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PubMed1975

Inhibitory and excitatory effects of CNS depressants on invertebrate synapses.

(1) The effects of pentobarbital were studied on the membrane properties and synaptic activity of crustacean neuromuscular junction preparations and molluscan neurons. (2) Pentobarbital selectivity depressed in a dose-dependent, reversible manner the exciatory postynaptic potentials (EPSPs) recorded at crustacean neuromuscular junctions without altering either inhibitory postsynaptic potentials (IPSPs) or post-synaptic membrane properties. (3) Pentobarbital depressed cholinergic EPSPs recorded in an identified molluscan neuron and depressed the depolarizing phase of biphasic PSP without affecting the hyperpolarizing phase of the BPSP on the same cell. Facilitation of the EPSP was not affected. (4) Pentobarbital did not appreciably alter the reversal potentials of the EPSP and IPSP. (5) Low concentrations of pentobarbital did not alter the appearance of spontaneously occurring IPSPs, while high concentrations changed the pattern of regular IPSP input to an irregular, burst-like pattern. (6) Pentobarbital and 5 other CNS depressants (cholralose, chloroform, ethanol, and urethane) increased the excitability and altered the current--voltage relations of a cell whose membrane properties have been proposed as a model of presynaptic terminal membranes. The effects were dependent on the species of external divalent cation present. (7) The results in these invertebrate systems may provide insight into the cellular basis of the depressant and excitatory effects of these agents.

Acetylcholine↗
PubMed1976

Ultrastructure and synaptic contacts in barrels of mouse SI cortex.

Barrels in the posteromedial barrel subfield (PMBSF) in layer IV of mouse somatosensory cortex are consistently identifiable and somatotopically related to the large whiskers on the animal's snout32,38. This is a study of the ultrastructure - in particular the synaptic connections - of mouse PMBSF barrels. A technique was developed which enabled the precise selection for electron microscopy of specific regions of barrels identified in the light microscope. Barrel "sides" containing a high density of neuronal cell bodies and myelinated axons, contrasted with barrel "hollows" in which these elements were relatively sparse. The types and frequencies of synapses were examined in series of thin sections through sides and/or hollows of barrels B2, C3, C7, D4, E4, E5, and E8 from 6 mice. In all, 3042 synapses from 20 fields, each at least 10 mum x 10 mum x 4.8 mum in size, were classified. Four distinct kinds of presynaptic terminal were identified: (1) darkly, and (2) lightly stained, asymmetrically synapsing terminals (AD, AL respectively), and (3) darkly, and (4) lightly stained, symmetrically synapsing terminals (SD, SL respectively). Synapses of these terminals were distributed in roughly similar proportions throughout the neuropil of barrel sides and hollows. Thus in all barrel regions approximately 92% of the synapses in neuropil were made by AD terminals, 1.0% by AL, 2.4% by SD and 4.0% by SL terminals.

Animals↗
PubMed1976

Cytochemical studies of lectin binding sites in smooth membrane cisternae of rat brain.

The cytochemical localization of concanavalin A (con A) binding sites has been studied in Purkinje cell axons and presynaptic terminals of rat cerebellum. Smooth membrane cisternae just beneath the axolemma contain con A binding sites on the side of the membrane facing the cisternal space. At certain regions, such as the node of Ranvier, these cisternae lie in virtual apposition to the axolemma. Such a specialized system of cisternae could serve as a channel through which some of the materials synthesized in the Purkinje somata are moved to the axon terminals. The close association of the cisternae and axolemma at certain regions could be a site at which some of the transported materials contribute to renewal of the axolemma. The con A binding sites on intracellular membranes of the Purkinje cell are removed by prior glycosidic and proteolytic enzyme digestions. The results suggest that at least some of the carbohydrates lining membrane cisternae are glycoprotein in nature.

Animals↗
PubMed1976

Facilitation and depression of synaptic transmission in amphibian sympathetic ganglia.

