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At least 1,657 records · Page 92Linked to original sources
PubMed2001

Paralytic zebrafish lacking acetylcholine receptors fail to localize rapsyn clusters to the synapse.

Physiological analysis of two lines of paralytic mutant zebrafish, relaxed and sofa potato, reveals defects in distinct types of receptors in skeletal muscle. In sofa potato the paralysis results from failed synaptic transmission because of the absence of acetylcholine receptors, whereas relaxed mutants lack dihydropyridine receptor-mediated release of internal calcium in response to the muscle action potential. Synaptic structure and function appear normal in relaxed, showing that muscle paralysis per se does not impede proper synapse development. However, sofa potato mutants show incomplete development of the postsynaptic complex. Specifically, in the absence of ACh receptors, clusters of the receptor-aggregating protein rapsyn form in the extrasynaptic membrane but generally fail to localize to the subsynaptic region. Our results indicate that, although rapsyn molecules are capable of self-aggregation, interaction with ACh receptors is required for proper subsynaptic localization.

Acetylcholine↗
PubMed1973

The formation of synapses in mammalian striated muscle reinnervated with autonomic preganglionic nerves.

1. A study has been made of the formation of synapses during reinnervation of the hemidiaphragm of adult rabbits with preganglionic fibres of the thoracic vagus, using histological, ultrastructural and electrophysiological techniques.2. Following reinnervation with preganglionic axons, silver-stained nerve terminals were found in association with cholinesterase-stained end-plates only in the region of the muscle corresponding to the original innervation band.3. The fine preganglionic axons retained their normal structure in striated muscle, but were found to synapse over discrete areas of dimensions not larger than those of the original end-plates.4. The regenerated varicose preganglionic nerve terminals were observed with the electronmicroscope in positions either overlying or in the vicinity of the old synaptic folds.5. Spontaneous potentials and evoked synaptic potentials were recorded only in the middle of the muscle fibres after vagus reinnervation.6. In a few cases, multiple synaptic potentials with similar time courses were recorded, suggesting that several axons had formed synapses at a single site on a muscle fibre.7. It has been shown that, during reinnervation of adult mammalian striated muscle fibres with nerves other than those of the somatic system, synapses are formed preferentially in the region of the old end-plates.

Animals↗
PubMed1992

Receptor subtypes involved in callosally-induced postsynaptic potentials in rat frontal agranular cortex in vitro.

A slice preparation of rat frontal agranular cortex preserving commissural inputs has been used for intracellular recording from layer V pyramidal cells, in order to characterize the synaptic potentials induced by stimulation of the corpus callosum and to reveal the subtypes of amino acid receptors involved. Stimulation of the corpus callosum induced EPSPs followed by early IPSPs with a peak latency of 30 +/- 2 ms and late IPSPs with a peak latency of 185 +/- 18 ms. Reversal potentials for early and late IPSPs were -75 +/- 5 mV (early) and -96 +/- 5 mV (late). Late IPSPs were more dependent on extracellular K+ concentration. The early IPSPs were blocked by GABAA antagonists, bicuculline and picrotoxin, whereas the late IPSPs were reduced by the GABAB antagonist, phaclofen. CNQX (6-cyano-7-nitroquinoxaline-2,3-dione), an antagonist of non-NMDA (N-methyl-D-aspartate) receptors, suppressed both EPSPs and late IPSPs at 5 microM. Early IPSPs remained at this concentration but were suppressed by 20 microM CNQX. In Mg(2+)-free solution, EPSPs were larger and more prolonged than in control solution. These enhanced EPSPs persisted after 5 to 20 microM CNQX, but were reduced in amplitude, and their onset was delayed by 3.6 +/- 0.8 ms. The remaining EPSPs were suppressed by 50 microM APV (DL-2-amino-5-phosphono-valeric acid), an antagonist of NMDA receptors. In Mg(2+)-free solution containing 5 to 20 microM CNQX, the late IPSPs were not diminished. The remaining late IPSPs were suppressed by APV or by phaclofen.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed2001

Application of N-methyl-D-aspartate induces long-term potentiation in the medial perforant path and long-term depression in the lateral perforant path of the rat dentate gyrus in vitro.

