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PubMed2006

Bilirubin potentiates inhibitory synaptic transmission in lateral superior olive neurons of the rat.

Bilirubin is a well-known neurotoxin that can result in multiple neurologic deficits. Previous studies have suggested that bilirubin affects aspects of synaptic transmission; however the acute effects of bilirubin on synaptic transmission have not been examined in real-time. In this study, using whole-cell voltage-clamp recordings, we observed the effect of bilirubin on inhibitory postsynaptic currents (IPSC) in postnatal 13-15-day-old neurons dissociated from lateral superior olive nuclei (LSO), one of the brainstem auditory nucleus that are highly vulnerable to bilirubin. The results showed that 10(-5)M bilirubin increased the frequency of spontaneous IPSC without causing change in their amplitudes or in the response to bath applied glycine, suggesting a presynaptic locus for the action. In the presence of tetrodotoxin, the frequency of miniature IPSC was also potentiated by 10(-5)M bilirubin. The facilitation by bilirubin was concentration dependent and increased with an increase in exposure time. Bicuculline only partially reduced the action of bilirubin. The action of bilirubin was observed in extracellular Ca(2+)-free ([Ca(2+)](o) free) solution but was fully occluded by pretreatment with BAPTA-AM in [Ca(2+)](o) free solution. Thus, in LSO neurons, bilirubin facilitates inhibitory synaptic transmission, in a manner independent of voltage-activated Na(+) and Ca(2+) channels but dependent on presynaptic [Ca(2+)](i). The increase of inhibitory synaptic transmission in response to acute bilirubin is a novel effect of bilirubin on the central nervous system and may have implications for neurotoxicity and the impairment of auditory transduction seen in hyperbilirubinemia.

Animals↗
PubMed1998

Tachykinins may modify spontaneous epileptiform activity in the rat entorhinal cortex in vitro by activating GABAergic inhibition.

The effects of substance P and related tachykinins on intrinsic membrane properties and synaptic responses of neurons in cortical slices were determined. Substance P had no detectable effect on membrane properties of principal neurons in layer II or V of the rat medial entorhinal cortex or on neurons in either layer of the anterior cingulate cortex. Specific agonists at the neurokinin1-receptor were also without effect as were agonists at both neurokinin1- and neurokinin3-receptors. Substance P hyperpolarized a small number of principal neurons. These responses were weak and desensitized with repeated applications. Similar effects were seen with other neurokinin1-receptor agonists. Excitatory synaptic potentials mediated by either alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate- or N-methyl-D-aspartate-receptors in principal neurons of the entorhinal cortex were unaffected by substance P. Responses of entorhinal neurons to iontophoretically applied glutamate and N-methyl-D-aspartate were also unaffected. Inhibitory synaptic potentials mediated by either GABA(A)- or GABA(B)-receptors in entorhinal neurons were slightly but consistently enhanced by substance P. Neurons identified as interneurons on the basis of their firing characteristics were consistently depolarized by substance P. These responses also desensitized with repeated applications. Spontaneous epileptiform discharges evoked in entorhinal cortex by perfusion with a GABA(A)-receptor antagonist (bicuculline), were reduced in frequency and, sometimes, in duration by substance P. This effect was mimicked by other neurokinin1-receptor agonists and blocked by neurokinin1-receptor antagonists. It was also mimicked by neurokinin A but not by a specific neurokinin1-receptor agonist. The reduction in frequency of discharges was also mimicked by a GABA(B)-receptor agonist, L-baclofen, and blocked by the GABA(B)-receptor antagonist, CGP55845A. Neurokinin B, and a specific neurokinin1-receptor agonist (senktide), increased the frequency and (sometimes) duration of epileptiform discharges. Substance P could also increase frequency but this usually succeeded or preceded a decrease in frequency. The effect of neurokinin B was reduced by a metabotropic glutamate receptor antagonist. Substance P appears to have little direct effect on principal neurons of the entorhinal cortex but may hyperpolarize them indirectly by activating interneurons and releasing GABA. This indirect inhibition may be responsible for the ability of substance P to reduce the frequency of epileptiform discharges in the entorhinal cortex and may suggest that neurokinin1-receptor agonists have potential as anticonvulsant drugs.

Animals↗
PubMed1990

Long-term potentiation-induced synaptic changes in hippocampal dentate gyrus of rats with an inborn low or high learning capacity.

