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PubMed1991

Developmental expression of the 25-kDa synaptosomal-associated protein (SNAP-25) in rat brain.

The developmental expression and subcellular distribution of the neuron-specific 25-kDa synaptosomal protein (SNAP-25) were investigated by using Northern (RNA) blots, immunoblots, and immunocytochemistry. Both SNAP-25 protein and mRNA were present at low levels in embryonic day 15 rat brain, and levels of both increased during early postnatal maturation. Developmental immunoblots with antipeptide antisera demonstrated that a 25-kDa peptide was the major isoform in brain, and this form increased steadily from embryonic day 15 through adulthood. A second 27-kDa immunoreactive isoform was present in brain only during early development. Immunoblots of two-dimensional SDS/polyacrylamide gels revealed the presence of a predominant 25-kDa isoform of SNAP-25 in adult brain. Immunocytochemical studies indicated that as immunoreactivity for SNAP-25 increased during development, the cellular localization of SNAP-25 immunoreactivity concomitantly shifted from axons and cell bodies to presynaptic terminals. These data suggest that the SNAP-25 protein shifts in subcellular localization during development and may play a role in the establishment and stabilization of specific presynaptic terminals in brain.

Animals↗

PubMed1997

Imaging of calcium in Drosophila larval motor nerve terminals.

Calcium measurements in the presynaptic terminal are essential in the investigation of mechanisms underlying neurotransmitter release. To enhance the genetic analysis of secretory mechanisms, we have developed Ca2+ imaging techniques for Drosophila larval motor nerve terminals. We studied Ca2+ signals in "big" (type Ib) and "small" (type Is) boutons that innervate ventral longitudinal muscles 6 and 7 in each abdominal segment of Canton-S (CS)-strain 3rd instar larvae. The indicator fluo-3 in conjunction with confocal microscopy was used to detect stimulus-dependent changes in [Ca2+]i. The Ca2+ signals were reliable and reproducible, and the resting fluorescence remained constant throughout the experiments. The Ca2+ signals increased with stimulus frequency from 5 to 20 Hz for both bouton types. No significant differences in the Ca2+ signals were seen between the two bouton types at 5 and 20 Hz, but there was a difference at 10 Hz. The decay of the Ca2+ signal was more prolonged after 20-Hz stimulation than after 5 and 10 Hz. At the single-synapse level, the secretory efficacy of Is synapses is greater than that of Ib synapses, but our data show that factors other than differences in Ca2+ entry may govern the strength of synaptic transmission.

Animals↗

PubMed1990

A monoclonal antibody specific to Müller cells and selective synaptic sites in the retina.

We have produced a monoclonal antibody which stains the Müller cells in the region of the photoreceptors, nerve terminals surrounding the horizontal cells, and nerve terminals in the inner plexiform layer in carp, goldfish, and white perch retinas. Electron microscopy showed that the staining in the outer and inner retina was confined to Müller cells and presynaptic terminals, respectively. In the teleost brain, the antibody stained only the optic tectum and efferent fibers from the stratum album centrale. Biochemical characterization by immunoblotting showed that this monoclonal antibody recognizes an approximately 70-kD molecule in both whole retina and brain homogenates, suggesting that the antibody recognizes an identical molecule. No staining was noted in the spleen or the liver. This monoclonal antibody appears to be specific to a molecule common to the Müller cells and presynaptic terminals in the teleost retina, and although it is present in other parts of the central nervous system, it is confined to the visual pathway.

Animals↗

PubMed2005

Monosynaptic pathway from rat vibrissa motor cortex to facial motor neurons revealed by lentivirus-based axonal tracing.

