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PubMed1990

Enhancement of NMDA receptor-mediated synaptic potential evoked in rat medial-amygdala neuron following olfactory bulbectomy.

Synaptic potentials evoked in the medial amygdala (m-AMG) neurons were studied in in vitro slice preparations obtained from normal and olfactory bulbectomized rats. Local stimulation induced a sequence of responses: a fast EPSP, a fast IPSP and a slow EPSP. The fast EPSP was suppressed by kynurenic acid (KYN) at a concentration of 1 mM but not by 3-[(+-)-2-carboxypiperazin-4-yl-]-propyl-1-phosphonic acid (CPP) at concentrations up to 20 microM. The slow EPSP was reversibly blocked by both KYN (1 mM) and CPP (5-10 microM). Addition of bicuculline methiodide (50 microM) to the bath suppressed the fast IPSP and augmented both the fast and slow IPSPs leading to burst discharges. In a small population of m-AMG neurons, the slow EPSP was followed by a slow IPSP. The slow IPSP was suppressed by phaclofen (500 microM) but not by bicuculline methiodide (up to 100 microM). In slice preparations obtained from olfactory bulbectomized rats, local stimulation evoked burst discharges, which were similar to those observed when bicuculline methiodide was applied to slice preparations obtained from normal rats. These results suggest that GABAA receptor mediating fast IPSP and N-methyl-D-aspartate (NMDA) receptors mediating slow EPSP regulate activities of m-AMG neurons and that the enhancement of NMDA receptor mediating slow EPSP is responsible for the hyperexcitability of m-AMG neurons following olfactory bulbectomy.

Action Potentials↗

PubMed1985

Significance of slow synaptic potentials for transmission of excitation in guinea-pig myenteric plexus.

Intracellular recordings were made from neurones in myenteric ganglia of the guinea-pig ileum in vitro. Synaptic potentials were evoked by electrically stimulating presynaptic fibres as they entered the ganglion, using a small focal electrode. Slow synaptic depolarizations (excitatory postsynaptic potentials) were evoked in most myenteric neurones of both types. A single stimulus was more likely to evoke a slow excitatory postsynaptic potential in cells with nicotinic synaptic input (S cells; 50%) than in cells with long-lasting after-hyperpolarizations following the soma action potential (AH cells; 20%). Two pulses often evoked a slow excitatory postsynaptic potential in AH cells when one pulse was ineffective. The optimally effective time between the pulses was about 100 ms. Ten pulses resulted in slow excitatory postsynaptic potentials even when delivered at frequencies as low as 0.5 Hz. For the same frequency of presynaptic stimulation, the duration of the slow excitatory postsynaptic potential was greater in AH cells than in S cells and the amplitude of the slow excitatory postsynaptic potential was slightly greater in S than AH cells. Spontaneous depolarizations were observed which had time-courses and amplitudes similar to the evoked slow excitatory postsynaptic potential. They were not blocked by tetrodotoxin or atropine. The calcium-dependent after-hyperpolarization which follows one or more action potentials in AH cells was reduced or even abolished during the slow excitatory postsynaptic potential. Presynaptic nerve stimulation at intensities lower than those required to cause a slow excitatory postsynaptic potential caused a reduction in the calcium dependent after-hyperpolarization. It is concluded that the slow excitatory postsynaptic potential is generated by an intracellular intermediate process which is sensitive to the intracellular calcium concentration. The results suggest that the postsynaptic action of the synaptic transmitter is to interfere with the intracellular process which couples the entry of calcium to the increase in potassium conductance.

Animals↗

PubMed1969

Non-linear summation of unit synaptic potentials in spinal motoneurones of the cat.

1. Monosynaptic excitatory post-synaptic potentials (EPSPs) produced in spinal motoneurones of the cat by stimulation of a single afferent fibre were recorded with intracellular electrodes.2. In total, seventy-three triceps surae motoneurones were studied with stimulation of thirty-six different afferent fibres.3. The mean amplitude of the EPSPs evoked by single afferent impulses ranged from 0.06 to 2.0 mV with an average of 0.27 mV.4. The mean number of unit EPSPs responding to a single afferent impulse (m) was calculated from the number of failures. The values ranged from 0.7 to more than 5. About 10% of the sample showed no failure of synaptic response in about 200 consecutive trials. The m values for these synaptic responses were estimated to range from 5 to 15.5. In the majority of tests, the observed amplitude fluctuations of monosynaptic EPSPs evoked by stimulation of a single fibre were less than those expected from Poisson's law. This discrepancy may be accounted for by non-linear summation of the unit EPSPs at dendritic synaptic sites.6. It is suggested that the synaptic responses initiated at different sites of a motoneurone may summate linearly at the soma, although summation of unit EPSPs is non-linear at individual synaptic sites.