Structural changes induced by high frequency (HF) stimulation on granule cells of the hippocampal dentate gyrus of rats with inborn high (HP) and low (LP) learning capacity was examined in this study. Two types of axodendritic synapses were processed morphometrically; the axonal bouton on dendritic shafts and those making contact through dendritic spines. The occurrence of granule cell spine synapses on LP rats before tetanus is less than the one in control animals. However, after long-term potentiation (LTP) produced by HF stimulation the number of spine synapses decreased, as happened in the control rats. Moreover, the number of granule cells shaft synapses counted on LP rats, before tetanus is less than the one on control rats, and after LTP this number increased greatly. There was no change in the number of granule cell shaft synapses in HP rats before and after LTP. LP rats which did not show LTP in spite of HF stimulation did not show changes in the number of spine and shaft synapses. From these results we can conclude that: (1) the great hippocampal synaptic plasticity observed in HP rats compared to LP rats can be attributed, at least in part, to the increased number of spine and shaft synapses observed in HP rats; (2) the minor number of spine and shaft synapses in LP rats may account for the impossibility to obtain LTP after HF stimulation in these animals.

Animals↗
PubMed1992

Pyrethroid insecticide-induced alterations in mammalian synaptic membrane potential.

The neuroexcitatory actions of two toxicologically distinct classes of pyrethroid insecticides were characterized in rat brain synaptosomes using [3H]tetraphenylphosphonium to measure changes in synaptosomal membrane potential and by measuring the release of [3H]acetylcholine. Both type I (permethrin) and type II (deltamethrin, cypermethrin and fenvalerate) pyrethroids produced a concentration-dependent tetrodotoxin-sensitive membrane depolarization which was stereospecific for the neurotoxic isomer of each pyrethroid. Deltamethrin was the most potent and efficacious pyrethroid in these studies, with an EC50 of 30 nM and a maximal estimated membrane depolarization of 27 mV, followed by cypermethrin, fenvalerate and permethrin. The phenoxybenzyl pyrethroids also increased the spontaneous release of [3H]acetylcholine from rat brain synaptosomes, further supporting a depolarizing action of these insecticides on nerve terminal membranes. Pyrethroid-induced release of [3H]acetylcholine was tetrodotoxin-sensitive and occurred over the same concentration range as membrane depolarization. These data indicate that type I and type II phenoxybenzyl pyrethroids act potently and stereoselectively on the voltage-sensitive sodium channel to increase sodium influx into synaptic terminals producing membrane depolarization and neurotransmitter release. Furthermore, they show that pyrethroid-induced alterations in synaptosomal membrane potential is a sensitive measure of pyrethroid action on the sodium channel and of pyrethroid toxicity.

Animals↗
PubMed2000

Altering the concentration of GABA in the synaptic cleft potentiates miniature IPSCs in rat occipital cortex.

We have tested the effect of dextran (40 kDa, 5%) on miniature IPSCs (mIPSCs) recorded in layer V cortical pyramidal cells. This compound increases the amplitude of mIPSCs at room and physiological temperatures by 15%, leaving their duration unaffected at room temperature and slightly increased at physiological temperature. The amplitude increase is attributable to an increase in the number of receptors bound by GABA during synaptic transmission, as shown by the occlusion between the effects of dextran and zolpidem on mIPSC amplitude at room temperature. As dextran presumably enhances the concentration and dwell time of GABA in the synaptic cleft, these results demonstrate that the postsynaptic GABAA receptors are not saturated at room and physiological temperatures.

Animals↗
PubMed1998

Gamma oscillations in the entorhinal cortex of the freely behaving rat.