The mammalian motor cortex typically innervates motor neurons indirectly via oligosynaptic pathways. However, evolution of skilled digit movements in humans, apes, and some monkey species is associated with the emergence of abundant monosynaptic cortical projections onto spinal motor neurons innervating distal limb muscles. Rats perform skilled movements with their whiskers, and we examined the possibility that the rat vibrissa motor cortex (VMC) projects monosynaptically onto facial motor neurons controlling the whisker movements. First, single injections of lentiviruses to VMC sites identified by intracortical microstimulations were used to label a distinct subpopulation of VMC axons or presynaptic terminals by expression of enhanced green fluorescent protein (GFP) or GFP-tagged synaptophysin, respectively. Four weeks after the injections, GFP and synaptophysin-GFP labeling of axons and putative presynaptic terminals was detected in the lateral portion of the facial nucleus (FN), in close proximity to motor neurons identified morphologically and by axonal back-labeling from the whisker follicles. The VMC projections were detected bilaterally, with threefold larger density of labeling in the contralateral FN. Next, multiple VMC injections were used to label a large portion of VMC axons, resulting in overall denser but still laterally restricted FN labeling. Ultrastructural analysis of the GFP-labeled VMC axons confirmed the existence of synaptic contacts onto dendrites and somata of FN motor neurons. These findings provide anatomical demonstration of monosynaptic VMC-to-FN pathway in the rat and show that lentivirus-based expression of GFP and GFP-tagged presynaptic proteins can be used as a high-resolution neuroanatomical tracing method.

Animals↗

PubMed1977

Synaptic activation of Helix ganglion cells by barium ions.

Experiments were carried out on Helix suboesophageal ganglion cells by use of microelectrodes in order to study the effects of barium ions applied in 1-8 mM concentration. The overall effect of barium ions consisted in a marked depolarization, the thresholds of the ganglion cells, however, were quite different. In case of the most sensitive cells, bursting transformation and paroxysmal depolarization shifts occurred. A minor part of the neurons responded to barium ions with interruption of the spike generation which, in most cases, was accompanied by hyperpolarization. For a considerable part of the cells, the application of barium ions resulted in appearance of repetitive EPSP's and, infrequently, IPSP's. This was ascribed to excitatory effects exerted on the presynaptic terminals. It is concluded that barium ions have at least 2 points of attack in the ganglion: 1, on the soma membrane of the neurones, and 2, on the presynaptic terminals controlling them.

Action Potentials↗

PubMed2005

Retrograde signalling at the synapse: a role for Wnt proteins.

The formation of functional synapses requires a proper dialogue between incoming axons and their future synaptic targets. As axons approach their target, they are instructed to slow down and remodel to form proper presynaptic terminals. Although significant progress has been made in the identification of the mechanisms that control axon guidance, little is known about the mechanisms that regulate the conversion of actively growing axon into a presynaptic terminal. We found that Wnt secreted proteins are retrograde signals that regulate the terminal arborization of axons and synaptic differentiation. Wnts released from postsynaptic neurons induce extensive remodelling on incoming axons. This remodelling is manifested by a decrease in axon extension with a concomitant increase in growth-cone size. This morphological change is correlated with changes in the dynamics and organization of microtubules. Studies of a vertebrate synapse and the Drosophila neuromuscular junction suggest that a conserved Wnt signalling pathway modulates presynaptic microtubules as axons remodel during synapse formation. In this paper I discuss the role of the Wnt-Dvl (Dishevelled protein)-GSK-3beta (glycogen synthase kinase-3beta) signalling pathway in axon remodelling during synapse formation in the central nervous system.

Adaptor Proteins, Signal Transducing↗

PubMed1985

The mechanism of the inhibitory action of adrenaline on transmitter release in bullfrog sympathetic ganglia: independence of cyclic AMP and calcium ions.