There have been few reports concerning facilitation and depression in sympathetic ganglia9,17,40. In the present investigation, pairs of excitatory postsynaptic potentials (EPSPs) were recorded intracellularly from bullfrog paravertebral sympathetic ganglia for an analysis of the site and mechanism responsible for the phenomena of facilitation and depression of ganglionic transmission. The ratio of the amplitude of the second of a depression of ganglionic transmission. The ratio of the amplitude of the second of a pair of EPSPs divided by the first was compared to the time interval between each pair of EPSPs divided by the first was compared to the time interval between each pulse. These ratios demonstrated two phases: an earlier phase of facilitation (20-500 msec pulse intervals) and a later phase of depression (500 msec-10 sec). Additional parameters-rate of rise of synaptic potentials (dV/dt), synaptic currents (EPSCs), and synaptic conductances (Gtr)-were determined and all confirmed the results obtained with EPSPs. Furthermore, the degree of facilitation or depression could be modulated by altering the extracellular concentration of calcium. On the other hand, comparison of the amplitude of pairs of presynaptic terminal spikes did not show any variability over similar stimulus intervals, nor were the amplitudes of miniature EPSPs significantly different before or after an evoked EPSP. Therefore, the processes of facilitation and depression of ganglionic transmission occur as a result of normal nerve terminal activity. The processes are occurring simultaneously, such that one or the other may predominate depending upon the interval between pulses, as well as the relative concentration of extracellular calcium.

Animals↗
PubMed1976

Developmental variations of tyrosine hydroxylase and acetylcholinesterase in embryonic and post-hatching chicken sympathetic ganglia.

The developmental variations of tyrosine hydroxylase (TH) and of acetylcholinesterase (AChE) were studied in embryonic and post-hatching chicken sympathetic ganglia. Different levels of TH activity were found in two different flocks of White Leghorn chicken, which are probably dependent on genetic differences. These enzymatic differences, however, do not become apparent before hatching and may indicate a combined effect of genetic variation and functional demands. During the period of incubation, TH activity is characterized by a pronounced and steady increase from the twelfth day of incubation up to day 2 after hatching. This corresponds to a period of intense maturation of the sympathetic neuron. In the period following hatching, the 'fourth day fall phenomenon' previously described by us for DOPA decarboxylase (DDC), dopamine-beta-hydroxylase (DBH), and monoamine oxidase (MAO) is not seen in the TH curve. Instead, TH activity tends to remain constant between days 2 and 14 after hatching (ah). Both ganglionic protein and weight remain constant in this period, indicating a phase of general pause in protein synthesis. AChE activity increases steadily from the eighth until the twenty-first day of incubation. A sudden and significant drop in AChE activity was found at day 2 ah followed by a period of rapid increase at day 3 ah and a levelling of activity up to day 30 ah. Comparing the present variations to those observed in our previous studies on DBH, a temporal relationship between TH and DBH activity is observed during the phases of synaptogenesis and maturation but not during the phase of intense functional activity. Our results strongly suggest that before hatching in chick embryo sympathetic ganglia, the cholinergic presynaptic terminals play a role in regulating the development of the adrenergic neurons. In the period following hatching, however, the DBH and TH levels in cell bodies seem to be principally regulated by the functional activity. This results in depletion of DBH, but not TH, through liberation along with the neurotransmitter at the periphery. Depletion of DBH at the terminals may result in increased transport and thereby depletion in the cell body. This mechanism is probably responsible for the difference in the profiles of activity of DBH and TH in the cell bodies observed in the first week after hatching.

Acetylcholinesterase↗
PubMed1976

Selective antagonism of frog cerebellar synaptic transmission by manganese and cobalt ions.

Parallel fiber-Purkinje cell synaptic transmission of the frog cerebellum can be selectively blocked by Mn2+ and Co2+. The interaction of these cations with Ca2+ indicates that they act, as has been found for other chemical synapses, at the presynaptic terminals where Ca2+ is required for release of neurotransmitters. Climbing fiber-Purkinje cell synaptic transmission was similarly blocked by Mg2+, Mn2+ and Co2+.

Animals↗
PubMed1979

Development of neocortical circuitry: quantitative ultrastructural analysis of putative monoaminergic synapses.

The distribution, numbers and morphology of presumed monoaminergic (MA) synapses were examined in somatosensory cortex of neonatal rats and mice (newborn to 16 days of age). MA synapses were identified using an ultrastructural cytochemical marker, 5-hydroxydopamine (5-OHDA), which results in the appearance of small granular vesicles (SGV) in their presynaptic terminals. From birth to 7 days of age, 20--30% of all synapses sampled in somatosensory cortex contain SGVs. However, few SGV synapses are seen in 8-day-old cortex and by 12 days of age, SGVs are no longer detectable in cortex. A specific laminar distribution for these SGV synapses -- which is distinct from the overall synaptic distribution -- is first seen at 3 days of age and is essentially unchanged until 7 days postnatally. During this entire period, the SGV synapses predominate in the primordium of layer IV, where they account for 50--70% of all synapses. Morphometric analysis of SGV synapses indicates that there are differences in junctional symmetry, vesicle shape and configuration of the contact zone between SGV and non-SGV synapses, as well as between SGV synapses themselves in the various cortical layers. The laminar distribution and morphological characteristics of SGV synapses suggest that the MA projection to neocortex exhibits a high degree of spatial specificity during its ingrowth. Also, the relatively high proportion of SGV synapses in the first postnatal week may reflect a potent influence exerted by the MA inputs on immature neocortex. The decreased numerical density of SGV synapses after 7 days of age is probably due to the development of the blood-brain barrier to 5-OHDA.