Animals↗

PubMed1998

Distinct expressions for synaptic potentiation induced by calcium through voltage-gated calcium and N-methyl-D-aspartate receptor channels in the hippocampal CA1 region.

Brief elevation in postsynaptic calcium in hippocampal CA1 neurons leads to prolonged changes in synaptic strength. The calcium may enter the postsynaptic neuron via different routes, such as voltage-gated calcium channels or glutamate receptor channels of N-methyl-D-aspartate type, and/or be released from intracellular stores. The manner in which the synapse is altered, leading to the expression of an enhanced/depressed synaptic strength, is still unclear. The present study, performed using whole-cell recording from CA1 pyramidal cells of three- to five-week-old guinea-pigs, shows that postsynaptic depolarization alone, allowing for calcium influx through voltage-gated calcium channels, leads to a synaptic potentiation characterized by an altered time-course of the evoked excitatory synaptic response, an unaltered coefficient of variation of that response and a decreased paired-pulse facilitation likely related to a postsynaptic mechanism. These characteristics contrasted with those of long-term potentiation induced via activation of N-methyl-D-aspartate receptor channels, where the time-course was unaltered, the coefficient of variation was decreased and no change in paired-pulse facilitation was observed. Synapses can thus have mechanistically separate, but co-existent, potentiations of synaptic transmission initiated from separate sources for postsynaptic calcium.

Animals↗

PubMed1988

Phorbol ester-induced synaptic potentiation differs from long-term potentiation in the guinea pig hippocampus in vitro.

The relationship between the synaptic potentiations evoked by the protein kinase C activator phorbol-12,13-diacetate and by afferent tetanization has been examined in the CA1 region of the hippocampal slice preparation using extracellular recording. It has been found that the potentiation of the field excitatory postsynaptic potential produced by 1 microM phorbol ester does not affect the amount of long-term potentiation (LTP) that can be evoked by afferent tetanization, and vice versa. A dissociation between phorbol ester-induced and tetanus-induced potentiation is also indicated by the fact that only the former was associated with changes in paired-pulse facilitation. On the other hand, as previously described, higher concentrations (10 microM) of phorbol ester blocked the tetanus-induced potentiation. Since the total potentiation given by 10 microM phorbol ester and tetanization depended on the order of presentation of the potentiation-inducing stimuli, it appears that the blockade of LTP is, at least partly, independent of the phorbol ester-induced potentiation.

Action Potentials↗

PubMed1976

[The effect of cholinesterase inhibitors on the synaptic potentials of frog neuromuscular junctions].

Prostigmine and the organophosphorus inhibitor armine acting upon synaptic potentials in the frog cutaneous pectori nerve--muscle preparation, increased the m.e.p.p. and e.p.p. amplitudes, lengthened the rise and the half--decline time of the e.p.p. in a-proximately similar way. The effect of armine developed faster than that of prostigmine. The presynaptic effects of both anticholinesterases (increase of mepp's frequency and quantal content of epp's) developed much more slowly than their post-synaptic effects. After prostigmine pretreatment during 2 hrs, addition of armine caused lengthening of the time-course of e.p.p.'s. but the presynaptic effect was not altered. After armine pretreatment, prostigmine did not cause any further effect. Possible mechanisms for the presynaptic effects of the inhibitors are discussed.

Animals↗

PubMed1995

Postsynaptic injection of CA2+/CaM induces synaptic potentiation requiring CaMKII and PKC activity.

CA2+-regulated protein kinases play critical roles in long-term potentiation (LTP). To understand the role of Ca2+/calmodulin (CaM) signaling pathways in synaptic transmission better, Ca2+/CaM was injected into hippocampal CA1 neurons. Ca2+/CaM induced significant potentiation of excitatory synaptic responses, which was blocked by coinjection of a CaM-binding peptide and was not induced by injections of Ca2+ or CaM alone. Reciprocal experiments demonstrated that Ca2+/CaM-induced synaptic potentiation and tetanus-induced LTP occluded one another. Pseudosubstrate inhibitors or high-affinity substrates of CaMKII or PKC blocked Ca2/CaM-induced potentiation, indicating the requirement of CaMKII and PKC activities in synaptic potentiation. We suggest that postsynaptic levels of free Ca2+/CaM is a rate limiting factor and that functional cross-talk between Ca2+/CaM and PKC pathways occurs during the induction of LTP.