The effects of adrenaline and dibutyryl adenosine 3':5' - cyclic monophosphate (db cyclic AMP) on nicotinic transmission in bullfrog sympathetic ganglia were compared by use of an intracellular recording technique. The evoked release of transmitter, acetylcholine (ACh), was decreased in the presence of adrenaline (10-100 microM), while the postsynaptic sensitivity to ACh was unchanged (10 microM adrenaline) or slightly reduced (100 microM). Transmitter release was similarly inhibited by dopamine (10 microM), but not by isoprenaline (10 microM). The inhibitory action of adrenaline on transmitter release was blocked by phenoxybenzamine but not by propranolol. The inhibition of transmitter release was independent of the external calcium concentration. The evoked release of transmitter and the electrical properties of the postsynaptic membrane were unchanged during exposure to db cyclic AMP (1-4 mM), while the postsynaptic sensitivity to ACh was slightly but significantly depressed. The spontaneous release of transmitter in a high K+ (10 mM) solution was decreased in the presence of adrenaline (100-300 microM), but unchanged with db cyclic AMP (4 mM). In contrast to the effects during exposure, both the evoked and spontaneous release of transmitter were enhanced after the removal of adrenaline or db cyclic AMP. Neither adrenaline (100 microM) nor db cyclic AMP (4 mM) affected the presynaptic spike and synaptic delay. It is concluded that adrenaline mainly inhibits the release of ACh from the presynaptic terminals through its alpha-action, while db cyclic AMP reduces slightly the postsynaptic sensitivity to ACh and that both agents facilitate transmitter release when they are removed from the presynaptic terminals. It is further suggested that the inhibitory action of adrenaline is independent of endogenous cyclic AMP and calcium ions.

Acetylcholine↗

PubMed1980

The pregeniculate nucleus of the monkey (Macaca multatta). II. A study at the electron microscopic level.

An electron microscope study of the ultrastructure of the pregeniculate nucleus of the monkey (Macaca mulatta) shows it to contain three neuronal types and four varieties of presynaptic terminals. Type I neurons are found only in the inner lamina, have small rounded profiles with few axosomatic synapses; the cytoplasm is poor in organelles and the nucleus is deeplly infolded. Type II neurons were observed infrequently and only in the outer lamina; they have large oblong profiles, exhibiting many axosomatic contacts, and containing abundant cytoplasm rich in organelles, particularly arrays of granular and agranular endoplasmic reticulum. Type III neurons were the most frequently seen and are found in both laminae; their profiles are elliptical and exhibit only a few axosomatic synapses. The cytoplasm surrounding the infolded nucleus is moderately rich in organelles with agranular endoplasmic reticulum predominating. These three neuronal types were found to correlate well with types of neurons found in material stained with cresylecht violet or impregnated by the Golgi method. Four presynaptic terminal types were discerned: a small cup-shaped profile containing spheroid vesicles and found predominantly in the outer lamina, a larger elliptical profile containing flattened spheroid vesicles, a large ramifying profile also containing round vesicles and largely restricted to the inner lamina, and a rounded profile containing larger flattened vesicles. Three days after eye enucleation, darkened degenerating profiles containing vesicles and forming asymmetric synapses were observed in the inner lamina, while the third terminal type described above could no longer be seen. The first three types are usually associated with asymmetric synaptic densities, whereas in the case of the last type, the postsynaptic synapse is symmetrical. The profile of this last terminal type was also sometimes observed to be both postsynaptic as well as presynaptic to other profiles; however, it was never observed to contain ribosomes. Such a pre- and postsynaptic terminal always forms part of the in series or triadic configuration of terminals occasionally observed in the pregeniculate nucleus.U

Animals↗

PubMed1988

Effects of lowering extracellular and cytosolic pH on calcium fluxes, cytosolic calcium levels, and transmitter release in presynaptic nerve terminals isolated from rat brain.