Gamma frequency field oscillations (40-100 Hz) are nested within theta oscillations in the dentate-hilar and CA1-CA3 regions of the hippocampus during exploratory behaviors. These oscillations reflect synchronized synaptic potentials that entrain the discharge of neuronal populations within the approximately 10-25 msec range. Using multisite recordings in freely behaving rats, we examined gamma oscillations within the superficial layers (I-III) of the entorhinal cortex. These oscillations increased in amplitude and regularity in association with entorhinal theta waves. Gamma waves showed an amplitude minimum and reversed in phase near the perisomatic region of layer II, indicating that they represent synchronized synaptic potentials impinging on layer II-III neurons. Theta and gamma oscillations in the entorhinal cortex were coupled with theta and gamma oscillations in the dentate hilar region. The majority of layer II-III neurons discharged irregularly but were phase-related to the negative peak of the local (layer II-III) gamma field oscillation. These findings demonstrate that layer II-III neurons discharge in temporally defined gamma windows (approximately 10-25 msec) coupled to the theta cycle. This transient temporal framework, which emerges in both the entorhinal cortex and the hippocampus, may allow spatially distributed subpopulations to form temporally defined ensembles. We speculate that the theta-gamma pattern in the discharge of these neurons is essential for effective neuronal communication and synaptic plasticity in the perforant pathway.

Animals↗
PubMed1970

Actions of noradrenaline and acetylcholine on sympathetic ganglion cells.

1. The responses of the post-synaptic membrane of sympathetic ganglion cells to noradrenaline (NA) and to acetylcholine (ACh) were studied in relation to the slow inhibitory post-synaptic potential (S-IPSP) and slow excitatory one (S-EPSP) respectively.2. NA produced an hyperpolarization of about 4 mV in cells of rabbit superior cervical ganglia.3. The hyperpolarizing response to NA was not accompanied by any detectable change in membrane resistance, and it was depressed by conditioning depolarization.4. NA also depressed all the post-synaptic potentials, presumably by an action on presynaptic function.5. ACh produced a large depolarization in ganglion cells of rabbit and of frog (paravertebral) ganglia, which was accompanied by a large decrease in membrane resistance.6. When ACh was applied during nicotinic blockade, achieved with high concentration of nicotine (frog ganglia) or D-tubocurarine (rabbit ganglia), it still produced a considerable depolarization. This response could be blocked by atropine, and is presumably a muscarinic type of action.7. The muscarinic-ACh response was not accompanied by a decrease in membrane resistance. Instead, the frog ganglion cells exhibited increased resistances of up to more than twice the resting value during both the muscarinic-ACh depolarization and the S-EPSP.8. The muscarinic-ACh depolarization and the S-EPSP were both depressed by conditioning hyperpolarization (in nicotinized frog cells). An initial hyperpolarizing phase now appeared in both of these responses.9. It is concluded that the hyperpolarizing response to NA and the depolarizing response to muscarinic-ACh action are not generated by increases in ionic mobilities in the post-synaptic membrane; and that these two responses are produced by the same electrogenic mechanisms which underlie the S-IPSP and the S-EPSP respectively.

Acetylcholine↗
PubMed1992

Actions of somatostatin on GABA-ergic synaptic transmission in the CA1 area of the hippocampus.

Somatostatin and gamma-aminobutyric acid (GABA) are co-localized in some neurons in the CA1 area of the hippocampus. Since it is possible that the peptide and the amino acid are co-released, the interactions between the actions of somatostatin and GABA-ergic inhibitory post-synaptic potentials (IPSPs) in the CA1 pyramidal neurons of guinea pig hippocampal slices have been investigated. Somatostatin (2 microM) induced a hyperpolarization of the CA1 neurons associated with a reduction in the input resistance of the cells. These effects were not blocked by picrotoxinin (20 microM) or phaclofen (1 mM). Chelation of intracellular Ca2+ (Ca2+i) with BAPTA or the inhibition of protein kinase C (PKC) with sphingosine (30 microM) had no significant effects on the hyperpolarizing actions of somatostatin. The peptide suppressed the GABAA receptor-mediated fast IPSPs and the GABAB receptor-mediated slow IPSPs, but had no significant effect on the excitatory post-synaptic potentials (EPSPs). Somatostatin-induced depression of the IPSPs was not due to the hyperpolarization of the neurons. Baclofen (20 microM) suppressed the EPSP, as well as the fast and the slow IPSPs. The hyperpolarization of the CA1 neurons caused by somatostatin was greatly reduced in the presence of baclofen, an effect that was not due to the hyperpolarization of the cell by baclofen. The presence of QX-314 in the CA1 neurons, which suppressed the Na+ spikes and the slow IPSPs, prevented the hyperpolarization of the neurons by somatostatin and baclofen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Recruitment of crab gastric mill neurons into the pyloric motor pattern by mechanosensory afferent stimulation.