Amino Acid Sequence↗

PubMed1998

GABA receptor-mediated post-synaptic potentials in the retrohippocampal cortices: regional, laminar and cellular comparisons.

Inhibitory post-synaptic potentials (IPSPs) were studied in neurons of presubiculum, parasubiculum and medial entorhinal cortex in horizontal slices from rat brains. Isolated IPSPs were evoked by extracellular electrical stimuli in the presence of glutamate receptor antagonists. Cellular morphology was identified using Neurobiotin labeling. IPSPs were compared: (a) across morphological cell types, (b) across laminae within regions, and (c) across regions. IPSPs were visible in stellate and pyramidal cells from layers II, III, and V of all retrohippocampal areas during bath application of glutamate antagonists. Qualitative and quantitative differences in IPSPs were only found when comparing responses by superficial layer II, III cells to responses by deep layer V cells. Responses by stellate and pyramidal cells within the same or adjacent layers did not differ, nor did responses differ from region to region. All cell types exhibited an early hyperpolarizing response. The majority (85%) of superficial layer cells in all regions, regardless of cell shape, exhibited a second hyperpolarizing component. Fewer (50%) deep layer cells exhibited the late peak with similar long latencies. IPSPs were typically larger in superficial layer cells. IPSPs were comprised of GABAA and GABAB (gamma-aminobutyric acid) receptor-mediated components. With repetitive stimulation, the peak amplitude of the GABAA receptor-mediated component decreased with successive stimuli, but stabilized during the first five or fewer stimuli to a level that did not vary with stimulation frequency. The GABAB receptor-mediated component also stabilized, but the final amplitude appeared to decrease as the stimulation frequency increased. With high-frequency repetitive stimulation, both components of the IPSP showed summation. We conclude that the most meaningful distinction for IPSPs among retrohippocampal neurons is a laminar distinction, between superficial and deep layer neurons, and not one across cell shape or retrohippocampal subregion. These laminar differences can contribute to synchronous activity by deep layer neurons and restrict the activity of superficial layer neurons.

Animals↗

PubMed1993

Synaptic potentiation in the rat dentate gyrus during exploratory learning.

To investigate whether hippocampal synaptic transmission is enhanced during learning, we recorded synaptic field potentials in the dentate gyrus in response to stimulation of the perforant path in rats exploring a novel environment. Because these signals rapidly grow during brain temperature elevation, caused by any motor activity, the potentials were compared with signals sampled at similar brain temperatures after passive warming. Both the field excitatory postsynaptic potential (f-EPSP) and the population spike increased significantly early in the exploration, relative to temperature-matched control potentials. The effect decayed within 15-30 minutes. This is the first demonstration of a temperature-independent synaptic potentiation in the hippocampus during learning about the environment. The time course is similar to that of short-term potentiation.

Animals↗

PubMed1983

The time course of synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in motoneurones by impulses in single group Ia axons. After recording the e.p.s.p., the motoneurone and the group Ia axon were injected with horseradish peroxidase. The morphological details of the connexion formed by each group Ia axon with a motoneurone were subsequently reconstructed. Four Ia axon-motoneurone pairs were obtained. The electrotonic distance from the soma to each synaptic bouton in the connexion was calculated. The electrotonic lengths of those dendrites on which synaptic connexions were found were also calculated. The shape indices of each recorded e.p.s.p. and the standard cable model of the motoneurone were used to calculate the electrotonic distance from the soma to the point on the equivalent dendritic cable at which the e.p.s.p. originated. This distance was compared with the distance obtained from the reconstruction of the synaptic connexion at which the e.p.s.p. was generated. For two of the four connexions, the locations calculated by both methods agreed to within 0.1 lambda. Similar agreement could only be obtained for the other two connexions if synaptic transmission did not occur at some of the boutons in the termination. Evidence that some boutons were not involved in transmission is presented in the following paper (Redman & Walmsley, 1983).

