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PubMed1989

Tongue-muscle-controlling motoneurons in the Japanese toad: neural inputs from the thalamus.

The anuran tongue is an effector organ specialized for snapping up prey during visually guided prey-catching behavior. As a step toward elucidating the control mechanisms of the tongue movement and overall organization of visually guided behavior, properties of neural inputs from the thalamus (of which electrical stimulation elicited a behavior very similar to the visually guided predator-avoidance behavior under freely behaving conditions) were investigated in paralyzed Japanese toads. Tongue-muscle-controlling motoneurons (tongue-protractor motoneurons (PMNs) and tongue-retractor motoneurons (RMNs)) were identified antidromically, and synaptic inputs in response to electrical stimuli applied to various points in the thalamus (mainly the posterocentral thalamic nucleus) were examined. Hyperpolarizing potentials were evoked in both PMNs and RMNs in response to single electrical stimuli applied to the thalamus contralateral or ipsilateral to the recording side. Since these potentials reversed to depolarizing ones after injecting Cl- ions into the cell interior, these hyperpolarizing potentials were concluded to be the usual fast type of inhibitory postsynaptic potentials (IPSPs). On the other hand, depolarizing potentials which were superimposed on the underlying IPSPs were evoked when repetitive electrical stimuli were applied to the thalamus. The amplitude of these depolarizing potentials was decreased when depolarizing currents were injected intracellularly, while it was increased when hyperpolarizing currents were injected, indicating that these depolarizing potentials are excitatory postsynaptic potentials (EPSPs).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1987

Antagonist discrimination of two muscarinic responses elicited by applied agonists and orthodromic stimuli in superior cervical ganglion of rabbit.

Pirenzepine and gallamine selectively and differentially antagonized two muscarinic responses, in the superior cervical ganglion of the rabbit, whether elicited by the muscarinic agonist methacholine or by orthodromic stimulation. Methacholine elicited a biphasic ganglionic response, consisting of hyperpolarizing and depolarizing components that were the agonist-induced equivalents of the slow-inhibitory and slow-excitatory postsynaptic potentials elicited by orthodromic stimulation. Superfusion of ganglia with pirenzepine resulted in a concentration-dependent suppression of depolarization induced by methacholine with no suppressant action on ganglionic hyperpolarization. In contrast, superfusion of ganglia with gallamine resulted in a concentration-dependent suppression of ganglionic hyperpolarization and the slow-inhibitory postsynaptic potential. These effects occurred without appreciable suppression of ganglionic depolarization or the slow-excitatory postsynaptic potential. The action of gallamine was specific for muscarinic hyperpolarization. Hyperpolarizations produced by superfusion with dopamine or norepinephrine were unaffected by gallamine, at concentrations that suppressed the muscarinic slow-inhibitory post-synaptic potential. Incubation with anti-cholinesterases produced a parallel shift, to the right, of concentration-response curves for suppression by gallamine of the slow-inhibitory postsynaptic potential. This was presumably the consequence of an increase in the acetylcholine available for interaction with the muscarinic receptor. The evidence suggests that the ability of gallamine and pirenzepine to suppress selectively the slow-inhibitory and slow-excitatory postsynaptic potentials, as previously demonstrated, is through an action at muscarinic receptors. Furthermore, the data suggest that these pharmacological agents produce their effects by interaction at different muscarinic recognition sites.

Animals↗

PubMed1978

Pentobarbital: differential postsynaptic actions on sympathetic ganglion cells.

The frog sympathetic ganglion has been used as a model to elucidate the cellular mechanism of barbiturate anesthesia. Anesthetic concentrations of pentobarbital markedly reduced the fast nicotinic excitatory postsynaptic potential while having no effect on the slow excitatory postsynaptic potential or slow inhibitory postsynaptic potential, even though all three synaptic potentials depend on the presynaptic release of acetylcholine. A similar differential effect was seen for nicotinic and muscarinic responses to exogenously applied agonists, while the depolarizing action of gamma-aminobutyric acid (GABA) was enhanced. These results indicate that pentobarbital has remarkably selective actions on the sympathetic ganglion and further indicate that blockade of ganglionic transmission by anesthetic concentrations of pentobarbital can be entirely explained by a postsynaptic action. The present results strengthen the concept that pentobarbital anesthesia results from a postsynaptic blockade of central excitatory synapses which increase sodium conductance coupled with a postsynaptic enhancement of GABA-mediated synaptic inhibition.