Aging↗
PubMed1979

Neurochemical and morphological studies of bulk isolated rat brain cells. II. Preparation of viable cerebral neurons which retain synaptic complexes.

The bulk isolation from rat cerebral cortex of viable neurons retaining synaptic complexes is described. The basis of this procedure is to dissociate the neurons in situ from the surrounding glial cells. The glial structures that are normally adjacent to the neuronal cell body and to the proximal parts of the neuronal processes are largely destroyed by perfusion of the brain under special conditions. The most important of these conditions was found to be a hyperosmolar concentration of hexoses in the perfusion medium. In addition, the presence of collagenase and hyaluronidase in the perfusion medium and specific perfusate flow characteristics were required to produce the structural changes throughout the brain tissue. When the perfused brain was further dissociated into a cell suspension by mincing and sieving, isolated neurons were obtained, the majority of which retained the proximal parts of their processes. A novel feature of these neurons was the retention of synaptic boutons on the plasma membrane. Presynaptic terminals with mitochondria and vesicles as well as pre- and postsynaptic membranes and densities were observed on the isolated neurons. The neurons were fractionated to 90--95% purity using discontinuous Ficoll density gradient centrifugation with a liquid fluorocarbon as cushion. Highly purified, viable cerebral neurons retaining synaptic complexes are thus available in bulk for neurobiological studies.

Animals↗
PubMed1980

Morphine does not antagonize the substance P mediated excitation of dorsal horn neurons.

Multibarrelled microelectrodes were used to test the effects of iontophoretically released substance P (SP), morphine, glutamate, and naloxone on spinal cord dorsal horn neurons. Cells excited by SP were also excited by noxious stimuli, a finding consistent with the hypothesis that SP is the neurotransmitter released by primary nociceptor afferents to excite dorsal horn neurons. Iontophoretic morphine failed to depress the SP-induced discharges. Indeed, iontophoretic morphine frequently potentiated the SP responses. In addition to potentiating SP-induced discharges, iontophoretic morphine frequently increased both the spontaneous activity of dorsal horn neurons and the activity evoked in these cells by noxious cutaneous heat and iontophoretic glutamate. Naloxone did not antagonize these excitatory effects. Intravenous morphine only depressed spontaneous discharges. Nevertheless, iontophoretic morphine still produced excitatory effects in spinal animals pretreated with analgesic doses of intravenous morphine. It is concluded that such excitatory effects are toxic actions indicative of supratherapeutic morphine concentrations in the vicinity of the neuron being studied. Intravenously administered morphine depressed the spontaneous activity of dorsal horn neurons of spinal cats, but failed to depress their responses to SP. Morphine also failed to antagonize SP's biological effects in peripheral systems (contraction of isolated guinea pig ileum, rabbit hypotensive effect, rat sialogogic response). It is concluded that morphine is not a substance P receptor antagonist. The results are discussed with respect to the hypotheses that (1) the spinal analgesic effects of systemically administered morphine occur on presynaptic terminals of sensory neurons, and (2) an SP antagonist might be a unique analgesic agent.

Animals↗
PubMed1981

Calcium accumulation in intracellular compartments of frog retinal rod photoreceptors.

The accumulation of calcium in the rod cells of isolated frog retinas was studied by methods involving the pretreatment of tissue with saponin, which reduces the permeability barrier posed by the plasma membrane, and the inclusion of a Ca2+ trapping agent, oxalate, in incubation media. X-ray microanalysis using an analytical transmission electron microscope was employed to verify the presence of calcium in the deposits produced by these methods. Ca2+ was found to accumulate in the rough endoplasmic reticulum (ER) and the agranular reticulum of the myoid region and in the presynaptic terminals of the rods. At least one aspect of this accumulation appears to depend upon the presence of ATP.

Animals↗
PubMed1981

Direct retinal input to the limbic system of the rat.

Retinal projections in rats were studied using anterograde horseradish peroxidase (HRP) tracing and electron microscopic (EM) degeneration. HRP-labeled axons were observed to leave the optic tract in the vicinity of the lateral geniculate nucleus and enter the stria terminalis where they coursed anteriorly to the bed nucleus of the stria terminalis (BNST), and the anterodorsal (TAD) and anteroventral (TAV) thalamic nuclei. After enucleation, selected areas studied with EM confirmed that retinal presynaptic terminals are located in the BNST and TAV. These results support the finding of Conrad and Stumpf that the retina has a direct link to the limbic system.