We examined the effects of extracellular and intracellular pH changes on the influx of radioactive 45Ca, the concentration of ionized Ca (pCai) as monitored with the Ca-sensitive fluorescent indicator fura-2, and the efflux of dopamine in presynaptic nerve endings (synaptosomes) isolated from rat brain corpora striata and preloaded with [3H]dopamine. Cytosolic pH (pHi) was monitored by loading the synaptosomes with the H+-sensitive fluorescent indicator 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) (see Nachshen, D. A., and P. Drapeau, 1988, Journal of General Physiology, 91:289-303). An abrupt decrease of the pH of the external medium, from 7.4 to 5.5, produced a slow decrease of pHi (over a 5-min period) from an initial value of 7.2 to a steady state level of approximately 5.8. When 20 mM acetate was present in acidic media, pHi dropped as fast as could be measured (within 2 s) to a level similar to that reached (more slowly) in the absence of acetate. It was therefore possible to lower pHi over short time periods to different levels depending on whether or not acetate was present upon extracellular acidification. Extracellular acidification to pH 5.5 (in the absence of acetate) had no significant effect on pCai and dopamine release over a 30-s period (pHi = 6.4). Acidification in the presence of acetate lowered pHi to 5.8 without affecting pCai, but dopamine efflux increased approximately 20-fold. This increase in basal dopamine release was also observed in the absence of extracellular Ca. Thus, intraterminal, but not extracellular, acidification could stimulate the efflux of dopamine in a Ca-independent manner. The high Q10 (3.6) of acid-stimulated dopamine efflux in the presence of nomifensine (which blocks the dopamine carrier) was consistent with an activation of vesicular dopamine release by H+. When synaptosomes were both depolarized for 2 s in high-K (77.5 mM) solutions and acidified (in the absence of acetate), there was a parallel block of 45Ca entry and evoked dopamine release (50% block at pH 6.0 with 0.2 mM external Ca). When acetate was included in the acidic media to further reduce pHi, Ca entry remained blocked, but evoked dopamine release was increased. Therefore, extracellular, but not cytosolic, acidification inhibited the release of dopamine by blocking voltage-gated Ca channels. The stimulation by cytosolic acidification of both basal and evoked dopamine release suggests that vesicular release in resting and depolarized synaptosomes was directly activated by cytoplasmic H+.

Animals↗

PubMed1979

Calcium channels in the high resistivity axonal membrane of photoreceptors of the giant barnacle.

1. The distribution of calcium channels in the cell membrane of the photoreceptor neurone of the giant barnacle, Balanus nubilus, was studied by recording intracellularly in or near the soma, in the axon, and near the presynaptic terminals. The membrane properties of these different regions of the cell could be studied by separately superfusing each region with test salines or by cutting the axon between two regions. 2. In the presence of tetraethylammonium (TEA) or 3-aminopyridine (3-AP), but not in their absence, Ca dependent action potentials could be evoked with depolarizing current pulses in the somatic, axonal, and terminal regions. Consequently, voltage-sensitive Ca channels and TEA-sensitive channels are present in all three regions of the cell. 3. The action potentials recorded from the three regions were similar in their slow times-to-peak (30-300 msec), long durations (0.2-2 sec in 100 mM-TEA), and long-lasting (0.2-10 sec) undershoots. The action potentials were inhibited by extracellular Co. 4. Clear differences were consistently observed between terminal action potentials and axonal or somatic action potentials in TEA. Terminal action potentials displayed a lower voltage threshold, faster rate of rise, and were less sensitive to inhibition by extracellular cobalt, suggesting that the Ca current is greater in the terminal region. 5. Bathing the receptor axon in low Ca or Co solutions led to a greater attenuation of large depolarizing components of the visual signal as they spread to the presynaptic terminals.

Action Potentials↗

PubMed1983

Neuronal changes induced by neonatal hypothyroidism: an ultrastructural study.

The postnatal development of the neurons of the cuneate nucleus was examined ultrastructurally in euthyroid and hypothyroid rats from birth to the sixth postnatal week. In the euthyroid animals, the neurons at birth displayed mild nuclear invaginations and a scanty cytoplasm with few organelles. By 2 weeks, there was a considerable increase in Nissl bodies. At 3 weeks, the neurons contained short lamellar arrays of endoplasmic reticulum. Between 3 and 6 weeks there was a reduction in the Nissl substance. In the hypothyroid animals, although the sequence of maturational changes generally resembled that of the controls, a number of differences were noted. The neurons at 1 week displayed dilations of perinuclear space, rough endoplasmic reticulum, Golgi complexes, and mitochondria. At 4 weeks both perikaryon and myelinated axons contained glycogen. Several neurons with cytoplasmic inclusions considered to be nonfunctional RNA were seen. The 6-week hypothyroid neuron exhibited large, clear, cytoplasmic vacuoles associated with a drastic reduction in cytoplasmic organelles. Presynaptic terminals showed a 50% reduction in mitochondrial numbers associated with the presence of glycogen granules. Three changes observed in neurites in all the age groups included: (1) large accumulation of glycogen in presynaptic terminals; (2) clear vacuoles; and (3) the presence of numerous lamellar bodies within reactive axons. Aberrant myelination, such as a single myelin sheath enclosing multiple processes, and instances of collapsed and redundant myelin were encountered.