The effect of application of N-methyl-D-aspartate (NMDA) on synaptic plasticity was studied in the medial and lateral perforant path-granule cell synapse in the outer blade of the dentate gyrus in vitro. Field excitatory post-synaptic potentials were recorded from the middle or outer molecular layer in response to stimulation of the medial or lateral perforant path. Bath perfusion of NMDA (10 microM, 5 min) resulted in induction of long-term potentiation in the medial perforant path, and induction of long-term depression in the lateral perforant path.

Animals↗
PubMed1990

Osmotic effects upon excitability in rat neocortical slices.

Acute osmotic disturbances can lead to profound neurological problems, yet there has been little experimentation at a cellular level to assess if neurophysiological changes are induced by altered osmolality. Using extra- and intracellular recording in the rat neocortical slice preparation, we examined pyramidal neurons of layers II-III under changing osmotic conditions. Single cell properties, field potentials, synaptic transmission and epileptiform discharges were studied in control saline (295 mOsm) and compared with corresponding data collected during exposure to osmolalities between 245 and 375 mOsm. Single cell properties (resting membrane potential, cell input resistance, action potential threshold and duration) did not change significantly, but neuronal interactions were considerably influenced by osmotic change within minutes. Hyposmolality increased the amplitude of evoked field potentials and of excitatory postsynaptic potentials recorded intracellularly. Hyperosmolality, induced with mannitol, decreased these parameters. Electrotonic coupling, as gauged by the degree of dye coupling and by cell input resistance, was not influenced by shifts in osmolality. The clinical finding that overhydration promotes seizure onset was examined in slices made epileptogenic in Mg2(+)-free saline. Hyposmolality increased the frequency and decreased the duration of interictal bursts, whereas raising osmolality with mannitol had opposite effects. None of the aforementioned effects occurred when osmolality was increased with a freely permeable substance such as dimethylsulfoxide, nor could they be ascribed to changes in saline Na+ or Ca2+ concentrations. The results are consistent with hyposmotic solutions reducing extracellular space by causing cells to swell. Theoretically, during population discharge, this should both concentrate K+ released extracellularly and possibly increase field (ephaptic) interactions. How lowered osmolality strengthens spontaneous and evoked excitatory synaptic transmission in neocortex is not yet clear. However, it may be an important mechanism underlying the increased seizure susceptibility of patients and experimental animals with lowered plasma osmolality. Conversely, suppression of excitatory postsynaptic potentials by osmotically active substances may be involved in the lowered seizure susceptibility observed clinically.

Action Potentials↗
PubMed2005

Factors mediating powerful voltage attenuation along CA1 pyramidal neuron dendrites.

We performed simultaneous patch-electrode recordings from the soma and apical dendrite of CA1 pyramidal neurons in hippocampal slices, in order to determine the degree of voltage attenuation along CA1 dendrites. Fifty per cent attenuation of steady-state somatic voltage changes occurred at a distance of 238 microm from the soma in control and 409 microm after blocking the hyperpolarization-activated (H) conductance. The morphology of three neurons was reconstructed and used to generate computer models, which were adjusted to fit the somatic and dendritic voltage responses. These models identify several factors contributing to the voltage attenuation along CA1 dendrites, including high axial cytoplasmic resistivity, low membrane resistivity, and large H conductance. In most cells the resting membrane conductances, including the H conductances, were larger in the dendrites than the soma. Simulations suggest that synaptic potentials attenuate enormously as they propagate from the dendrite to the soma, with greater than 100-fold attenuation for synapses on many small, distal dendrites. A prediction of this powerful EPSP attenuation is that distal synaptic inputs are likely only to be effective in the presence of conductance scaling, dendritic excitability, or both.

