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PubMed1984

Concentration of F-actin in synaptic formations of the hippocampus as visualized by staining with fluorescent phalloidin.

Polymerized actin (F-actin) was localized in the guinea pig hippocampus by fluorescent staining with rhodamine-labeled phalloidin. Phalloidin displayed a preferential affinity for the main synaptic areas where the fluorescence was confined to 0.5-1 micron particles, roughly the size of synaptic structures (dendritic spines and presynaptic terminals). These particles appeared to stud the surface of dendrites. Particularly large and strongly fluorescent particles mainly 1-3 micron in diameter were found in the termination zone of mossy fibres which form the largest synapses of the hippocampus. The apparent high concentration of F-actin in synaptic formations suggests a role for actin in synaptic function.

Actins↗
PubMed1984

Phenytoin reduces frequency potentiation of synaptic potentials at the frog neuromuscular junction.

The action of the commonly used antiepileptic drug phenytoin on frequency potentials was studied at the frog neuromuscular junction. Whereas the drug, at concentrations of 0.1-0.3 mM, had only a slight effect on EPPs evoked by nerve stimulation at a frequency of 0.5 Hz, it strongly suppressed their potentiation during tetanic nerve stimulation at 30 Hz. The post-tetanic potentiation of the EPPs was also reduced by the drug. These effects occurred without a blockade of invasion of the nerve impulse into the presynaptic terminal during the tetanus, and thus indicate a specific frequency-dependent depressant action of the drug on neurally-evoked transmitter release.

Animals↗
PubMed1985

Cerebral cortex slices in sodium-free medium: depletion of synaptic vesicles.

Rat cerebral cortex slices superfused for 5 min in sodium-free medium after 30-min stabilization and 25-min superfusion periods in sodium-containing medium displayed a well-preserved tissue structure and mostly intact neurons and glial cells. Electron-microscopic morphometry showed the number of presynaptic terminals containing few (less than or equal to 10) vesicles to increase 3-fold after the 5-min depletion of sodium. The 90-min sodium depletion resulted in increased swelling and an additional decrease in synaptic vesicles. The results show that from a morphological point of view the substitution of sodium by choline with brain slice techniques is an eminently suitable method for studies on synaptic neurochemistry.

Animals↗
PubMed1985

Neurons with whorl bodies have increased numbers of synapses.

The endoplasmic reticulum in some neurons of the rat hypothalamic arcuate nucleus forms concentric sheets of smooth cisternae which are known as whorl bodies. It has been reported that the number and size of these structures change under varying endocrine conditions. For example, the number of rat arcuate nucleus neurons containing whorl bodies increases after gonadectomy. In studying their relationship to other components of the cell, we found that neuron profiles which contain whorl bodies receive a significantly increased number of axosomatic presynaptic terminals (P less than 0.001). Whorl bodies may mark a subpopulation of endocrine sensitive cells which are characterized by a different pattern of connections and whose response to stimuli includes changes in endoplasmic reticulum organization.

Animals↗
PubMed1985

Neuronal/glial plasticity in the supraoptic dendritic zone in response to acute and chronic dehydration.

The magnocellular neurosecretory cells of the supraoptic nucleus increase production and secretion of oxytocin and/or vasopressin in response to dehydration, gestation and lactation. Dynamic neuronal/glial interactions have also been shown to occur in response to these stimuli, resulting in a reversible increase in soma-somatic direct membrane apposition at these times. Chronic (lactation, 10 days of saline drinking) but not acute stimuli (4-24 h water deprivation) are further accompanied by the reversible formation of axo-somatic double synapses (one presynaptic terminal contacting two postsynaptic elements), which are virtually absent in control animals. The dendrites of these cells course ventrolaterally toward the ventral glial lamina, and have also been shown to be involved in this plasticity: dendro-dendritic direct membrane apposition and axo-somatic double synapses significantly vary with gestation and parturition. The present study investigated the dendritic zone response to both chronic and acute dehydration and rehydration. Increased dendro-dendritic membrane contacts resulted from both stimuli. Rehydration following acute dehydration resulted in a dose-dependent return to control levels, while rehydrated chronic dehydrates did not show such a return until 35 days of rehydration. The percentage of dendrites contacted by double synapses did not vary with treatment, and there were no sex differences. The recalcitrance on the part of the dendrites to return to normal following chronic dehydration may reflect a readiness to respond to renewed hormone demand.