1. The gastropyloric receptor (GPR) cells are stretch-sensitive muscle receptors in the crab stomatogastric nervous system that use both 5-hydroxytryptamine (serotonin) and acetylcholine as cotransmitters. Brief stimulation of these afferent neurons causes two gastric mill neurons to be recruited into the pyloric motor pattern. 2. The GPR cells evoke complex synaptic potentials in the lateral gastric (LG) and medial gastric (MG) motor neurons, two component neurons of the gastric mill central pattern generator. When the gastric mill is quiescent (as often happens in vivo), GPR stimulation transiently inhibits LG and MG. After this transient inhibition, these cells undergo a prolonged excitation during which they fire bursts of action potentials at a constant phase relation to the pyloric motor pattern. 3. To determine the causes for this effect, we examined the effects of GPR stimulation on these two cells and on the inferior cardiac motor neuron, which is electrically coupled to them. When GPR is stimulated, all three cells receive rapid biphasic synaptic potentials that are blocked by nicotinic antagonists, followed by a slow, prolonged depolarizing potential. 4. The slow, prolonged depolarizing potential is not blocked by nicotinic or muscarinic cholinergic antagonists but is mimicked and occluded by exogenously applied serotonin. 5. The prolonged excitation, mediated at least in part by serotonin, may be responsible for the recruitment of the gastric mill neurons into the pyloric motor pattern. Thus sensory input can directly exert prolonged modulatory effects that change the functional cellular composition of pattern-generating circuits.

Acetylcholine↗
PubMed1993

Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro.

1. The effect of brief primary afferent inputs on the amplitude and duration of the synaptic potentials evoked in ventral horn (VH) neurons by the activation of other unconditioned primary afferents was studied by current-clamp intracellular recording in the neonatal rat hemisected spinal cord in vitro. Low-frequency (1 Hz) trains of stimulation were applied to a lumbar dorsal root (Conditioning root) for 20-30 s. Test excitatory synaptic potentials (EPSPs) were evoked by single electrical shocks applied to an adjacent Test dorsal root. 2. Test and Conditioning inputs were generated at stimulation strengths sufficient to activate A beta-, A delta- and C-afferent fibers successively. At A delta- and C-fiber strength the EPSPs lasted for 4-6 s, and, during the repetitive Conditioning inputs, these summated to produce a progressively incrementing cumulative depolarization that slowly decayed back to the control Vm over tens of seconds. 3. Dorsal root conditioning produced heterosynaptic facilitation, defined as an enhancement of Test EPSPs above their DC matched controls, in 7 out of 20 neurons. To facilitate the unconditioned afferent input, the intensity of conditioning stimulation had to exceed the threshold for the activation of thin myelinated (A delta) afferents: conditioning at A beta-fiber strength had no effect, whereas A delta- and C-fiber strength conditioning were equally effective. 4. Heterosynaptic facilitation of only A beta- or A delta-fiber-evoked Test EPSPs was observed, no enhancement of C-fiber strength Test EPSPs could be demonstrated. The facilitation manifested as increases in the EPSP peak amplitude, area or the number of action potentials evoked. 5. Conditioning trials that produced heterosynaptic facilitation generated cumulative depolarizations larger than those produced by ineffective conditioning trials (9.1 +/- 3.1 vs. 3.3 +/- 0.5 mV after 20 s conditioning at resting Vm, mean +/- SE, n = 6 and 13, respectively; P < 0.05). The slope of the Vm trajectory during the summation of the conditioning EPSPs was higher in trials resulting in heterosynaptic facilitation, at 0.31 +/- 0.10 mV/s in neurons with heterosynaptic facilitation and 0.06 +/- 0.02 mV/s in cells without heterosynaptic facilitation (P < 0.05). 5. Four of the 20 VH neurons in our sample responded to A delta/C-fiber conditioning with action-potential windup: all 4 also displayed heterosynaptic facilitation. 6. Heterosynaptic facilitation decayed after the completion of the conditioning stimulus with a time course that was parallel to but not superimposable on that of the slow Vm depolarization evoked by the conditioning.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1997

Effect of chronic ethanol treatment in vivo on excitability in mouse cortical neurones in vitro.