Animals↗

PubMed2001

The neurobiology and evolution of cannabinoid signalling.

The plant Cannabis sativa has been used by humans for thousands of years because of its psychoactivity. The major psychoactive ingredient of cannabis is Delta(9)-tetrahydrocannabinol, which exerts effects in the brain by binding to a G-protein-coupled receptor known as the CB1 cannabinoid receptor. The discovery of this receptor indicated that endogenous cannabinoids may occur in the brain, which act as physiological ligands for CB1. Two putative endocannabinoid ligands, arachidonylethanolamide ('anandamide') and 2-arachidonylglycerol, have been identified, giving rise to the concept of a cannabinoid signalling system. Little is known about how or where these compounds are synthesized in the brain and how this relates to CB1 expression. However, detailed neuroanatomical and electrophysiological analysis of mammalian nervous systems has revealed that the CB1 receptor is targeted to the presynaptic terminals of neurons where it acts to inhibit release of 'classical' neurotransmitters. Moreover, an enzyme that inactivates endocannabinoids, fatty acid amide hydrolase, appears to be preferentially targeted to the somatodendritic compartment of neurons that are postsynaptic to CB1-expressing axon terminals. Based on these findings, we present here a model of cannabinoid signalling in which anandamide is synthesized by postsynaptic cells and acts as a retrograde messenger molecule to modulate neurotransmitter release from presynaptic terminals. Using this model as a framework, we discuss the role of cannabinoid signalling in different regions of the nervous system in relation to the characteristic physiological actions of cannabinoids in mammals, which include effects on movement, memory, pain and smooth muscle contractility. The discovery of the cannabinoid signalling system in mammals has prompted investigation of the occurrence of this pathway in non-mammalian animals. Here we review the evidence for the existence of cannabinoid receptors in non-mammalian vertebrates and invertebrates and discuss the evolution of the cannabinoid signalling system. Genes encoding orthologues of the mammalian CB1 receptor have been identified in a fish, an amphibian and a bird, indicating that CB1 receptors may occur throughout the vertebrates. Pharmacological actions of cannabinoids and specific binding sites for cannabinoids have been reported in several invertebrate species, but the molecular basis for these effects is not known. Importantly, however, the genomes of the protostomian invertebrates Drosophila melanogaster and Caenorhabditis elegans do not contain CB1 orthologues, indicating that CB1-like cannabinoid receptors may have evolved after the divergence of deuterostomes (e.g. vertebrates and echinoderms) and protostomes. Phylogenetic analysis of the relationship of vertebrate CB1 receptors with other G-protein-coupled receptors reveals that the paralogues that appear to share the most recent common evolutionary origin with CB1 are lysophospholipid receptors, melanocortin receptors and adenosine receptors. Interestingly, as with CB1, each of these receptor types does not appear to have Drosophila orthologues, indicating that this group of receptors may not occur in protostomian invertebrates. We conclude that the cannabinoid signalling system may be quite restricted in its phylogenetic distribution, probably occurring only in the deuterostomian clade of the animal kingdom and possibly only in vertebrates.

Animals↗

PubMed1978

Presynaptic modulation of voltage-dependent Ca2+ current: mechanism for behavioral sensitization in Aplysia californica.