Animals↗
PubMed1982

Electroshock afterdischarges are related to neuronal oscillability: neuronal models of Aplysia.

Identifiable giant neurons of Aplysia explored intracellularly behave differently at the offset of an intracellular electroshock (IES) or after a synaptic 'tetanization', according to their functional type: neurons of the stable type depolarize and fire at the offset of the IES, anodal or cathodal, thus eliciting an afterdischarge (AD). The threshold of this AD is lowered if the neuron is destabilized, i.e. converted from the stable to an oscillatory type (for instance by decalcification). Neurons normally of the tonic type are more sensitive to an IES, eliciting a longer afterdischarge than the stable neurons. Extracellular electroshock (EES) anodal or cathodal, applied directly on desheathed somata of Helix give long-lasting afterdischarges at the offset. In addition, EES stimulating presynaptic terminals or axons leads to a high frequency synaptic input on remote neurons. At the offset of this input either prolonged synaptic afterdischarges or postsynaptic rebounds of the membrane potential sustaining bursts of decreasing amplitude denote apparent oscillatory properties of the synaptically activated neuron. Finally, any conversion by convulsants of tonic neurons to oscillators highly facilitates the elicitation of afterdischarges of axons simultaneous to paroxysmal depolarization shifts of the homologous somata. These results indicate that afterdischarge elicitation is highly facilitated (low threshold) in normal oscillatory neurons and/or chemically destabilized neurons.

Animals↗
PubMed1982

Long-term facilitation of amphetamine-induced rotational behavior and striatal dopamine release produced by a single exposure to amphetamine: sex differences.

Amphetamine (AMPH)-induced rotational behavior in non-lesioned rats and AMPH-stimulated dopamine (DA) release from striatal tissue fragments in vitro were used to study the long-term effects of a single injection of AMPH on activity in the mesostriatal DA system. A single injection of a low dose of AMPH (1.25 mg/kg) greatly enhanced the rotational behavior produced by a second injection of AMPH given 3-4 weeks later in intact female, ovariectomized female and castrated male rats. The effect of AMPH pretreatment in intact males differed from that in the other groups. When only 7-8 days separated the two test sessions both intact male and female rats showed sensitization of rotational behavior, but the magnitude of the change was greater in females. In addition, a single injection of 1.25 mg/kg of AMPH in vivo produced a long-lasting (3-5 weeks) enhancement of AMPH-stimulated DA release from striatal tissue in vitro. It is suggested that: (1) repeated injections of AMPH are not necessary to produce a long-lasting facilitation of behaviors mediated by the mesostriatal DA system; (2) gender and/or hormonal state influences the development of long-term changes in the mesostriatal DA system; and (3) changes in DA release from presynaptic terminals may contribute to the behavioral sensitization produced by stimulant drugs. The phenomena reported here may provide complementary in vitro and in vivo models for studying neuroplasticity in brain DA systems.

Animals↗
PubMed1982

Delayed neuronal death in the gerbil hippocampus following ischemia.

In the CA1 subfield of the gerbil hippocampus, an unusual series of changes were noticed after ischemia. Mongolian gerbils were subjected to bilateral carotid occlusion for 5 min. Perfusion fixation was performed 3, 6 and 12 h or 1, 2, 4, 7 and 21 days afterwards. Specimens obtained from the dorsal hippocampus were processed for light and electron microscopy. Three different types of changes were observed in the CA4, CA2 and CA1 subfields. In CA4, the change was rapid and corresponded to ischemic cell change. The alteration in CA2 was relatively slow, and identical to what has been called reactive change. On the contrary, the change in the CA1 pyramidal cells was very slow, only becoming apparent by light microscopy 2 days following ischemia. The CA1 subfield was selected for electron microscopic observation. The lamellar alignment of proliferated cisterns of the endoplasmic reticulum was the most conspicuous finding in these cells. Four days following ischemia, almost all of the pyramidal cells in CA1 were destroyed. In the CA1 neuropil, numerous presynaptic terminals remained without being apposed to normal postsynaptic sites. These changes in CA1, called here 'delayed neuronal death', may differ from those thought to be typical of ischemic neuronal damage. It was unlikely that the disturbance of local blood vessels was the cause of these changes.

Animals↗
PubMed1982

Selective inhibition by methysergide of the monosynaptic reflex discharge in the isolated spinal cord of the newborn rat.

