Correlation of the inhibitory post-synaptic potential of motoneurones with the latency and time course of inhibition of monosynaptic reflexes.
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Neurons↗
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Identification of a prolonged post-synaptic potential of cerebral cortex.
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Cerebral Cortex↗
Distinct mechanisms for neurotrophin-3-induced acute and long-term synaptic potentiation.
Although neurotrophins elicit both acute and long-term effects, it is unclear whether the two modes of action are mediated by the same or different mechanisms. Using neuromuscular junction (NMJ) as a model system, we identified three characteristic features required for long-term, but not acute, forms of synaptic modulation by neurotrophin-3 (NT-3): endocytosis of NT-3-receptor complex, activation of the PI3 kinase substrate Akt, and new protein synthesis. Long-term effects were eliminated when NT-3 was conjugated to a bead that was too large to be endocytosed or when dominant-negative dynamin was expressed in presynaptic neurons. Presynaptic inhibition of Akt also selectively prevented NT-3-mediated long-term effects. Blockade of protein translation by the mammalian target of rapamycin inhibitor rapamycin prevented the long-term structural and functional changes at the NMJ, without affecting the acute potentiation of synaptic transmission by NT-3. These results reveal fundamental differences between acute and long-term modulation by neurotrophins.
Animals↗
THE INHIBITORY POST-SYNAPTIC POTENTIAL IN INTESTINAL SMOOTH MUSCLE INVESTIGATED WITH INTRACELLULAR MICROELECTRODE.
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Animals↗
The difference in shape of spontaneous and uniquantal evoked synaptic potentials in frog muscle.
1. Spontaneous and stimulation-induced uniquantal synaptic activity at the frog cutaneous pectoris muscle, treated with neostigmine, was recorded by focal extracellular microelectrodes. A monoexponential curve was fitted to the decay of each synaptic response. 2. A highly significant positive relationship was found between the amplitude and the decay time constant of spontaneous extracellular miniature endplate potentials (MEPPs(o)), whereas the relationship displayed by evoked uniquantal extracellular endplate potentials (EPPs(o)) was only slightly greater than zero. 3. The difference did not stem from changes in the muscle membrane conductance or from inclusion of outstanding MEPPs(o) formed as a result of the block of acetylcholinesterase. 4. The dependence of the rise time on the amplitude was also stronger in MEPPs(o) than in EPPs(o). 5. In the absence of neostigmine, MEPPs(o) exhibited a positive correlation between decay time constant and amplitude, while EPPs(o) did not show such a correlation. 6. In view of previously published models of transmitter release, it is suggested that spontaneous secretion of quanta occurs both within and outside the active zones facing postsynaptic areas of variable receptor density.
Acetylcholinesterase↗
Synaptic potentiation and depression in slices of mediorostral neostriatum-hyperstriatum complex, an auditory imprinting-relevant area in chick forebrain.
Long-term potentiation, a tetanic stimulation-evoked, persistent increase in synaptic efficiency, is the most extensively studied form of synaptic plasticity. Intracellular correlates of long-term potentiation have been analysed in mammalian hippocampus and cortex, but not in bird cortical analogues. We present here studies on long-term potentiation in slices of the chick forebrain area mediorostral neostriatum-hyperstriatum complex which receives thalamic afferents and is relevant for auditory filial imprinting. Following afferent tetanic stimulation, population spike potentiation was extracellularly recorded in 25% of the tested neurons for longer than 40 min. Using intracellular recordings, the membrane potential, the amplitude of excitatory postsynaptic potentials, the latency between the test stimulus and the evoked action potentials, and the cellular excitability (excitatory postsynaptic potential-spike relationship) were found to change after the tetanus. A long-term depression following the tetanus was also seen in some units in this area. Furthermore, the mechanisms underlying long-term potentiation were investigated. A large depolarization of resting membrane potential (approx. 36 mV) was characteristic after the tetanic stimulation. N-methyl-D-aspartate receptor channels are necessary for induction of this depolarization, as well as for long-term potentiation, as demonstrated by the effect of DL-2-amino-5-phosphonovaleric acid. After intracellular recordings, the cells were injected with Lucifer Yellow. The combination of electrophysiological characterization and morphological identification suggested that the potentiation came chiefly from type I neurons, which have the largest soma among the neuron types in this area and up to eight dendrites. The results demonstrate that the recognized major phenomena of long-term potentiation are found in an auditory imprinting-relevant area of the chick forebrain, and that this potentiation is dependent on N-methyl-D-aspartate receptor channels. It is noteworthy that behavioural imprinting was previously shown to induce a reduction of up to 47% of the spine frequency of type I neurons and a growth of the remaining spine synapses, all resembling a synaptic selection process. Therefore, the intriguing possibility emerges that mechanisms underlying long-term potentiation are instrumental for this selection process, which involves regressive and proliferative morphological changes.