1. The effects of cessation of chronic ethanol ingestion on seizure activity in vivo and on the characteristics of the evoked synaptic potentials in cortical neurones in vitro have been investigated in mice. Withdrawal from chronic ethanol treatment increased handling seizure ratings in mice between 4 and 16 h post-withdrawal. This ethanol-induced increase in seizure rating was unaffected by carbamazepine (30 mg kg(-1)) but significantly reduced at a higher concentration (130 mg kg(-1)). 2. Intracellular recordings were made from cortical layer II neurones in vitro from control mice and from mice following chronic ethanol ingestion. Evoked synaptic potentials were generated in these neurones through intralaminar stimulation. 3. Neurones from control mice displayed an evoked potential consisting of a fast excitatory postsynaptic potential (e.p.s.p.) mediated by AMPA-type glutamate receptors and an inhibitory postsynaptic potential (i.p.s.p.) mediated via GABA(A) receptors. Application of pentylenetetrazole (PTZ) or bicuculline onto these neurones inhibited the i.p.s.p., caused a large increase in both the amplitude and duration of the e.p.s.p. and initiated spontaneous excitatory activity. The resulting large evoked e.p.s.p. was mediated via both NMDA- and AMPA-type glutamate receptors. 4. Most neurones (77%) from ethanol treated mice displayed an evoked potential which comprised a large e.p.s.p. and no i.p.s.p. The e.p.s.p. consisted of several distinct components and in addition these neurones displayed spontaneous paroxysmal depolarizing shifts. This multi-component e.p.s.p. was mediated through both NMDA- and AMPA-type glutamate receptors. A population (23%) of neurones from ethanol treated mice exhibited evoked potentials which possessed both inhibitory and excitatory components and these neurones were effectively identical to those obtained from control mice. 5. Carbamazepine reduced the duration of the e.p.s.p. in neurones from ethanol treated mice and in PTZ-treated control neurones. 6. Prolonged ethanol ingestion is known to create a neurochemical imbalance in cortical neurones resulting in abnormal neurotransmission. The present study highlights the functional consequences that arise as a result of these neurochemical changes leading to over-excitation of neurones and pronounced epileptiform activity.

Alcoholism↗
PubMed2003

Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons.

In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial parasympathetic ganglion neurons, including depolarization, causing phasic neurons to fire with a repetitive action potential pattern and potentiating synaptic transmission. In the present study, guinea pigs were passively sensitized to the antigen ovalbumin. After sensitization, the bronchi were prepared for in vitro electrophysiological intracellular recording of parasympathetic ganglia neurons to investigate the contribution of cyclooxygenase activation and prostanoids on parasympathetic nerve activity. Cyclooxygenase inhibition with either indomethacin or piroxicam before in vitro antigen challenge blocked the change in accommodation. These cyclooxygenase inhibitors also blocked the release of prostaglandin D(2) (PGD(2)) from bronchial tissue during antigen challenge. We also determined that PGE(2) and PGD(2) decreased the duration of the action potential after hyperpolarization, whereas PGF(2alpha) potentiated synaptic transmission. Thus prostaglandins released during antigen challenge have multiple effects on the excitability of guinea pig bronchial parasympathetic ganglia neurons, which may consequently affect the output from these neurons and thereby alter parasympathetic tone in the lower airways.

Action Potentials↗
PubMed2003

Study of the effects of electroacupuncture in a rodent model of cerebral ischaemia.

The effects of electroacupuncture (EA) has been studied in a model of global cerebral ischaemia performed in gerbils through the bilateral carotid artery occlusion (BCAO). Animals, under isofluorane anaesthesia, underwent 5 min of BCAO and were killed after 7 days. The effects of EA were evaluated both on functional (with electrophysiological recordings of synaptic potentials in hippocampal slices) and morphological parameters (by counting the number of survived neurons in CA1 area of the hippocampus). The results demonstrated that the treatment of animals with EA (5 min before, during and 20 min after BCAO and 30 min per day in the following 5 days) did not modify either the ischaemia-induced reduction of synaptic potentials amplitude, either ischaemia-induced neuronal loss in the hippocampus. We conclude that, at least in this animal model of cerebral ischaemia, EA does not exert a neuroprotective effect.

Animals↗
PubMed1992

Dissociation of mu and delta opioid receptor-mediated reductions in evoked and spontaneous synaptic inhibition in the rat hippocampus in vitro.