Acute Disease↗
PubMed1986

The sources of extracellular potassium accumulation in the CA1 region of hippocampal slices.

To estimate the relative contributions of pre- and postsynaptic elements, and of synaptic and action potential-related currents, to the elevation of interstitial potassium ([K+]o) that occurs during neural activation, we measured [K+]o and focal electrical potential (Vec) during ortho- and antidromic stimulation, before and after blocking synaptic transmission, in the CA1 region of hippocampal tissue slices in vitro. Single stimulus pulses could cause delta [K+]o as large as 0.25 mM in stratum (st.) pyramidale and 0.27 mM in st. radiatum; stimulus trains could cause delta [K+]o as large as 10.5 mM in st. pyramidale and 6.25 mM in st. radiatum. Stimulus trains also caused negative Vec shifts; these shifts were related in a linear fashion to delta [K+]o. For a given increase in [K+]o, the change in Vec was greater in st. radiatum than in st. pyramidale. In st. pyramidale, the delta [K+]o evoked by antidromic stimulation was 65% of the delta [K+]o evoked by orthodromic stimulation (with equal population spike amplitudes). Blockade of synaptic transmission by removal of Ca2+ reduced orthodromically evoked delta [K+]o in st. radiatum by 52%; delta [K+]o in st. pyramidale was abolished. Removal of Ca2+ caused an 11% decrease in the delta [K+]o evoked in st. pyramidale by antidromic stimulation. We conclude that in the layer of dendritic trees (st. radiatum), approximately half of the K+ ions released into the interstitial space during orthodromic stimulation come from presynaptic terminals, with the remainder probably resulting from the ion currents of postsynaptic potentials. Among the pyramidal cell bodies (st. pyramidale), almost all of the excess K+ is released by action potential currents.

Animals↗
PubMed1986

Ultrastructural localization of brain 'vitamin D-dependent' calcium binding proteins.

Rat brain vitamin D-dependent calcium-binding protein (D-CaBP) was assessed for vitamin D dependency, calcium binding and ultrastructural localization within neurons. No evidence of vitamin D dependency could be derived from the experiments on vitamin D-deficient rats. A 95% pure extract of the 27-kDa brain D-CaBP was shown to bind 45Ca on nitrocellulose membrane after sodium dodecyl sulphate-electrophoresis, specifically on the 27-kDa CaBP band. Immunogold staining with electron microscopy allowed detection of D-CaBP into Purkinje cells and climbing fibers of the cerebellum. The immunoreactivity was found to be hyaloplasmic and never membrane-bound. It was present in neuronal soma, neurites and postsynaptic as well as presynaptic terminals. These findings rule out D-CaBP as a possible neurotransmitter and bring further support to the hypothesis that the protein functions as a cytosolic calcium buffer. Immunohistochemical detection of D-CaBP is proposed as a means for morphologic detection of neurons with high calcium metabolism.

Animals↗
PubMed1986

Gonadotropin responses to naloxone may depend upon spontaneous activity in noradrenergic neurons at the time of treatment.

The opiate system is thought to modulate gonadotropin secretion by its effect on catecholamine secretion. This action may be produced by opiates regulating the amount of catecholamine released from presynaptic terminals at a given frequency of depolarization and/or by increasing the rate of impulse traffic within catecholamine neurons. We examined the effects of naloxone, an opiate receptor antagonist, on luteinizing hormone (LH) and prolactin (Prl) secretion in 3 sex steroid-treated, gonadectomized rat models in which we have considerable information on the rates of turnover of norepinephrine (NE) and dopamine (DA) in the hypothalamus. In 7 day ovariectomized rats treated for 2 days with estradiol (E2), the injection of naloxone (10 mg/kg) at 09.15 h produced a small 3-fold rise in LH and a short-lived decline in Prl. In contrast, naloxone, given at 12.15 h, markedly amplified (10-fold) and advanced the time of the LH surge but did not affect afternoon Prl surges. Hypothalamic NE turnovers are low in the morning and high in the afternoon for such animals. Other ovariectomized (OVX) rats received E2 for 2 days and progesterone (P4) on day 2. Such treatment extinguishes the LH surges which normally occur the next day (day 3) but does not affect phasic Prl secretion. Naloxone, given at 09.15 h to E2P4-treated rats on day 3, did not affect basal LH levels but serum Prl declined for about 1 h. When given at 12.15 h, naloxone produced a small 3-fold rise in LH but did not affect phasic Prl release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Immunocytochemical localization of GABA in the cochlear nucleus of the guinea pig.