Behavioral sensitization of the gill-withdrawal reflex of Aplysia is the result of a prolonged increase in transmitter release from the presynaptic terminals of sensory neurons. Earlier work suggested that this presynaptic facilitation might be mediated by a serotonin-sensitive adenylate cyclase in the sensory neuron terminals. Here we present evidence that presynaptic facilitation results from a cyclic AMP-dependent increase in the calcium current that underlies action potentials in the sensory neurons. The action potentials of sensory neuron cell bodies have, in addition to a sodium current, a calcium current that is enhanced by blocking the opposing potassium current with tetraethylammonium. Under these conditions, the action potentials show a slowly repolarizing plateau that follows the Nernst potential for a calcium electrode and serves as a sensitive assay for changes in calcium current. Stimulation of the pathway that mediates sensitization, incubation with serotonin or phosphodiesterase inhibitors, or intracellular injection of cyclic AMP produces an increase in the calcium plateau in the presence of tetraethylammonium. In addition, both before and after sensitizing stimulation, the duration of the plateau potential parallels transmitter release as measured by the amplitude of monosynaptic excitatory postsynaptic potentials evoked in the motor neurons by intracellular stimulation of single sensory neurons. These results are consistent with the idea that presynaptic facilitation is caused by a cyclic AMP-mediated increase in a voltage-sensitive calcium current in sensory neuron presynaptic terminals. This synaptic action is novel in that it can produce little or no change in the resting potential, is of long duration, and exerts its influence directly on a conductance triggered by the action potential, rather than on non-voltage-sensitive conductances, as is typical of conventional synaptic actions.

Action Potentials↗

PubMed1990

Increased MEPP frequency as an early sign of experimental immune-mediated motoneuron disease.

Intracellular recordings of miniature end-plate potentials were performed in extensor digitorum longus muscles from guinea pigs with experimental immune-mediated motoneuron destruction. In the early stages of the disease, the miniature end-plate potential frequency was elevated compared to that in control and normal animals. The amplitude and time course of the miniature end-plate potentials as well as the resting potential of the muscle fibers were not altered, which implies integrity of the postjunctional membrane. The increase in frequency of miniature end-plate potential reflects an increase of basal acetylcholine release and documents dysfunction of the presynaptic terminal of the neuromuscular junction. The increased frequency was associated with high levels of antimotoneuronal IgG in the blood and the presence of IgG at motor end-plates. These data suggest that the presynaptic terminal of the neuromuscular junction may be involved in the immune attack in animal models of motoneuron degeneration.

Animals↗

PubMed2006

Immunolocalization of the Ca2+-activated K+ channel Slo1 in axons and nerve terminals of mammalian brain and cultured neurons.

Ca(2+)-activated voltage-dependent K(+) channels (Slo1, KCa1.1, Maxi-K, or BK channel) play a crucial role in controlling neuronal signaling by coupling channel activity to both membrane depolarization and intracellular Ca(2+) signaling. In mammalian brain, immunolabeling experiments have shown staining for Slo1 channels predominantly localized to axons and presynaptic terminals of neurons. We have developed anti-Slo1 mouse monoclonal antibodies that have been extensively characterized for specificity of staining against recombinant Slo1 in heterologous cells, and native Slo1 in mammalian brain, and definitively by the lack of detectable immunoreactivity against brain samples from Slo1 knockout mice. Here we provide precise immunolocalization of Slo1 in rat brain with one of these monoclonal antibodies and show that Slo1 is accumulated in axons and synaptic terminal zones associated with glutamatergic synapses in hippocampus and GABAergic synapses in cerebellum. By using cultured hippocampal pyramidal neurons as a model system, we show that heterologously expressed Slo1 is initially targeted to the axonal surface membrane, and with further development in culture, become localized in presynaptic terminals. These studies provide new insights into the polarized localization of Slo1 channels in mammalian central neurons and provide further evidence for a key role in regulating neurotransmitter release in glutamatergic and GABAergic terminals.

Animals↗

PubMed2003

Cilnidipine as an agent to lower blood pressure without sympathetic nervous activation as demonstrated by iodine-123 metaiodobenzylguanidine imaging in rat hearts.