Animals↗
PubMed1976

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

The most consistent effects produced by intracellular injections of guanosine 3',5'-cyclic monophosphate (cGMP) (but not 5'-guanosine 5'-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction, cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Acetylcholine↗
PubMedDate not supplied

[Recent findings on generators of evoked potentials].

In the study of potential generators the dipole localization method is often used. The "equivalent dipole" represents the resultant of all the neurobiological processes (excitatory and inhibitory post-synaptic potentials, action potentials) that concur to generate the evoked potentials. According to the dipole's distance from the active electrode, "near-field" and "far-field" potentials will be recorded, with differences in the spatiotemporal distribution to the skin. The main hypotheses about the generators of standard components of somatosensory evoked potentials (SEP) from median and posterior tibial nerve, visual evoked potentials (VEP), auditory brainstem evoked potentials (BAEP) and P300, are analyzed.

Brain Stem↗
PubMed1996

Morphometric analysis of intrinsic axon terminals of Cebus monkey area 17.

A morphological study of intrinsic projection in area 17 of Cebus monkey was conducted after iontophoretic injection of biocytin. Thirty axon terminals located in supragranular layers were qualitatively and quantitatively analyzed using 3-d automatic microscopy. Three types of axon terminals could be identified: Ia, Ib and II. Group I was characterized by a sparse and/or long-distance branch pattern, while type II presented compact and localized arborization. Ia axon terminals formed "clusters" and "terminaux" boutons while Ib did not. On average, group II axon terminals tended to present straight or obtuse branching angles and a much more ramified pattern, and occupy a smaller cortical territory with shorter intermediate segments and higher density of synaptic potential sites than group I. The common characteristics of group I included innervation of larger cortical territories, longer intermediate segments, acute branching angles and lower synaptic density compared to group II. The results are compatible with the major subdivisions of neocortical neuronal morphology that classifies them as smooth and spine neurons. Smooth neurons may be related to axon terminals of group II while spine neurons may be related to group I.

Animals↗
PubMed2006

Fornix lesions decouple the induction of hippocampal arc transcription from behavior but not plasticity.

The immediate-early gene (IEG) Arc is transcribed after behavioral and physiological treatments that induce synaptic plasticity and is implicated in memory consolidation. The relative contributions of neuronal activity and learning-related plasticity to the behavioral induction of Arc remain to be defined. To differentiate the contributions of each, we assessed the induction of Arc transcription in rats with fornix lesions that impair hippocampal learning yet leave cortical connectivity and neuronal firing essentially intact. Arc expression was assessed after exploration of novel environments and performance of a novel water maze task during which normal rats learned the spatial location of an escape platform. During the same task, rats with fornix lesions learned to approach a visible platform but did not learn its spatial location. Rats with fornix lesions had normal baseline levels of hippocampal Arc mRNA, but unlike normal rats, expression was not increased in response to water maze training. The integrity of signaling pathways controlling Arc expression was demonstrated by stimulation of the medial perforant path, which induced normal synaptic potentiation and Arc in rats with fornix lesions. Together, the results demonstrate that Arc induction can be decoupled from behavior and is more likely to indicate the engagement of synaptic plasticity mechanisms than synaptic or neuronal activity per se. The results further imply that fornix lesions may impair memory in part by decoupling neuronal activity from signaling pathways required for long-lasting hippocampal synaptic plasticity.

Animals↗
PubMed1996

Effects of the antiepileptic drug felbamate on long-term potentiation in the CA1 region of rat hippocampal slices.

