Serotonin-IR fibers and varicosities were located only along blood vessels near the junction of the pneumatic duct and posterior chamber. Our results suggest that the zebrafish swim bladder is a complex and richly innervated organ and that buoyancy-regulating effectors may be controlled by multiple populations of autonomic neurons.

Acetylcholinesterase↗
PubMed1980

Uptake, intra-axonal transport and fate of horseradish peroxidase in embryonic spinal neurons of the chick.

Horseradish peroxidase (HRP) was injected in ovo into the ventral muscle mass of the hind limb of 5- to 7-day-old chick embryos or into the gastrocnemius muscle of 8- to 18-day embryos and localized histochemically. HRP is extensively incorporated via endocytosis into axonal growth cones or presynaptic terminals in the proximity of the injection site. Much of the tracer is taken up in vesicles and small vacuoles. Most of these are smooth-surfaced and only a few are bristle-coated. A small amount of the tracer is also incorporated into the axon terminal through the openings between the axolemma and an intricate membrane channel. The majority of the tracer-laden vesicles and vacuoles rapidly fuse with one another to become large vacuoles, some of which are transformed into multivesicular bodies (MVBs). In axon shafts, many labeled vacuoles and MVBs are transferred to tubule-like organelles, which appear to be the primary carrier for transporting the tracer back to the cell bodies in the lumbar spinal cord. HRP arrives in the sensory ganglia about 0.5-1 hour earlier than in the motoneurons of the lateral motor column. The maximal rate of the retrograde axoplasmic transport is about 3.5 mm/hour. After arriving in the cell bodies, HRP is transferred from tubule-like organelles to discrete vacuoles of various sizes and appearance. Lysosomal dense bodies and HRP-labeled vacuoles can be distinguished ultrastructurally. A fusion of HRP-labeled vacuoles with lysosomal dense bodies or Golgi vesicles was occasionally observed and the density of HRP-labeled vacuoles diminished after 2 to 3 days. Most of the HRP-labeled organelles were found to contain acid phosphatase activity. Therefore, the complete disappearance of HRP by 4 days postinjection is most likely related to lysosomal degradation. Neuronal cell bodies diffusely labeled with HRP were only observed prior to day 6. After day 6, despite various attempts to injure the peripheral axons, only granularly labeled cell bodies were found. This difference may imply that "mature" neurons have a more efficient mechanism for the sequestration of "free" HRP in the cytoplasmic matrix into membrane-bounded organelles. A mature-like retrograde transport mechanism appears to exist at the earliest stages of axonal growth in vivo.

Animals↗
PubMed1980

The synaptic organization of the motor nucleus of the trigeminal nerve in the opossum.

The motor nucleus of the opossum trigeminal nerve consists of a main body and a small dorsomedial cell cluster. The cell bodies form a unimodal population with areas that range from 150-2700 mum2. Golgi impregnations reveal that each neuron has three to six primary dendrites which radiate in all planes from the cell body. Within 300 mum from the soma, the primary dendrites divide into secondary branches and these, in turn, bifurcate into thinner distal dendrites. The overall diameter of the dendritic tree often extends as much as 1 mm, with a rare branch leaving the confines of the nucleus to enter the neighboring reticular formation. Somatic and dendritic spines are often present and are either sessile or complex appendage forms. The perikarya and initial dendritic trunks of trigeminal neurons are contacted by four types of presynaptic terminals which cover more than 40% of the membrane. Most endings are 1-3 mum long and contain either spherical (S) or pleomorphic (P) synaptic vesicles. Another, less common, type of bouton is marked by large dense-core (DC) vesicles. Approximately 8% of the terminals on trigeminal cell bodies are large (2-5 mum) with spherical synaptic vesicles and are always associated with a subsynaptic cistern (C-boutons). These terminals very often interdigitate with adjacent synaptic endings. S-, P-, and C-boutons synapse on the dendritic tree of trigeminal neurons in the following characteristic pattern: proximal dendrites (greater than 5 mum in diameter) are contacted by all three types of terminals; intermediate-sized dendrites (between 2.5 and 5.0 mum in diameter) are most often contacted by S-boutons although P-boutons are also present; and small, distal dendrites (less than 2.5 mum in diameter) are almost always contacted by S- boutons. Both S- and P-boutons contact spines. In order to determine the ultrastructural identity of some of the major afferent systems to the trigemina motor nucleus, adult opossums were subjected to two different types of lesions. Three and 5 days subsequent to lesions which destroyed most of the trigeminal mesencephalic nucleus, degenerating terminals containing spherical vesicles were found. These endings were S-boutons on more distal parts of the dendritic tree while on the cell body and proximal dendrites they were C-boutons. Seven days after a mesencephalic lesion, expanded glial processes approximated the trigeminal cell membrane. Two days subsequent to lesions which transected commissural fibers from the contralateral trigeminal complex, degenerating S- and P-boutons were found in contact with intermediate and distal parts of the trigeminal dendritic tree.