Acoustic Stimulation↗
The effects of the adenosine reuptake inhibitor soluflazine on synaptic potentials and population hypoxic depolarizations in area CA1 of rat hippocampus in vitro.
Adenosine has recently been shown to play a potentially important role in the regulation of synaptic excitability during experimental hypoxia in the hippocampus of the rat. Endogenous adenosine, rapidly released at the initiation of a hypoxic episode, produced synaptic depression, which could protect sensitive neurons. In the present experiments, an inhibitor of the reuptake of adenosine, soluflazine (R64719) was employed to increase the levels of endogenous adenosine under normoxic and hypoxic conditions in slices of the hippocampus of the rat. Soluflazine produced a slow-onset, concentration-dependent depression of population excitatory postsynaptic potentials, which was reversed by the specific A1 adenosine receptor antagonist, 8-cyclopentyltheophylline. During severe N2-induced hypoxia, soluflazine significantly delayed hypoxic depolarization. These results suggest that inhibition of the reuptake of adenosine may have therapeutic potential in the amelioration of hypoxic/ischemic neuronal damage, particularly in the hippocampus.
Adenosine↗
QUANTAL COMPONENTS OF THE SYNAPTIC POTENTIAL IN THE CILIARY GANGLION OF THE CHICK.
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Animals↗
Giant GABAB-mediated synaptic potentials induced by zinc in the rat hippocampus: paradoxical effects of zinc on the GABAB receptor.
The interaction of zinc with pre- and postsynaptic GABAB receptors was studied in adult rat hippocampal slices using intracellular recording in CA1 and CA3 pyramidal neurons. Zinc (50-300 microM) antagonized baclofen responses with a variable potency, whereas CGP-35348 (100 microM) or barium (300 microM) produced a more substantial and consistent inhibition. Zinc also induced giant GABAA-mediated depolarizing potentials (GDP) in these neurons. After blocking GABAA and excitatory synaptic transmission, monosynaptic hyperpolarizing inhibitory postsynaptic potentials (IPSP) mediated by GABAB receptors (IPSPB) were inhibited by CGP-35348 or barium; however, zinc increased the latency and prolonged the duration of the IPSPB and also induced the appearance of spontaneous giant GABAB-mediated hyperpolarizing potentials (GHP). In some cells, IPSPBs in zinc exhibited a multiphasic appearance. The early component was partially inhibited by 300 microM zinc and was followed by a late GHP. CGP-35348 at 100 microM inhibited the early monosynaptic IPSPB but not the GHP; however, at 300 microM both components were blocked. Paired-pulse inhibition of the IPSPB was used to assess the effect of zinc on presynaptic GABAB receptors. Neither the zinc-chelating agent CP94 (400 microM) nor zinc affected this phenomenon. CGP-35348, barium and polyvalent cations, such as cadmium, copper, cobalt, manganese, iron and aluminum, failed to induce giant potentials in hippocampal neurons. It is concluded that zinc is apparently unique in synchronizing the release of GABA to produce GDPs and GHPs.
Animals↗
Synaptic potentials recorded in cell cultures of nerve and muscle.