In the CA1 region of rat hippocampal slices, the antiepileptic drug 2-phenyl-1,3-propanediol dicarbamate (felbamate; 100-1300 microM) concentration-dependently decreased extracellularly recorded synaptic potentials. The effect was significant at 200 microM, and became maximal at 700 microM felbamate, with a 70% decrease in population spike amplitude and 25% reduction of dendritic field excitatory postsynaptic potential (fEPSP) slope. Both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of the fEPSP were decreased by 700 microM felbamate. Up to 300 microM felbamate did not affect long-term potentiation (LTP), whereas 500 microM decreased the magnitude of LTP. Higher concentrations of felbamate (700-1300 microM) blocked induction of somatic and dendritic LTP completely, but reversibly. It appears that the concentrations of felbamate which affect LTP are higher than those needed for its antiepileptic action.

Animals↗
PubMed1986

Long-term potentiation of transmitter release induced by adrenaline in bull-frog sympathetic ganglia.

Long-term potentiation (l.t.p.) of transmitter release induced by adrenaline in bull-frog sympathetic ganglia was studied using intracellular recording techniques. The quantal content of the fast excitatory post-synaptic potentials (fast e.p.s.p.s: evoked by the nicotinic action of acetylcholine) was potentiated for more than several hours after treatment with adrenaline (1-100 microM). A similar l.t.p. of quantal content was produced consistently by isoprenaline (10 microM) and only in a certain fraction of cells by dopamine (10 microM). The l.t.p. induced by adrenaline (10 microM) was blocked by a beta-antagonist, propranolol (1 microM), but not by an alpha-antagonist, phenoxybenzamine (1 microM). Dibutyryl adenosine 3',5'-phosphate (dibutyryl cyclic AMP) (0.8-1.0 mM), adenosine 3',5'-phosphate (cyclic AMP) (4 mM), 3-isobutyl-1-methylxanthine (10 microM), caffeine (1-2 mM), and cholera toxin (2 micrograms ml-1) applied for 20-30 min, all caused the l.t.p. of quantal content. By contrast, adenosine 5'-phosphate (AMP) (4 mM) and adenosine (4 mM) had no potentiating action. Treatment of the ganglion with adrenaline (2.5-160 microM) or dibutyryl cyclic AMP (4 mM) for 15-30 min resulted in the l.t.p. of the frequency of miniature e.p.s.p.s. The l.t.p. of quantal content induced by adrenaline was markedly suppressed by lowering temperature from 20-25 degrees C to 11-13 degrees C, and blocked by dibutyryl guanosine 3',5'-phosphate (dibutyryl cyclic GMP) (100 microM) consistently when applied together, but inconsistently when given after adrenaline. The post-synaptic sensitivity to acetylcholine was unchanged for at least 1 h after exposure to adrenaline (2.5-160 microM) or dibutyryl cyclic AMP (0.8-4 mM). It can be concluded that adrenaline produces l.t.p. of transmitter release by activating a cyclic-AMP-dependent metabolic process through the activation of beta-adrenoceptors, and that this mechanism is presumably regulated by a process involving endogenous guanosine 3',5'-phosphate (cyclic GMP).

1-Methyl-3-isobutylxanthine↗
PubMed1982

Effects of local anesthetic QX-314 on the membrane properties of hippocampal pyramidal neurons.

The quaternary lidocaine derivative QX-314 was applied internally to CA1 pyramidal neurons of the guinea-pig hippocampal slice preparation. This local anesthetic blocked both fast, Na+-dependent action potentials and the voltage-dependent, non-inactivating Na+ conductance. Partially blocked Na+ spikes exhibited pronounced frequency-dependent depression at rates as low as 0.2 Hz. Ca++-dependent electrogenesis, synaptic potentials and glutamate-induced depolarizations were apparently unaffected even after large doses of QX-314. The results indicate that the cellular mechanisms of local anesthetics on central neuronal membranes are similar to those described for peripheral axons. The frequency-dependence of spike blockade may account for some of the effects of local anesthetics on the central nervous system in vivo. Additionally, the localized intracellular application of QX-314 may prove useful as a specific pharmacological tool in studies of central neurons.