Modulation of gamma-aminobutyric acid (GABA)-mediated inhibition, and glutamate-mediated excitation by highly selective mu and delta opioid agonists was studied using intracellular recordings of CA1 pyramidal neuron synaptic responses in superfused hippocampal slices. Equimolar concentrations of the selective mu agonist, [Tyr-(D-Ala)-Gly-(N-Me-Phe)-Gly-ol]-enkephalin (DAGO), or the delta selective agonist, [D-Pen2,D-Pen5]-enkephalin (DPDPE), reversibly increased the amplitudes of excitatory post-synaptic potentials (EPSPs), evoked by Schaffer collateral/commissural stimulation, without altering the input resistance or resting membrane potential of these CA1 pyramidal neurons. The increased EPSP amplitudes resulting from superfusion with the enkephalin analogs were qualitatively similar to those caused by the GABAA receptor antagonist, bicuculline methiodide (BMI). Specific stimulation/recording protocols and micro-lesions of the slices were used to evoke relatively pure forms of recurrent and feed-forward GABA-mediated inhibitory post-synaptic potentials (IPSPs). The mu opioid agonist DAGO reduced both recurrent and feed-forward IPSPs, while the delta agonist DPDPE had no effect upon these responses. To test the hypothesis that the enhancement of pyramidal neuron EPSPs by delta (and mu) opioids was due to the reduction of an inhibitory potential that was coincident with the EPSP, DPDPE or the mu agonist, DAGO, were applied while recording monosynaptic IPSPs following the elimination of EPSPs by the glutamate receptor antagonists, D,L-2-amino-5-phosphonovalerate (APV) and 6,7-dinitroquinoxaline-2,3-dione (DNQX). The mu agonist, DAGO, reversibly reduced these pharmacologically isolated IPSPs, while the delta agonist, DPDPE, had no effect upon these responses. Despite the fact that the delta agonist, DPDPE, had no effect on recurrent, feed-forward or monosynaptic evoked IPSPs, this enkephalin did reversibly reduce the frequency of spontaneously occurring IPSPs, measured using whole-cell recordings with pipettes containing 65 mM KCl. The mu agonist, DAGO, and the GABAA antagonist, BMI, similarly reduced spontaneous IPSP rates. We conclude from these data that mu and delta opioid receptor activation increases EPSPs via the reduction of a form of GABAergic inhibition that is difficult to characterize, and which may be distinct from conventional feed-forward and recurrent inhibition. Furthermore, delta opioids seem to reduce this form of GABAergic inhibition selectively, while mu opioids reduced this inhibition, and conventional feed-forward and recurrent IPSPs as well.

2-Amino-5-phosphonovalerate↗
PubMed1993

Rabbit cerebellar slice analysis of long-term depression and its role in classical conditioning.

Cerebellar long-term depression (LTD) has been proposed as a mechanism underlying classical conditioning of the rabbit nictitating membrane/eyelid response (NMR). However, LTD has only been obtained reliably when (1) cerebellar slices are bathed in GABA antagonists which abolish disynaptic inhibitory post synaptic potentials, and (2) the temporal sequence of stimulation used in slice or intact preparations is the opposite of that used in classical conditioning. Based on intradendritic Purkinje cell recordings obtained from rabbit cerebellar slices, we report that stimulation of climbing fibers and then parallel fibers in the presence of the GABA antagonist, bicuculline, produced significant depression of parallel fiber excitatory post synaptic potential (epsp) amplitude that continued to increase for at least 20 min after stimulation. However, application of the same stimulation protocol without GABA antagonists produced a brief depression of parallel fiber epsps that disappeared within minutes. Activation of parallel fibers and then climbing fibers in an order opposite to the LTD-producing sequence (i.e. a classical conditioning-like order) produced a brief depression that dissipated quickly. Stimulation of parallel fibers alone produced a small, slowly developing potentiation, but stimulation of parallel fibers during depolarization-induced local dendritic calcium spikes produced significant depression almost immediately which then declined slowly to more modest levels. Finally, stimulation of parallel fibers at frequencies used in in vivo parallel fiber-climbing fiber stimulation experiments (e.g. 100 Hz) produced an immediate and profound long-lasting epsp depression. The depression occurred, however, whether parallel and climbing fibers were stimulated separately (unpaired) or in a classical conditioning-like protocol (paired) where parallel fiber stimulation coterminated with climbing fiber stimulation (10 Hz).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Analysis of synaptic quantal depolarizations in smooth muscle using the wavelet transform.