Animals↗
PubMed1983

Cerebellar output regulation by the climbing and mossy fibers with and without the inferior olive.

The activity of the olivocerebellar complex and the structures related in series with it have been studied using the complementary action of harmaline and 3-acetylpyridine to isolate the two principal inputs to the cerebellar Purkinje cells. The activities of the various nuclei as well as the entire brain have been simultaneously monitored using the [14C]2-deoxy-glucose method under the various combined effects of the pharmacological agents. (1) Tremogenic doses of harmaline increased the frequency of discharge in selected parts of the olivocerebellar system, increasing climbing fiber input and reducing Purkinje cell simple spike discharges in corresponding parts of the cerebellar cortex. The metabolic activity increased in the inferior olive and in the red nucleus. The results are interpreted as a net reduction of Purkinje cell inhibition on their target neurons, leading to a facilitatory cerebellar output. (2) Systemic injection of neurotoxic doses of 3-acetylpyridine selectively produced total degeneration of the neurons in the inferior olive, resulting in the suppression of complex spikes and a net increase in simple spike output from the Purkinje cells. The metabolic consequences were a reduction or absence in the inferior olive, decrease in the red nucleus, and increases in the Purkinje cell target neuron regions, including the intracerebellar and vestibular nuclei. The study of long survival times following the neurotoxic treatment revealed a transient metabolic marking of the inferior olive during the active glial processes accompanying the degeneration. In other parts the radioautographic changes caused by the destruction of the inferior olive persisted for about 1 month after the administration of the drug. (3) Tremogenic doses of harmaline were given to rats at different times following treatment with 3-acetylpyridine. It was demonstrated that: (a) intoxication of the inferior olive started within the second hour after 3-acetylpyridine administration, corresponding to the time at which the metabolic response to harmaline was also abolished; and (b) the increased metabolic activity produced by harmaline in the olivocerebellar complex was a consequence of an increased activity of the neurons of the inferior olive rather than a direct pharmacological effect of the drug. (4) Partial lesions of the inferior olive led to increased metabolic activity of those parts of the intracerebellar nuclei topographically related to the destroyed parts of the inferior olive. (5) In 3-acetylpyridine-treated animals, local ablation as well as local inactivation of the cerebellar cortex produced localized suppression of the intense labeling in the intracerebellar nuclei obtained in these animals. Since these regions receive synapses which are normally inhibitory, suppression of labeling clearly supports the hypothesis that regional marking may very well be produced by the activity of the presynaptic terminals themselves...

Animals↗
PubMed1983

An intracellular HRP study of the rat globus pallidus. II. Fine structural characteristics and synaptic connections of medially located large GP neurons.

In order to classify the presynaptic elements contacting the principle class of globus pallidus neurons, electron microscopic examination of serial sections made from a medially located large globus pallidus neuron, labeled with intracellular horseradish peroxidase, was undertaken. In addition, the use of labeled and light microscopically reconstructed material allowed us to quantitatively determine the distribution of each bouton type along the soma and dendrites. Six types of presynaptic terminals contacting the labeled cell have been recognized. Type 1 endings, the most numerous (84%), make symmetrical contacts on all portions of the cell, except spines, contain large pleomorphic, and a few large dense-core vesicles. Type 2 endings are filled with small spherical-to-ellipsoidal synaptic vesicles. They make asymmetrical contacts only with higher-order dendrites and account for 12% of synaptic contacts onto the labeled neuron. Type 3 endings are large, contain sparsely distributed large pleomorphic vesicles, and make two symmetrical synapses per bouton, one onto a spine head and the other onto the underlying dendritic shaft. They are infrequent (0.2%), being found only in association with dendritic spines. Type 4 endings contain large pleomorphic synaptic vesicles and no dense-core vesicles. They make symmetrical contacts with the short primary dendrites. Type 5 endings contain a mixture of small clear pleomorphic vesicles and numerous large dense-core vesicles. They contact only the cell body and the short primary dendrites, making up 20% of somatic synaptic contacts but less than 1% of contacts onto dendrites. Type 6 boutons contain oval and flattened synaptic vesicles and establish symmetrical contacts with higher-order dendritic branches and the cell body.