Action Potentials↗
PubMed2003

Chronic ethanol treatment reduces the magnitude of hippocampal LTD in the adult rat.

Human alcoholics and animals that have received chronic ethanol treatment (CET) display memory deficits. Previous work in our laboratory has shown that CET produces damage to the hippocampus and a reduction in the magnitude of hippocampal long-term synaptic potentiation. In the present report we examined the effects of CET on hippocampal long-term depression (LTD). We used in vitro hippocampal slices to examine LTD after rats received 38-41 weeks of paired feeding on liquid diets containing ethanol or isocaloric sucrose. Stimulation delivered through electrodes in the CA3-CA1 Schaffer collateral pathway activated synaptic population responses in CA1. LTD of CA1 stratum radiatum evoked field potential slope was not induced by 900 single pulses at 1 Hz, but was elicited by 900 pulse pairs separated by 50 or 200 msec delivered at 1 Hz (pLFS50, pLFS200). LTD evoked by pLFS200, but not by pLFS50, was significantly reduced in slices from ethanol-treated rats. The N-methyl D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) (50 micro M) blocked LTD induced by pLFS50 and pLFS200 equally, but the L-type calcium channel blocker nimodipine (10 micro M) had no effect on either type of LTD. Thus, direct effects on these channels cannot explain how CET selectively reduces the magnitude of pLFS200 LTD. Finally, we describe a novel and robust LTD of the presynaptic afferent volley that is resistant to CET, NMDAR antagonists, GABA-A receptor blockade, and blockade of L-type calcium channels.

Animals↗
PubMed1992

Computer simulation of carbachol-driven rhythmic population oscillations in the CA3 region of the in vitro rat hippocampus.

1. We used simulations of the in vitro CA3 region of the hippocampus to analyse the 5 Hz population oscillations recorded experimentally in carbachol. 2. A simulation model of the in vitro CA3 region was constructed with 1000 pyramidal neurones and 200 inhibitory neurones (100 producing fast inhibitory postsynaptic potentials (IPSPs) and 100 producing slow IPSPs of delayed onset). Each neurone contained nineteen soma-dendritic compartments. Pyramidal neurones contained six voltage- and/or calcium-dependent ionic currents, whose kinetics were consistent with voltage-clamp data. The connectivity and waveform of unitary synaptic events for excitatory and fast inhibitory synapses were consistent with dual intracellular recordings. This network was shown to generate previously described network oscillations, including synchronized bursts recorded in the presence of GABAA blockers, and synchronized synaptic potentials observed during partial blockade of GABAA inhibition. 3. The model generated 5 Hz oscillations as recorded in carbachol under the following conditions: (a) excitatory synaptic conductance was within a limited range; (b) there was blockade of fast and slow IPSPs (consistent with the experimental lack of effect of bicuculline and phaclofen on carbachol oscillations and the known depression of IPSPs by acetylcholine); (c) the after hyperpolarization (AHP) conductance was reduced (consistent with the known pharmacology of carbachol); (d) the apical dendrites of the pyramidal cells were depolarized, as suggested by the carbachol-induced depolarization of pyramidal neurones. Each oscillation was associated in pyramidal cells with a burst of action potentials riding on a depolarizing wave. The N-methyl-D-aspartate (NMDA) type of excitatory synapse was not necessary for the oscillations to occur. 4. Progressive reduction of excitatory synaptic strength led to an oscillation of the same frequency, with bursts riding on smaller EPSPs (consistent with the experiment). Further reduction of excitatory synaptic strength abolished the population oscillation by uncoupling the neurones. When excitatory synaptic conductance was too large, population oscillations were attenuated as the cells switched from a bursting mode to a repetitively firing mode. 5. Increasing the AHP conductance prolonged the interburst interval as expected. Inclusion of slow IPSPs exerted a similar effect. 6. When fast IPSPs were included, an oscillation with different characteristics emerged: a 10 Hz oscillation that was gated by compound GABAA IPSPs. On any oscillatory wave, few pyramidal neurones fired, and the firing of individual neurones was irregular.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Fast Na+ spike generation in dendrites of guinea-pig substantia nigra pars compacta neurons.