BACKGROUND: Administration of short-acting antihypertensive agents to patients with ischemic heart disease results in increased sympathetic nervous activity and is associated with worsened outcomes. Cilnidipine is an agent which blocks not only L-type calcium channels at the smooth muscle in the artery, but also N-type calcium channels at the presynaptic terminal. The goal of the present study was to determine the effect of cilnidipine on sympathetic nervous activity as on agent which blocks both L-type and N-type calcium channels at the presynaptic terminal, on sympathetic nervous activity in an experimental rat model using iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging. METHODS: Fourteen-week-old Wistar-Kyoto rats were divided into 3 separate groups: CTR group (control: distilled water administered), Nif group (nifedipine administered), or Cil group (cilnidipine administered). Agents were administered via a stomach tube, followed by injection of MIBG via the femoral vein. Systolic blood pressure (SBP) and heart rate (HR) were measured by tail-cuff plethysmography just prior to administration of antihypertensive drugs and 150 minutes later. Initial imaging (Ce) and delayed imaging (Cd) were defined as the sum of density counts in the region of interest created by adjusting to myocardial edge, and were corrected for both physical decay and weight. The myocardial washout rate (WR) was defined as the percent change in the count density from the initial to delayed images. RESULTS: Significant decreases in SBP were seen in the Nif group (from 132 +/- 3 mmHg to 85 +/- 5 mmHg, p < 0.0001) and the Cil group (from 128 +/- 4 mmHg to 92 +/- 7 mmHg, p = 0.0008), whereas no significant change in SBP was noted in the CTR group (from 123 +/- 5 mmHg to 127 +/- 3 mmHg). HR significantly increased in the Nif group (from 290 +/- 12/min to 378 +/- 14/min, p < 0.0001) but not in the CTR (from 278 +/- 3/min to 300 +/- 6/min) or Cil (from 291 +/- 6/min to 303 +/- 5/min) groups. WR was significantly greater in the Nif group (64.7 +/- 0.5%) when compared to the CTR (56.4 +/- 1.2%, p = 0.0031) or the Cil (55.4 +/- 2.2%, p = 0.0016) groups. CONCLUSION: In contrast to nifedipine, administration of cilnidipine did not result in increased myocardial sympathetic nervous activation.

3-Iodobenzylguanidine↗

PubMed1974

The electrostatic basis of Mg++ inhibition of transmitter release.

The inhibition by Mg(++) of stimulus-evoked transmitter release is attributed to a decrease in surface potential, Psi(0), on the outer surface of the presynaptic terminal and hence a lower surface calcium concentration, [Ca(++)](0). Data on the frog neuromuscular junction are quantitatively fit by assuming that there is a negative charge density, sigma, on the outer surface of the presynaptic terminal of 6.5 x 10(13) charges per cm(2) and that simple diffuse double layer theory is applicable. No specific binding of Mg(++) or Ca(++) is required. Without any additional assumptions, the inhibitory effect of univalent cations is also quantitatively predicted.

Acetylcholine↗

PubMed1981

The influence of protein restriction, rehabilitation and changing nutritional status on synaptic development: a quantitative study in rat brain.

Quantitative ultrastructural technique were employed to compare the development and maturation of cortical synapses in rats subjected to protein deprivation, control diet, nutritional rehabilitation and a normal-low crossover diet. Osmicated preparations of the molecular layer of occipital cortex were prepared at 15, 20, 28, 75 and 224 days postnatal in male rats. At 15 and 30 days the values for mitochondrial and synaptic densities, vesicle number and packing per terminal, synaptic length, terminal area and brain weight were lower in the protein-deprived than in the control animals. These initial deficits were progressively transformed to excesses, with the most marked crossover period occurring between 20 and 28 days. By 224 days only brain weight and presynaptic terminal area were lower in the protein-deprived material. A further parameter, synaptic curvature, showed a decrease in negativity in protein-deficient junctions between 15 days (64%) and 224 days (41%). Well-nourished tissue had fewer negatively-curved synapses during early development. These data suggest that the morphological development of the presynaptic terminals is not simply delayed, but is ultimately different in the protein-deprived animals. The nature of these changes may facilitate an adaptation to provide more efficient functioning in the adverse condition. Nutritionally rehabilitated tissue ultimately approaches the control, although significant differences occur in synaptic and mitochondrial densities and in brain weight. The normal--low crossover procedure intensities the differences noted in animals subjected to continuous deprivation.

Animals↗