The immunocytochemical distribution of gamma-aminobutyric acid (GABA) was determined in the cochlear nucleus of the guinea pig using affinity-purified antibodies made against GABA conjugated to bovine serum albumin. Light microscopic immunocytochemistry shows immunoreactive puncta, which appear to be GABA-positive presynaptic terminals, distributed throughout the cochlear nucleus. In the ventral cochlear nucleus, these puncta are often found around unlabeled neuronal cell bodies. While occasional labeled small cells are found in the ventral cochlear nucleus, most GABA-immunoreactive cell bodies are present in the superficial layers of the dorsal cochlear nucleus. Based on size and shape, immunoreactive cells in the dorsal cochlear nucleus are divided into 3 classes: medium round cells with diameters averaging 16 microns, small round cells with average diameters of 9 microns and small flattened cells with major and minor diameters averaging 11 and 6 microns, respectively. Labeled fusiform and granule cells are not seen. A similar distribution of label was seen using antibodies against glutamic acid decarboxylase. Electron microscopic immunocytochemistry of the anteroventral cochlear nucleus shows GABA immunoreactive boutons containing oval/pleomorphic synaptic vesicles on cell bodies and dendrites. Other major classes of terminals, including those with small round, large round and flattened synaptic vesicles are unlabeled.

Animals↗
PubMed1987

GABAergic synapses and benzodiazepine receptors are not identically distributed in the primate retina.

The distribution of benzodiazepine receptors (BZR) was compared to the distribution of gamma-aminobutyric acid (GABA)-ergic synapses in the rhesus monkey retina using monoclonal antibodies against the BZR and polyclonal antisera to glutamate decarboxylase (GAD), the GABA-synthesizing enzyme which labels the presynaptic terminals of the GABAergic synapses. Indirect immunofluorescence including dual fluorochroming for both BZR and GAD indicates that although both were localized to the inner plexiform layer and adjacent cell body layers, their distributions were largely non-overlapping. Thus, in the primate retina, BZRs are not exclusively associated with GABAergic synapses.

Animals↗
PubMed1987

The Golgi apparatus-complex of neurons and astrocytes studied with an anti-organelle antibody.

An antiserum reacting with a 135-kDa antigen of rat liver Golgi apparatus-complex was used to stain, by light microscopic and ultrastructural immunocytochemistry, sections of rat cerebellum and by immunoblot homogenates of whole brain, isolated neurons and a fraction of enriched neuronal Golgi apparatus. In sections of rat cerebellum fixed with periodate-lysine-paraformaldehyde and immunostained with the direct peroxidase or peroxidase-antiperoxidase methods, the Golgi apparatus-complex in perikarya of neurons and glia was stained. Occasionally, nuclear envelopes and cisternae of the rough endoplasmic reticulum of neurons and glia were stained. Immunostain was not observed in peripheral dendrites, axons and presynaptic terminals. In striking contrast, peripheral smooth cisternae of astrocytic perikarya and processes were stained. Immunoblots of whole-brain membrane fractions, homogenates of isolated neurons and an enriched neuronal fraction of the Golgi apparatus-complex showed a principal single band of 64-kDa apparent mol. wt. We have concluded that the putative 64-kDa antigen(s) is distributed in cisternae of the Golgi apparatus-complex and occasionally in the nuclear envelope and rough reticulum, within the perikarya of neurons and glia. A second important distribution of the 64-kDa antigen(s), involving peripheral cisternae in perikarya and processes of astrocytes, is consistent with the hypothesis that the Golgi apparatus-complex of these cells extends to the periphery of these cells. The functional implications of the peripheral localization of the 64-kDa antigen(s) in astrocytes are discussed.