Electric fields were applied to study the regenerative properties of substantia nigra pars compacta neurons in guinea-pig brain slices. Two types of spikes, of high or low amplitude, were generated in both the soma-hyperpolarizing and the soma-depolarizing directions of the field. The different sensitivity of the spikes to somatic polarization suggested that the high-amplitude spikes were generated near the cell body, whereas the low-amplitude spikes were generated at a distance from the soma. Application of tetrodotoxin or intracellular injection of QX 314 abolished both types of spike. The spikes were not inhibited in the presence of glutamate receptor antagonists or during Ca2+ channel blockade. Blockers of gap junctional conductance (sodium propionate, octanol and halothane) did not affect the field-induced spikes. The spike generation was highly sensitive to changes in membrane conductance induced by current injection in the soma or by external field application. The ability of a conditioning field stimulation to affect the spike generation in different neuronal compartments suggested that a transient outward current was generated in the dendrites. The field-induced spikes were facilitated by synaptic stimulation and, in some neurons, low-amplitude spikes were generated by synaptic potentials in the absence of field application. These results suggest that channels responsible for Na+ spike generation reside in the dendrites, and are influenced by spatially distributed voltage-dependent K+ currents and by synaptic input.

Anesthetics, Local↗
PubMed2005

SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability.

Synaptic activity-dependent gene expression is critical for certain forms of neuronal plasticity and survival in the mammalian nervous system, yet the mechanisms by which coordinated regulation of activity-induced genes supports neuronal function is unclear. Here, we show that deletion of serum response factor (SRF) in specific neuronal populations in adult mice results in profound deficits in activity-dependent immediate early gene expression, but components of upstream signaling pathways and cyclic AMP-response element binding protein (CREB)-dependent transactivation remain intact. Moreover, SRF-deficient CA1 pyramidal neurons show attenuation of long-term synaptic potentiation, a model for neuronal information storage. Furthermore, in contrast to the massive neurodegeneration seen in adult mice lacking CREB family members, SRF-deficient adult neurons show normal morphologies and basal excitatory synaptic transmission. These findings indicate that the transcriptional events underlying neuronal survival and plasticity are dissociable and that SRF plays a prominent role in use-dependent modification of synaptic strength in the adult brain.

Animals↗
PubMed1995

Patterns of synaptic activity in forward and feedback pathways within rat visual cortex.

1. The laminar and temporal distribution of synaptic activity supplied by forward and feedback connections between different areas of rat visual cortex was determined with the use of current source density (CSD) analysis in in vitro slices. In forward connections, synaptic potentials were evoked by electrically stimulating area 17 and recording in the extrastriate area LM (lateromedial), that ranks at the second hierarchical level, one step above primary visual cortex. For activating feedback connections, the location of stimulating and recording electrodes was reversed. 2. The synaptic interactions in reciprocal intracortical circuits are excitatory, and they are mediated through glutamate receptors that are blocked by kynurenic acid. 3. Forward connections from area 17 to area LM provide input to all layers including a strong input to layer 4. In contrast, feedback input to layer 4 is weak and is mainly directed to superficial and deep layers. This laminar distribution closely resembles that seen anatomically. 4. Both forward and feedback connections evoke distinct temporal patterns of synaptic activation in different layers. Although onset and peak latencies are slightly shorter in the forward than in the feedback pathway, the difference is not statistically significant. 5. The spatiotemporal distribution of synaptic activation by forward connections resembles the pattern evoked by geniculocortical inputs. Feedback connections show greater similarities to long-range connections within area 17, although they are not identical. Our results support the notion derived from anatomic and in vivo physiological studies that forward and feedback pathways belong to functionally distinct cortical circuits.

Animals↗