In the isolated spinal cord of the newborn rat, methysergide and LSD-25 depressed the monosynaptic reflex discharge selectively. Cyproheptadine and dimethothiazine did not inhibit the monosynaptic reflex. The selective inhibitory effect of methysergide on the monosynaptic reflex was not due to a presumptive low safety factor of this reflex. The inhibition was restored under a condition such as the compound action potential in the dorsal root was enhanced by 4-aminopyridine. Methysergide did not decrease the sensitivity of the motoneuron to substance P and L-glutamic acid. It is suggested that methysergide acts at the presynaptic terminal of Ia afferent fibers and depresses evoked transmitter release.

Action Potentials↗
PubMed1983

Light and electron microscopic demonstration of guanylate cyclase in rat brain.

Guanylate cyclase (GTP pyrophosphate-lyase (cyclizing), EC4.6.1.2.) was histochemically demonstrated in rat brain with light and electron microscopes by using a specific monoclonal antibody to soluble guanylate cyclase from rat brain. Under a light microscope, intense reactions were seen in caudate-putamen complex, neocortex and cerebellar cortex. Immunoreactive cells were mainly some types of neurons such as small neurons in caudate-putamen complex, Purkinje cells in cerebellar cortex and pyramidal cells in neocortex. Some astroglial cells were also stained. Not all neurons or glial cells exhibited the positive guanylate cyclase reactivity. Electron microscopic examination revealed that guanylate cyclase was localized within postsynaptic components (perikaryon and dendrites) in neurons and in the cytoplasm and plasma membrane of astroglia. Presynaptic terminals were free of reaction. The observation supports a possibility that cyclic GMP is involved in the postsynaptic events of neuronal transmission and the regulation of intracellular processes.

Animals↗
PubMed1983

Does acute L-DOPA increase active release of dopamine from dopaminergic neurons?

L-DOPA is believed to be decarboxylated by the residual striatal dopaminergic presynaptic terminals with formation of the putative neurotransmitter dopamine (DA) and with increased availability of DA at post-synaptic receptors. However there is no direct evidence that the DA formed is released into the synaptic cleft. We therefore investigated the biochemical modifications occurring in the dopaminergic system after acute administration of L-DOPA. After acute L-DOPA (100 mg/kg plus 25 mg/kg of benserazide p.o.) the levels of 3-methoxytyramine (3-MT), a metabolite reflecting release of the neurotransmitter DA, were significantly raised, following the same pattern as DA levels, indicating that DA release from DA nerve terminals is increased after L-DOPA administration. The increased DA release and 3-MT formation were not reduced by pretreatment with direct DA agonists such as apomorphine (5 mg/kg i.p.) or piribedil (120 mg/kg p.o.). Thus in this case DA release is not under the control of the compensatory mechanisms induced by post-synaptic receptor hyperstimulation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Evidence for the presynaptic localization of opiate binding sites on striatal efferent fibers.

Using quantitative receptor autoradiography, [3H]D-Ala-D-Leu-enkephalin (DADL) and [3H]naloxone binding were studied in rat striatum and striatal projection areas (globus pallidus (GP) and substantia nigra pars reticulata (SNr] after unilateral striatal kainic acid lesions. [3H]DADL and [3H]naloxone binding were each examined by two methods. Initially, [3H]DADL binding was performed in 50 mM Tris-HCl (pH 7.4), 30 mM NaCl, 3 mM manganese acetate and 2 microM GTP; [3H]naloxone binding was carried out in 50 mM Tris-HCl (pH 7.4) and 100 mM NaCl. Subsequent studies were carried out in 150 mM Tris-HCl (pH 7.4) and either [3H]DADL plus 500 nM morphiceptin (to block [3H]DADL binding to mu receptors) or [3H]naloxone plus 10 nM delta receptor peptide (to block [3H]naloxone binding to delta receptors). At one and eight weeks in the lesioned striatum, [3H]DADL binding was reduced by 70% and 82%, respectively, when compared to the control side. [3H]Naloxone binding was reduced by 35% and 20%. In GP and SNr, [3H]DADL binding was reduced by 31% and 41%, respectively, at one week and 27% and 26% at eight weeks. [3H]Naloxone binding was reduced 19% in GP at eight weeks. A parsimonious explanation of these results is that opiate binding sites are located on presynaptic terminals of striatal efferent fibers to globus pallidus and substantia nigra pars reticulata as well as on local striatal axon collaterals. Since opiate peptides have recently been found to coexist with GABA in some striatal neurons, opiate peptides may play a role in striatal function by controlling GABA release from striatal efferent fibers. It is possible that pallidal and nigral opiate binding could be utilized as a marker for striatal terminals.

Animals↗