Animals↗

PubMed1983

Amplitude fluctuations in synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in spinal motoneurones (of anaesthetized cats) by impulses in single group Ia axons. The morphological details of the Ia axon-motoneurone connexion involved in generating each e.p.s.p. were subsequently reconstructed, as described by Redman & Walmsley (1983). The fluctuation pattern of the peak amplitude of each e.p.s.p. was determined using a deconvolution method, taking into account the recording noise. Four e.p.s.p.s were analysed. One did not fluctuate in amplitude; the others fluctuated between discrete amplitudes which were separated by quantal increments. The number of increments which must be added to produce the largest peak amplitude of each e.p.s.p. was always less than, or equal to, the number of synaptic boutons in the connexion at which the e.p.s.p. was generated. The results are consistent with the hypothesis that transmission occurs in an all-or-none manner at each synaptic bouton. Different boutons in the termination of a Ia axon with a motoneurone have different probabilities of releasing transmitter, and this probability is sometimes zero at low stimulation rates. The results support the idea that the discrete amplitudes of an evoked e.p.s.p. result from intermittent transmission, in an all-or-none manner, at some or all of the boutons in the termination.

Animals↗

PubMed2002

Synaptic potentials mediated by alpha 7 nicotinic acetylcholine receptors in supraoptic nucleus.

Brain slice preparations preserving projections from nearby forebrain cholinergic neurons to the supraoptic nucleus (SON) were used to study synaptic potentials mediated by nicotinic acetylcholine receptors (nAChRs) in the hypothalamus. Paired-pulse electrical stimulation in an area anterior to the SON that was rich in cholinergic cells confirmed the monosynaptic nature of the connections to putative oxytocin and vasopressin SON neurons. With ionotropic glutamate and GABA(A) transmission blocked, this stimulation evoked fast, atropine-insensitive EPSPs that were sensitive to nAChR antagonists. Evoked EPSPs were blocked by methyllycaconitine and alpha-bungarotoxin, antagonists that are selective for nAChRs containing the alpha7 subunit, but not by dihydro-beta-erythroidine at concentrations known to antagonize alpha4beta2 nAChRs. Although anatomical evidence exists for postsynaptic alpha4beta2 nAChRs in the SON, these results indicate that postsynaptic alpha7 nAChRs are primarily responsible for the cholinergically mediated EPSPs. Repetitive stimulation suggested partial desensitization of the receptors. With ionotropic glutamate transmission blocked, inhibition of AChE increased spontaneous EPSP frequency and amplitude, suggesting spontaneous ACh release. ACh, nicotine, and choline (a selective alpha7 nAChR agonist) were effective in evoking action potentials and repetitive firing with synaptic transmission blocked by low Ca2+, high Mg2+ medium. These agonists were also effective in evoking the type of phasic bursts characteristic of vasopressin neurons, long thought to be completely dependent on activation of NMDA receptors (NMDARs). Because phasic bursting is Ca2+-dependent, the functional equivalence of alpha7 nAChR and NMDAR activation in this regard is likely attributable to their large Ca2+ fluxing capacities. This is the first demonstration that synaptically released ACh results in fast, alpha7 nAChR-mediated EPSPs in hypothalamic neurons.

Acetylcholine↗

PubMed1982

On the nature of histamine-mediated slow hyperpolarizing synaptic potentials in identified molluscan neurones.

1. Standard intracellular stimulating and recording techniques were used to test the correspondence between monosynaptic post-synaptic potentials (p.s.p.s) evoked by histamine-containing C-2 neurones and responses to focally applied histamine recorded from two classes of identified post-synaptic neurones in the cerebral ganglion of Aplysia californica.2. Two types of p.s.p.s were examined: (1) a monophasic slow hyperpolarizing potential (I(s)p.s.p.) lasting 1-2 sec; and (2) a biphasic p.s.p. consisting of a fast depolarizing component <0.5 sec in duration (E(f)p.s.p.) plus a slow hyperpolarizing potential (I(s)p.s.p.) designated the E(f)I(s)p.s.p.3. Ionophoretic or pressure applied histamine mimicked both p.s.p.s and produced conductance increases in the post-synaptic neurones similar to those associated with the evoked p.s.p.s.4. The reversal potentials (E(rev)) for the I(s)p.s.p. and E(f)I(s)p.s.p., estimated by extrapolation, were -85+/-5.3, -35+/-5.5, and -83+/-8.1 mV (mean+/-S.D.), respectively. The I(s)p.s.p.s were produced by an increase in potassium conductance because their E(rev)s were shifted about 16 mV by doubling or halving the concentration of extracellular potassium and they could be eliminated by cooling or by intracellular injection of TEA ions.5. The average E(rev) values for the slow hyperpolarizing histamine responses were similar to those for the I(s)p.s.p.s; about -83 and -86 mV in neurones receiving the monophasic I(s)p.s.p.s and biphasic E(f)I(s)p.s.p., respectively.6. Cimetidine, an antihistamine drug that selectively blocks histamine receptors associated with potassium conductances in Aplysia, reversibly abolished the I(s)p.s.p.s and slow hyperpolarizing responses to focally applied histamine. In similar concentrations, cimetidine had no discernible effects on the E(f)p.s.p. and depolarizing response to histamine or on several different types of p.s.p.s mediated by the C-2 neurones.7. It is proposed that the I(s)p.s.p.s are mediated by histamine released from the C-2 neurones.