Animals↗
PubMed1987

Localization of a developmentally regulated neuron-specific protein S54 in dendrites as revealed by immunoelectron microscopy.

We sought to determine the ultrastructural localization of the developmentally regulated neuron-specific protein S54 in the chicken cerebellar cortex and optic tectum. The brains were fixed by perfusion with paraformaldehyde and glutaraldehyde. Frozen sections were immunocytochemically labeled with a monoclonal antibody to S54 protein. The immunoreactivity for S54 protein was localized in dendrites. No immunoreactivity for S54 protein was detected in axons and their presynaptic terminals.

Animals↗
PubMed1988

Immunohistochemical detection of GTP-binding regulatory protein (Go) in the autonomic nervous system including the enteric nervous system, superior cervical ganglion and adrenal medulla.

The localization of a GTP-binding regulatory protein, Go, in the autonomic nervous system including the enteric nervous system, superior cervical ganglion, and adrenal medulla, has been immunohistochemically examined by use of affinity-purified antibody against the alpha-subunit of Go. In the small intestine, dense Go-immunoreactive products were localized on the enteric nervous system, i.e. the myenteric plexus of Auerbach and the submucosal plexus of Meissner. In the superior cervical ganglion, presynaptic terminals were strongly immunoreactive to the Go antibody. The adrenal medulla was stained with this antibody, but the adrenal cortex was not immunoreactive to this antibody. Thus, the present study strongly suggests that Go is localized in the autonomic nervous system and plays its role in transmembrane signal transmission in this system.

Adrenal Medulla↗
PubMed1988

CCK-A receptors in the rat interpeduncular nucleus: evidence for a presynaptic location.

Using autoradiography, 'peripheral type' or cholecystokinin-A (CCK-A) receptor binding was measured in the interpeduncular nucleus (IPN) of rats which had received electrolytic lesions of the habenular nucleus. Presynaptic GABAB receptor binding was also determined in the IPN in order to verify the loss of input to the nucleus. In animals which showed almost total loss of GABAB receptors. 125I-Bolton Hunter CCK binding in the IPN was reduced from 1.83 +/- 0.28 pmol/g wet weight to 0.87 +/- 0.16 pmol/g wet weight. This was not significantly different from non-specific levels, determined in the same region using 10(-7) M L-365,031 (0.97 +/- 0.14 pmol/g wet weight). These data suggest that CCK-A receptors in rat IPN are localized on presynaptic terminals within the nucleus.

Animals↗
PubMed1989

Changes in extracellular calcium and magnesium and synaptic transmission in isolated mouse spinal cord.

Hemisected mouse spinal cords were maintained in vitro and the concentrations of calcium [CA2+] and of magnesium [Mg2+] in the bath were varied. In control solution containing 1.2 mM of both [Ca2+] and [Mg2+] stimulation of a dorsal root (DR) evoked in an adjacent DR an initial fiber volley representing 'input'; a postsynaptic compound spike recorded by volume conduction from dorsal gray matter, the dorsal horn response (DHR); and a slow dorsal root potential (DRP). In the ventral root of the stimulated segment a monosynaptic reflex (VRR1) was evoked. The fiber volley was enhanced by lowering [Ca2+] or [Mg2+] and depressed when either ion concentration was raised. The DRP, DHR and VRR1 were enhanced in low [Mg2+] and in moderately elevated [Ca2+]. At 1.8 mM [Ca2+] and above, the 'classical' dorsal root reflex (DRR) and a GABA-dependent delayed VR reflex (VRR2) appeared. Transmission of reflexes was maximal between 2.4 and 3.6 mM [Ca2+], while DRP was maximal at about 4.8 mM. In elevated [Mg2+] and in low [Ca2+] all synaptically transmitted responses (DRR, DRP and VRR) were depressed. The influence of both [Ca2+] and [Mg2+] was stronger on DRP, DRR and VRR2 than on DHR and VRR1. The effects of simultaneous changes of [Ca2+] and [Mg2+] partially cancelled each other. We conclude that low to moderately elevated [Ca2+] mainly influences the release of transmitter from presynaptic terminals; at very high [Ca2+] the depression of neuronal excitability dominates. The effects of Ca2+ and Mg2+ on GABAergic transmission are especially marked.