Animals↗

PubMed1992

Developmental and regional differences in the vulnerability of rat hippocampal slices to lack of glucose.

Field excitatory postsynaptic potentials were recorded in stratum radiatum of CA1 and CA3 in submerged hippocampal slices from adult or newborn (postnatal days 5-25) Wistar rats. In adult slices, excitatory postsynaptic potentials were depressed by glucose removal ("aglycemia") more rapidly and to a greater extent in CA1 than in CA3 [respective mean times to 50% reduction in peak amplitude were 7.5 +/- 0.83 (standard error) min and 12.5 +/- 0.27 (standard error) min]. Subsequent recovery of excitatory postsynaptic potentials in normoglycemic medium was correspondingly quicker in CA3 than in CA1. Transmission failure at the synapses was indicated by the preservation of the afferent volley, and sharp depression of synaptic input-output plots. In the early postnatal period, CA1 excitatory postsynaptic potentials were much more resistant to aglycemia, substantially persisting for as long as 75 min, with full subsequent recovery in normoglycemic medium. The higher resistance of slices from newborn rats progressively disappeared over the first two postnatal weeks.

Aging↗

PubMed1985

The function of dendritic spines: a theoretical study.

A modeling procedure is proposed which introduces the cable equivalent of dendritic spines into the Rall model of spiny interneurons in the spinal cord. At this point combined morphological and physiological works have given some insight into the possible role of a single spine and the function of a single spine has been studied by theoretical computations [Jack, Noble and Tsien (1975) Electric Current Flow in Excitable Cells, pp. 218-223. Oxford University Press, Oxford; Koch and Poggio (1983) Trends Neurosci. 6, 80-83; Perkel (1983) J. Physiol., Paris 78, 695-699]. The goal of the present paper is two-fold: (a) to stress the gross function of the spine system in the excitability of dendrites; and (b) to emphasize the role of spines in the dynamic input/output function of neurons. The simulation procedure is based on the well-known compartmental method. (1) The kinetics of active somatic and dendritic compartments are taken from a currently available spinal interneuron model to match the physiological data of large dorsal horn neurons carrying spines. (2) Beside the prolongation of the somatic excitatory postsynaptic potential, the model suggests that the spiny neuron increases the differences in the latency and height of excitatory postsynaptic potential as a function of the electrotonic position of input. The characteristics of the excitatory postsynaptic potential can be modified by the changes in spine geometry and the ratio of cytoplasmic resistances of spine stalk to that of main dendritic shaft. (3) Dendritic electroresponsiveness, which was already postulated for dorsal horn neurons, is analysed by the model including calcium and slow potassium systems. It is concluded that the participation of the spine stalk in active processes can highly modify the input dependence of response pattern. Depolarization-dependent Ca2+ accumulation in spines may reflect the interaction of spine stalks. (4) Passive antidromic spread of action potential can be suppressed in spiny cells. Analysis of active antidromic spread shows the probable importance of spines located near the soma. Centripetal vs centrifugal conduction of dendritic action potential may depend on the spine distribution along the tree and change in electrical parameters of spines.

Action Potentials↗

PubMed1989

Histamine H2 receptor mediates postsynaptic excitation and presynaptic inhibition in submucous plexus neurons of the guinea-pig.

Intracellular recordings were made from submucous plexus neurons of the guinea-pig cecum maintained in vitro. Histamine (0.3-10 microM) produced a dose-dependent membrane depolarization (congruent to 13 mV with 3 microM) in about 28% of the cells tested; most of these cells showed a prominent calcium-activated potassium conductance (AH cells). The depolarization was due primarily to an inactivation of potassium conductance which is available at the resting membrane potential of -60 mV. Peak amplitude of the fast excitatory postsynaptic potential was depressed by histamine (0.1-10 microM) in a dose-dependent manner (congruent to 62% depression with 1 microM). This was observed even in those cells in which histamine did not produce any membrane depolarizations (mostly S cells). The depression of the fast excitatory postsynaptic potential resulted from the presynaptic inhibition of acetylcholine release. Histamine also reduced the amplitude of the non-cholinergic, presumably peptidergic, slow excitatory postsynaptic potential by suppressing peptide release from presynaptic nerve terminals. Peak amplitude of the adrenergic inhibitory synaptic potential was not depressed by histamine suggesting that histamine receptors are not present on presynaptic terminals of sympathetic nerve fibres. Both postsynaptic and presynaptic actions of histamine were blocked by cimetidine or ranitidine but not by pyrilamine implying that H2 receptors are involved.