Animals↗

PubMed1987

On the excitatory post-synaptic potential evoked by stimulation of the optic tract in the rat lateral geniculate nucleus.

1. The electrophysiological and pharmacological properties of the excitatory post-synaptic potentials (e.p.s.p.) evoked by electrical stimulation of the optic tract were studied in projection neurones of the ventral and dorsal lateral geniculate nucleus (l.g.n.) of the rat in vitro. 2. No difference was found in the rise time of e.p.s.p.s. recorded in the dorsal and ventral l.g.n. and in their threshold for action potentials. At membrane potentials more negative than -60 mV, e.p.s.p.s. in the dorsal l.g.n. were always followed by a Ca2+-dependent potential. Its amplitude could easily reach threshold for generating an action potential and thus evoke firing from an e.p.s.p. that was subthreshold at resting potential. No Ca2+ potential was observed to follow e.p.s.p.s. recorded in the ventral l.g.n. 3. At resting potential the excitability of dorsal and ventral cells was unaffected following an initial shock to the optic tract. However, in dorsal neurones, at potentials more negative than -60 mV, the presence of Ca2+ potentials evoked by the e.p.s.p.s. resulted in a period of decreased excitability. 4. Using intrasomatic injection of Cs+ the reversal potential (E) of the e.p.s.p. and of the depolarization produced by glutamate could be measured in the same l.g.n. neurone. They were: Eepsp, -0.9 mV; and Eglut, -3.9 mV. 5. gamma-D-glutamylglycine (DGG), an excitatory amino acid antagonist, reversibly inhibited the e.p.s.p. and depolarization produced by quisqualate and glutamate by a competitive action. The concentration of DGG that produced 50% inhibition (IC50) was 2.7 mM. 6. D-2-amino-5-phosphonovalerate (APV), the potent and selective N-methyl-D-aspartate (NMDA) antagonist, had no effect on the e.p.s.p. both in the presence and absence of Mg2+. The isomers of 2-amino-4-phosphonobutyrate (APB) were inactive or had a non-specific action on the e.p.s.p. 7. No difference could be detected in either the reversal potential or the action of the antagonists between neurones of the dorsal and the ventral l.g.n. 8. These results suggest that Ca2+-dependent potentials play an important role in modulating synaptic efficacy in principal neurones of the dorsal l.g.n. The quisqualate/kainate nature of the optic nerve receptors and the similarity of Eepsp and Eglut constitute strong support in favour of a glutamate-like substance as the transmitter of the optic nerve.

2-Amino-5-phosphonovalerate↗

PubMed1981

The components of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia afferents.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in cat spinal motoneurones by impulses in single group Ia afferent fibres. The probability density of the fluctuations in peak amplitude of each e.p.s.p. was calculated from the recorded peak amplitude and the probability density of the recording noise. 2. Most e.p.s.p.s fluctuated between different components (i.e. individual e.p.s.p.s of a particular discrete amplitude) with peak amplitudes which were integer multiples of the increment between successive components. The average peak amplitude of this incremental e.p.s.p. was about 90 microV for e.p.s.p.s generated at or near the soma. 3. In general, the probability density of the peak amplitude could not be described using Poisson or binomial distributions. 4. For many e.p.s.p.s the complete time course of each component could be calculated. There was no variability in the amplitude of these components nor in their latency of onset. For some e.p.s.p.s there were differences in the latency and time course of the components. 5. The increments between successive components of e.p.s.p. generated proximally were no larger (at the soma) than the corresponding increments for e.p.s.p.s generated at more distal dendritic sites. 6. These results and those from subsequent papers (Jack, Redman & Wong, 1981; Hirst, Redman & Wong, 1981) reinforce earlier suggestions that each bouton behaves in an all-or-nothing manner with respect to post-synaptic effect, and the probability of failure varies at different boutons arising from the same afferent.

Animals↗

PubMed1984

Influence of post-synaptic properties on the time course of synaptic potentials in different types of cat lumbar alpha-motoneurons.