The time-frequency characteristics of synaptic potentials contain valuable information about the process of neurotransmission between nerves and their target organs. For example, at the synapse between autonomic nerves and smooth muscle, two central issues of neurophysiology, i.e., 1) the probability of neurotransmitter release and 2) the quantal behavior of transmission can be deduced from analysis of the rising phases of evoked excitatory junction potentials (eEJP's) recorded from smooth muscle. eEJP rising phases are marked by prominent inflexions, which reflect these features of neuronal activity. Since these inflexions contain time-varying frequency information, we have applied recent techniques of time-frequency analysis based upon wavelet transforms to eEJP's recorded from the guinea-pig vas deferens in vitro. We find that these techniques allow accurate and convenient characterization of neuronal release sites, and that their probability of release falls between 0.001-0.004. We have also analyzed eEJP's recorded in the presence of the chemical 1-heptanol, which reveals quantal depolarizations. These results have helped clarify the nature of the quantal depolarizations that underly eEJP's. The present method offers significant advantages over those previously employed for these tasks, and holds promise as a novel approach to the analysis of synaptic potentials.

Animals↗
PubMed1991

Potentiation of synaptic responses in slices from the chick forebrain.

Coronal slices, containing part of the medial hyperstriatum ventrale (MHV), were cut from the left forebrains of domestic chicks and maintained in vitro. Records were made of the field responses evoked in the MHV by local electrical stimuli provided at 0.1 Hz. Two 1 min periods of stimulation at 5 Hz, separated by 10 min, were used in attempts to induce a persistent increase in the size of the postsynaptic response to test stimulation at 0.1 Hz. This procedure produced a potentiation which usually lasted longer than 2 h. The probability of inducing this persistent potentiation of the response (PPR) is not distributed evenly over the whole anteroposterior length of the MHV but is higher in slices that also contain the septo-mesencephalic tract ventrally. These are the slices that contain the intermediate part of the medial hyperstriatum ventrale (IMHV); an area that is essential for early behavioural learning. At this level PPR is not confined to the IMHV. It can also be produced in the lateral neostriatum in response to similar local stimulation at 5 Hz. No PPR was observed in either the caudal ectostriatum, or the paleostriatum.

Animals↗
PubMed1994

Y2-receptor-mediated selective inhibition of slow, inhibitory postsynaptic potential in submucous neurones of guinea-pig caecum.

1. The subtype of neuropeptide Y receptor mediating the selective inhibition of the slow inhibitory postsynaptic potential (i.p.s.p.) of submucous neurones in guinea-pig caecum was investigated by use of conventional intracellular electrophysiological recording techniques. 2. Neuropeptide Y (NPY) (1-300 nM) was found to depress or abolish reversibly the slow i.p.s.p. evoked by focal stimulation of internodal fibre tracts. At low concentrations (1-30 nM), a reduction in the duration of the slow i.p.s.p. was often apparent before any inhibition of the amplitude of this synaptic potential. 3. These inhibitory effects of NPY were mimicked by peptide YY (PYY; 0.3-100 nM), NPY13-36 (1-300 nM) and NPY22-36 (10-100 nM); [Leu31,Pro34]NPY ([Pro34]NPY) and bovine pancreatic polypeptide (bPP) were without pre- or postsynaptic effects at concentrations of up to 300 nM. The IC50 +/- s.e. mean values for PYY, NPY, and NPY13-36 were 2.7 +/- 0.3, 7.8 +/- 2.1 and 30 +/- 4.8 nM, respectively, and were significantly different from each other. Thus, the apparent rank order of potency was PYY > NPY > NPY13-36 >> [Pro34]NPY and bPP. 4. In concentrations of up to 300 nM, NPY and its analogues had no depressant effects on the active and passive properties of the impaled neurone and did not affect the amplitude or duration of either cholinergic fast synaptic potentials or non-cholinergic, slow excitatory postsynaptic potentials (e.p.s.ps). Furthermore, none of these peptides altered the amplitude or time-course of changes in membrane potential induced by focal application of acetylcholine or noradrenaline. 5. It is, therefore, concluded that the selective inhibition of the slow i.p.s.p. is mediated by Y2-receptors,located presynaptically on noradrenergic nerve terminals.

Action Potentials↗