Initially dissociated spinal cord and muscle cells derived from chick embryos differentiate sufficiently in tissue culture to form functional synaptic contacts. Spontaneous and evoked potentials recorded with intracellular microelectrodes resemble synaptic responses of adult spinal cord and neuromuscular junctions.
Action Potentials↗
Presynaptic mechanism underlying cAMP-induced synaptic potentiation in medial prefrontal cortex pyramidal neurons.
cAMP, a classic second messenger, has been proposed recently to participate in regulating prefrontal cortical cognitive functions, yet little is known about how it does so. In this study, we used forskolin, an adenylyl cyclase activator, to examine the effects of cAMP on excitatory synaptic transmission in the medial prefrontal cortex (mPFC) using whole-cell patch-clamp recordings from visually identified layer II-III or V pyramidal cells in vitro. We found that bath application of forskolin significantly increased the amplitude of excitatory postsynaptic currents (EPSCs) in a concentration- and age-dependent manner. This enhancement was completely abolished by coapplication of cAMP-dependent protein kinase (PKA) inhibitor and p42/p44 mitogen-activated protein kinase (MAPK) kinase inhibitor, but not application of either drug alone. The membrane-permeable cAMP analog adenosine 3',5'-cyclic monophosphorothioate, Sp-isomer, triethylammonium salt, or activation of beta-adrenergic receptor by isoproterenol mimicked the effect of forskolin to potentiate EPSCs. However, neither exchange protein activated by cAMP (Epac) inhibitor brefeldin A nor hyperpolarization and cyclic nucleotide-activated channel blocker 4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride (ZD7288) affected forskolin response. The augmentation of EPSCs by forskolin was accompanied by a reduction of the synaptic failure rate, coefficient of variation and paired-pulse ratio of EPSCs, and an increase in release probability and number of releasable synaptic vesicles. Forskolin also significantly increased the frequency of miniature EPSCs without altering their amplitude distribution. These results indicate that cAMP acts presynaptically to elicit a synaptic potentiation on the layer V pyramidal neurons of mPFC through converging activation of PKA and p42/p44 MAPK signaling pathways.
Adenylyl Cyclases↗
Contribution of a calcium-activated non-specific conductance to NMDA receptor-mediated synaptic potentials in granule cells of the frog olfactory bulb.
We studied granule cells (GCs) in the intact frog olfactory bulb (OB) by combining whole-cell recordings and functional two-photon Ca(2+) imaging in an in vitro nose-brain preparation. GCs are local interneurones that shape OB output via distributed dendrodendritic inhibition of OB projection neurones, the mitral-tufted cells (MTCs). In contrast to MTCs, GCs exhibited a Ca(2+)-activated non-specific cation conductance (I(CAN)) that could be evoked through strong synaptic stimulation or suprathreshold current injection. Photolysis of the caged Ca(2+) chelator o-nitrophenol-EGTA resulted in activation of an inward current with a reversal potential within the range -20 to +10 mV. I(CAN) in GCs was suppressed by the intracellular Ca(2+) chelator BAPTA (0.5-5.0 mM), but not by EGTA (up to 5 mM). The current persisted in whole-cell recordings for up to 1.5 h post-breakthrough, was observed during perforated-patch recordings and was independent of ionotropic glutamate and GABA(A) receptor activity. In current-clamp mode, GC responses to synaptic stimulation consisted of an initial AMPA-mediated conductance followed by a late-phase APV-sensitive plateau (100-500 ms). BAPTA-mediated suppression of I(CAN) resulted in a selective reduction of the late component of the evoked synaptic potential, consistent with a positive feedback relationship between NMDA receptor (NMDAR) current and I(CAN). I(CAN) requires Ca(2+) influx either through voltage-gated Ca(2+) channels or possibly NMDARs, both of which have a high threshold for activation in GCs, predicting a functional role for this current in the selective enhancement of strong synaptic inputs to GCs.
2-Amino-5-phosphonovalerate↗
Substrates for coincidence detection and calcium signaling for induction of synaptic potentiation in the neonatal visual cortex.