Shape indices of excitatory post-synaptic potentials (EPSPs) have been calculated on compartmental models assembled using average properties obtained from two motoneuron groups classified as fast and slow, on the basis of rheobase current and input conductance. The calculated EPSP time courses differed considerably between the two models, the rise-time and half-width being more prolonged in the slow model. With a conductance change distributed uniformly among compartments 3-6 in a 10-compartment model, the resulting shape indices in the slow and fast model, respectively, were quite similar to the apparent average values previously observed experimentally for composite Ia EPSPs in types S (slow) and F (fast) motoneurons. The results of the calculations suggest that differences in EPSP shape indices observed between F and S motoneurons arise from systematic differences in motoneuron postsynaptic properties (specific membrane resistivity and dendritic geometry) rather than differences in dendritic location of synaptic input. The results also suggest that changes in EPSP time course, following section of the motor axon, may similarly be related to changes in motorneuron postsynaptic properties.

Animals↗

PubMed1991

Involvement of GABA systems in feedback regulation of glutamate-and GABA-mediated synaptic potentials in rat neostriatum.

1. Neostriatal neurones were recorded intracellularly from a rat corticostriatal slice preparation. Depolarizing postsynaptic potentials (DPSPs) were evoked by either cortical or intrastriatal stimulation. 2. Kynurenic acid (600 microM), an antagonist of excitatory amino acids, reduced the cortically-evoked DPSPs by 88% while the intrastriatally evoked potentials were reduced by 48%. Bicuculline (100 microM) produced only a slight inhibition of the cortically evoked DPSPs (12%), but clearly depressed intrastriatal potentials (52%). 3. The effects of (-)-baclofen, a gamma-aminobutyric acid (GABA)B receptor agonist, were studied on the cortically evoked DPSPs. In all the tested neurones (-)-baclofen, added to the superfusion medium, caused a concentration-dependent decrease of these potentials (half-maximal effect (EC50) = 800 nM). This effect was not affected by bicuculline. (-)-Baclofen did not change the membrane potential, the input resistance, current-evoked firing frequency, or postsynaptic responses to exogenously applied glutamate. 4. The effects of (-)-baclofen on the DPSPs were compared to those produced by application of GABA and muscimol. GABA and muscimol decreased the DPSPs and caused a membrane depolarization coupled with a decrease of the membrane resistance. Bicuculline (100 microM) blocked the GABA-induced changes of the membrane potential and of the resistance, but not the decrease of the synaptic potentials. All the effects produced by muscimol were blocked by bicuculline. 5. Following intrastriatal stimulation a residual kynurenate-insensitive potential persisted; this potential was blocked by bicuculline (100 microM). (-)-Baclofen produced a dose-dependent decrease of this potential (EC50 = 800 nM). The postsynaptic responses to exogenously applied GABA were unchanged by (-)-baclofen. 6. The amplitude of kynurenate and bicuculline-sensitive DPSPs were stable at a frequency of 0.1 Hz. At frequencies between 0.3 and 3 Hz both these potentials were attenuated with the second stimulus and after about five stimuli a steady state was reached. Membrane potential and input resistance were not affected by these frequencies of stimulation. 7. Application of the GABA uptake inhibitor nipecotic acid (100-300 microM) clearly reduced the amplitude of both kynurenate-and bicuculline-sensitive DPSPs evoked at low frequencies of stimulation (0.01-0.3 Hz), but had lower effects at higher stimulation rates (1-3 Hz). Application of nipecotic acid increased the duration of membrane responses to exogenously applied GABA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMedDate not supplied

Effect of cholinesterase inhibitors on synaptic potentials of the frog neuromuscular junction.

The action of neostigmine and armin on the parameters of synaptic potentials of the m. cutaneus pectoris of the frog was investigated. Both drugs caused an approximately equal increase in amplitude of miniature end-plate potentials (MEPP) and end-plate potentials (EPP), and lengthened the rise time and the half-decay time of EPP, but the effect of armin developed faster. The presynaptic action of both inhibitors was demonstrated (an increase in the frequency of MEPP and in the quantum composition of EPP), but it developed much more slowly than the postsynaptic effects; it was more marked in the case of neostigmine. Administration of armin after preliminary contact with neostigmine increased the duration of EPP somewhat, but did not potentiate the presynaptic effects. No significant changes were observed when neostigmine was given after armin. The possible mechanism of the presynaptic effects of the cholinesterase inhibitors is discussed.

Action Potentials↗