Action Potentials↗
PubMed1989

Hypogastric ganglion perinatal development: evidence for androgen specificity via androgen receptors.

The hypogastric ganglion (HG) has previously been shown to be sensitive to both the organizational and activational influences of testosterone. The current investigations examined whether testosterone exerts similar effects prenatally, whether these events are specifically controlled by androgen, and whether androgens might directly masculinize the HG. Prenatal treatment with an anti-androgen, flutamide, resulted in significant decreases in the adult levels of tyrosine hydroxylase (TH) activity, an index of postsynaptic noradrenergic ontogeny, and choline acetyltransferase (ChAT) activity, a marker for presynaptic terminal formation. In addition, testosterone propionate and dihydrotestosterone benzoate reversed the effects of neonatal castration on the development of TH and ChAT activities. In contrast estradiol benzoate was unable to restore enzyme activities. To determine whether the above observations might be produced by direct effects on the HG, androgen cytosol receptor characteristics were studied. Competition and saturation analyses demonstrate that the affinity and specificity of the androgen cytosol receptor in the HG are similar to that displayed in the pituitary, which has previously been shown to contain androgen receptors. These results suggest that the adult levels of TH and ChAT activities are organized during prenatal and early postnatal development. In addition, the organization of the HG appears to be androgen specific. The presence of cytosol androgen receptors suggests that the organizational effects of androgens are possibly induced by a direct mechanism.

Adrenergic Fibers↗
PubMed1989

A morphometric analysis of Torpedo synaptic vesicles isolated by iso-osmotic sucrose gradient separation.

The presynaptic terminal vesicle population of Torpedo electric organ is heterogeneous in size, consisting of two prominent subpopulations that comprise 80% of the total. The use of standard iso-osmotic sucrose gradients with zonal centrifugation to isolate vesicle fractions that co-localize with the acetylcholine (ACh) peak results in the recovery of: (1) 10% of the total estimated vesicle population; and (2) a single 68-nm diameter vesicle size class. The whereabouts of the major 90-nm subclass, which accounts for 60% of the total terminal population and which has long been considered to represent the resident ACh population, has been investigated. Assuming this subclass to have undergone severe osmotic stress, the effects of hypo- and hyper-osmotic salines, buffers and fixatives were examined and found to produce only negligible changes on vesicle size. Isolation of vesicles by hypo-osmotic shocking of synaptosomes purified on a Ficoll gradient, however, resulted in a reasonable approximation of the in situ distribution. As the iso-osmotic sucrose gradient procedure utilizes frozen blocks of electric tissue, this step is suspected of being involved in the loss, perhaps because of the slow freezing rates employed. These findings indicate that the 90 nm subclass is lost rather than transformed during isolation by sucrose gradient separation and that dimensionally, the cholinergic vesicle is a constant-sized and relatively stable structure.

Animals↗
PubMed1989

Autoradiographic distribution of [3H]hemicholinium-3 binding sites in human brain.

Since previous radioligand binding studies support the evidence that [3H]hemicholinium-3 ([3H]HC-3) selectively labels the high-affinity choline uptake (HACU) process, we have studied the autoradiographic characteristics and regional distribution of [3H]HC-3 binding to post mortem human brain tissue. [3H]HC-3 specific binding was saturable, of high affinity and exhibited an uneven distribution. High densities were observed in caudate-putamen, nucleus basalis accesorius of the amygdala, hippocampal gyrus dentatus and CA3 field, locus niger, nucleus interpeduncularis and motor trigeminal and facial nuclei. Low densities were found in areas such as neocortex, thalamus, hypothalamus or cerebellum. Our results agree with those obtained in human brain membranes and are comparable to previous autoradiographic data from rat brain. Remarkably, the distribution of [3H]HC-3 binding sites closely corresponds with that of cholinergic enzymatic presynaptic markers and HACU. These findings, together with previous data from membrane studies, allow the use of [3H]HC-3 as a selective anatomical marker of cholinergic presynaptic terminals.

Aged↗