Regulation of the efficacy of synaptic transmission by activity-dependent processes has been implicated in learning and memory as well as in developmental processes. We previously described transient potentiation of excitatory synapses onto layer 2/3 pyramidal neurons in the visual cortex that is induced by coincident presynaptic stimulation and postsynaptic depolarization. In the adult visual cortex, activation of N-methyl-d-aspartate (NMDA) glutamate receptors is necessary to induce this plasticity. These receptors act as coincidence detectors, sensing presynaptic glutamate release and postsynaptic depolarization, and cause an influx of Ca(2+) that is necessary for the potentiation. In the neurons of the neonatal visual cortex, on the other hand, coincident presynaptic stimulation and postsynaptic depolarization induce stable long-term potentiation (LTP). In addition, reduced but significant LTP can be induced in many neurons in the presence of the NMDA receptor (NMDAR) antagonist, 2-amino-5-phosphonovaleric acid despite the Ca(2+) requirement. Therefore there must be an alternative postsynaptic Ca(2+) source and coincidence detection mechanism linked to the LTP induction mechanism in the neonatal cortex operating in addition to NMDARs. In this study, we find that in layer 2/3 pyramidal neurons, release of Ca(2+) from inositol trisphosphate (InsP(3)) receptor-mediated intracellular stores and influx through voltage-gated Ca(2+) channels (VGCCs) provide alternative postsynaptic Ca(2+) sources. We hypothesize that InsP(3)Rs are coincidence detectors, sensing presynaptic glutamate release through linkage with group I metabotropic glutamate receptors (mGluRs), and depolarization, through VGCCs. We also find that the downstream protein kinases, PKA and PKC, have a role in potentiation in layer 2/3 pyramidal neurons of the neonatal visual cortex.
Animals↗
Dual-component synaptic potentials in the lamprey mediated by excitatory amino acid receptors.
The synaptic mechanisms underlying amino acid-mediated excitation in the lamprey spinal cord have been investigated. Fine stimulating electrodes were used to stimulate single axons in the spinal cord and evoke unitary EPSPs in lamprey motoneurons and one type of premotor interneuron, the CC interneuron. Three types of EPSP, distinguished by their time course and sensitivity to amino acid antagonists, were seen. Fast EPSPs had a fast rise time (mean, 6.5 msec) and a short half-decay time (mean, 22.5 msec). Slow EPSPs lasted at least 200 msec, had a slow rise time (mean, 28 msec), and a long half-decay time (mean, 109 msec). The third type of unitary potential, called "mixed" EPSP, also lasted at least 200 msec, had a fast rise time (mean, 12 msec), and a long half-decay time (mean, 105 msec). Lamprey neurons were found to possess 3 types of excitatory amino acid receptor: N-methyl-D-aspartate (NMDA), kainate, and quisqualate receptors. 2-Amino-5-phosphonovaleric acid (APV) or Mg2+ blocked the depolarizations caused by N-methyl-D,L-aspartate (NMA) but not those of kainate or quisqualate. Cis-2, 3-piperidine dicarboxylic acid (PDA) blocked the depolarizations caused by NMA and kainate but not those of quisqualate. Fast EPSPs were unaffected by the bath application of APV or Mg2+ but were greatly reduced by PDA, suggesting that these EPSPs were mediated by non-NMDA, possibly kainate receptors. Both APV and Mg2+ blocked the slow EPSPs, suggesting that they were mediated by NMDA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
ATP mediates fast synaptic potentials in enteric neurons.