Animals↗
PubMed1986

Distribution and ultrastructure of synapses on a premotor local nonspiking interneuron of the crayfish.

Many premotor local nonspiking interneurons are involved in the control of the uropod movements of a crayfish. One of these interneurons was impaled intracellularly, characterized physiologically, and then labeled by intracellular horseradish peroxidase (HRP) injection to examine the distribution and ultrastructure of synapses. Depolarization of this interneuron by a current injection excited the closer motoneurons of the uropod and inhibited its opener motoneurons, but hyperpolarization had no effect. Input and output synapses are distributed all over the major branches and the finer neurites except for the main neurite (7-10 micron in diameter), which runs near the dorsal surface of the neuropil. Both types of synapse are located on the same neurite and are often intermingled in close proximity, often less than 1 micron apart. Presynaptic terminals of the interneuron contain round, clear vesicles that are densely packed in fine branches and spines. The number of synaptic vesicles associated with a particular output synapse was estimated to be about 2,000. No dense-cored granules are observed in the labeled neurites. Our results support the proposal that synaptic transmission in this class of interneurons of the crayfish can sometimes be restricted to a very small region of the branches and that, therefore, different regions of the interneuron can function independently.

Animals↗
PubMed1987

Fine structural studies of growth-hormone-releasing-factor (GRF)-immunoreactive neurons and their synaptic connections in the guinea pig arcuate nucleus.

The fine structure of neurons containing human growth-hormone-releasing factor (hGRF) immunoreactivity located in the arcuate nucleus of the guinea pig was studied by means of the preembedding immunohistochemical technique. The perikaryon of labeled neurons was fusiform or ovoid; the nucleus was regular in shape and contained a prominent nucleolus. The main ultrastructural features of the hGRF-immunoreactive neurons were the presence of numerous labeled secretory granules (100-120 nm in diameter) and the abundance and the enlargement of the organelles involved in the synthesis of the peptides: a well-developed rough endoplasmic reticulum and a conspicuous Golgi apparatus. Synaptic inputs were observed on immunoreactive perikarya but, above all, on the labeled dendrites. The unstained presynaptic nerve endings most often contained only small clear vesicles and formed symmetrical contacts. In rare cases, the presynaptic terminals exhibited both small clear and large dense vesicles and constituted asymmetrical contacts. Immunoreactive nerve endings were also observed in this area: the synaptic boutons contained large, stained vesicles and small, unlabeled, clear vesicles. These axon terminals made synaptic contacts with unstained dendritic processes; the contacts were symmetrical. The results indicate that hGRF-immunoreactive neurons of the guinea pig arcuate nucleus present morphological features of neuroendocrine cells. Moreover, the presence of hGRF-labeled nerve endings in the arcuate nucleus itself suggests that a substance related to hGRF might be a neuromodulator, at least in this area.

Animals↗
PubMed1990

Immunocytochemical localization of protein kinase C subspecies in the rat spinal cord: light and electron microscopic study.

Distinct expression of protein kinase C (PKC) subspecies in the central nervous system suggested that each subspecies has a distinct neural function in the processing and modulation of a variety of physiological responses to external signals. In this study, the cellular and subcellular distributions of beta I-, beta II- and gamma-subspecies of PKC were demonstrated by using subspecies-specific antibodies in the rat spinal cord. By light microscopy both gamma- and beta II-subspecies immunoreactivities were found only in neurons of the substantia gelatinosa and axons of the dorsal corticospinal tract in the spinal cord. Use of a double staining method, however, revealed that beta II-subspecies immunoreactivity was localized in the outer part of the lamina II, whereas gamma-subspecies immunoreactivity was found in the inner part of lamina II. Immunoreactive neurons containing beta I-subspecies were scattered in the substantia gelatinosa. Beta I-subspecies immunoreactivity varied in neuronal types. Furthermore, electron microscopic analysis clearly showed the subcellular distribution of these subspecies to be different from one another. Dense gamma-subspecies immunoreactivity was found in the cytoplasm except within cell organelles of the perikarya and dendrites. Some nuclei were stained as strongly as the cytoplasm and others were stained less heavily. The nucleoli had faint or no immunoreactivity. Reaction products of beta II-subspecies were located against the inner plasma membrane but not seen in the nuclei or nucleoli. Beta I-subspecies immunoreactivity appeared to be associated with the Golgi complex. No immunoreactive products of any PKC subspecies were detected in the presynaptic terminals. The different patterns of expression described above imply that individual PKC subspecies may have a specific function in modulating the neuronal activity in the different neurons of the spinal cord.

Animals↗