Conventional intracellular electrophysiological methods were used to study fast synaptic transmission in the myenteric plexus of guinea pig ileum in vitro. Fast excitatory postsynaptic potentials (fEPSPs) were evoked in 98 neurons following single stimuli applied to interganglionic connectives. The nicotinic antagonist hexamethonium (100 microM) reduced fEPSPs by 83% in 37 neurons; these fEPSPs were considered to be cholinergic. In 61 neurons, hexamethonium reduced fEPSPs by 33%; fEPSPs recorded in the presence of hexamethonium were considered to be noncholinergic. Similar data were obtained using the nicotinic antagonist mecamylamine (10 microM) to block fEPSPs. Hexamethonium or mecamylamine completely blocked depolarizations caused by acetylcholine (ACh) applied by ionophoresis. The P2 receptor antagonist suramin (1-300 microM) inhibited noncholinergic fEPSPs in 30 cells; the suramin IC50 was 4 microM. Suramin (100 microM) did not block depolarizations caused by ACh or 5-HT, but suramin blocked depolarizations caused by ATP. Hexamethonium did not block ATP-induced depolarizations. The estimated reversal potential for suramin-sensitive fEPSPs and ATP-induced depolarizations was -25 and -16 mV, respectively. ATP responses were reduced in low-sodium (26 mM) extracellular solution, suggesting that ATP activates a cation channel. These data indicate that in myenteric nerves ATP, in addition to ACh, contributes to fast synaptic transmission.
Acetylcholine↗
A spectral analysis of the integration of artificial synaptic potentials in mammalian central neurons.
In order to simulate the interaction between synaptic input and intrinsic membrane properties in mammalian central neurons a well-defined current was injected into the neurons through a recording electrode. The stimulus was white noise bandpass filtered at 0.5 and 75 Hz and the power spectra of the responses were calculated. Recordings were obtained from neurons of the neocortex, the hippocampus, the thalamus and the cerebellar cortex. The neurons were either located in newly cut slices from adult guinea pig brains or in 3-10-weeks-old slice cultures from brains of newborn rats. In hippocampal and cortical cells the passive membrane properties dominated the shape of the power spectra. In general, when the average membrane potential was made more positive the power of the response increased. When neurons had active subthreshold responses like delayed rectification, sag-and-hump responses or delayed depolarization there was a depression of the response power at frequencies below 10-20 Hz. The depression was voltage dependent in the same way as the current that produced the active subthreshold response. In thalamic cells with a low-threshold Ca2+ spike (lts) the power of the responses grew in the 3-20-Hz range with hyperpolarization. The spectra of the responses of thalamic neurons had multiple peaks indicating multiple frequencies of resonance. Purkinje cells of the cerebellar cortex have prominent plateau potentials. When these cells were stimulated with the white noise at levels where the plateau potentials could be activated the spectra were dominated by a large peak at the lowest frequencies, i.e., below 5 Hz. Few cells in our data base generated spontaneous membrane potential oscillations. When the current stimulus was injected into such neurons the intrinsic rhythm was unaffected by the input and the power spectrum showed a marked peak at the frequency of the intrinsic oscillations. We conclude that bandpass filtered white noise as simulation of synaptic input is valuable for quantification of how passive and active membrane properties affect synaptic integration. The technique can also provide information on the role of transmitters and modulators in the CNS.
Animals↗
[Changes in synaptic potentials and axonal delays as factors causing epileptic instability of neuronal networks].
Synaptic weights, axonal delays and excitability thresholds are three basic parameters influencing the function of neuronal network as a dynamic system. Changes of the general level of the signal flow, without changes in relation between excitatory and inhibitory connections can cause pathologic oscillations in the network. The conductivity in neuronal nets depends on electrochemical processes and may be influenced by the pH-status, ion concentrations, among other parameters. Also different pathological processes can change it. Even slight changes of axonal delays, as shown above, can cause in certain situations unstable, epileptic oscillations of the net.
Action Potentials↗
Linearity of summation of synaptic potentials underlying direction selectivity in simple cells of the cat visual cortex.
Intracellular recordings from simple cells of the cat visual cortex were used to test linear models for the generation of selectivity for the direction of visual motion. Direction selectivity has been thought to arise in part from nonlinear processes, as suggested by previous experiments that were based on extracellular recordings of action potentials. In intracellular recordings, however, the fluctuations in membrane potential evoked by moving stimuli were accurately predicted by the linear summation of responses to stationary stimuli. Nonlinear mechanisms were not required.
Animals↗