Action Potentials↗

PubMed1987

Antagonists discriminate muscarinic excitation and inhibition in sympathetic ganglion.

The effect of muscarinic antagonists was studied on the muscarinic slow IPSP (inhibitory postsynaptic potential) and slow EPSP (excitatory postsynaptic potential) in bullfrog sympathetic ganglia using the sucrose-gap recording method. Pirenzepine, alcuronium and atropine reduced slow IPSP amplitude more than slow EPSP amplitude. The most selective antagonists studied were pancuronium and gallamine which blocked or substantially reduced the slow IPSP without significantly affecting slow EPSP amplitude. The results suggest that the muscarinic inhibitory response may involve a different muscarinic receptor subtype, and/or receptor-ion-channel complex, than the muscarinic excitatory response.

Alcuronium↗

PubMed1990

The C-terminal glycopeptide of propressophysin potentiates excitatory transmission in the rat lateral septum.

Effects of peptides synthesized from the same precursor as vasopressin, i.e. the C-terminal 39-amino acid long glycopeptide and neurophysin II, were investigated for biological activities in electrophysiological experiments in brain slices of the rat lateral septum. These slices contained the glycopeptide as the predominant form and a fragment of it, amino acid sequence 22-39, as a minor form (8% of the glycopeptide 1-39), as shown by high performance liquid chromatography of extracts and by radioimmunoassay. None of the peptides, neurophysin II, the glycopeptide 1-39 and the fragment 22-39, tested in a concentration of 10(-12) M, had measurable effects on the resting membrane potential of the neurons. The glycopeptide and the fragment 22-39, however, increased, in some cells, for tens of minutes the excitatory postsynaptic potentials evoked in these neurons by stimulation of the fimbria fibers. The increase in input resistance, seen in many septal neurons treated with either of the peptides was not correlated with the excitatory postsynaptic potential increase. Neurophysin II affected neither the excitatory postsynaptic potentials nor the input resistance of the neurons. It is concluded that the glycopeptide 1-39 and the fragment 22-39 possess biological activities amongst which the facilitation of excitatory amino acid transmission on lateral septum neurons. Therefore, these peptides derived from the vasopressin precursor may act in concert with vasopressin to establish facilitation of excitatory transmission in the brain.

Animals↗

PubMed1986

Effects of 4-aminopyridine on the action potential and the after-hyperpolarization of cat spinal motoneurons.

In cats under pentobarbital anaesthesia, intramotoneuronal administrations of 4-aminopyridine significantly prolong the falling phase of the antidromic action potential but have much less effect on the orthodromic action potential. 4-aminopyridine probably blocks the fast K channels involved in the repolarization of the membrane and indirectly activates ionic channels through enhancement of synaptic transmission, also suggested by the potentiation of excitatory postsynaptic potentials. In many cells, 4-aminopyridine depresses the amplitude and prolongs the time course of the after-hyperpolarization; therefore 4-aminopyridine may also partly block Ca2+-activated K+ channels.

4-Aminopyridine↗

PubMedDate not supplied

Perspectives on physiological monitoring: junctional-type potentials in the food ventricle.

1. Many toads monitored throughout survival with no support other than protection against drying, pass terminally through a remarkable evolution which is described here in the full details of a single experiment lasting some 40 hours. 2. The essential features of this particular sequence is block of the Luciani-Wenckebach type affecting SA, AV, and intraventricular conduction. SA block was apparently the major cause of periods of arrest and of cycles of heart beats. Periodically PR delay based on progressive AV block was observed but it was not an outstanding feature. 3. Progressive, rate-determined intraventricular block during the cycles of ventricular beats was the first new feature of these observations. 4. As intraventricular block progressed, an initial ventricular deflection separated itself from the rest of QRS. 5. This initial deflection diminished in amplitude throughout each cycle of ventricular beats, its rate of rise diminished, and the interval separating it from the rest of the ventricular complex increased until the whole initial deflection was revealed. 6. Thereafter, with a small decrease in amplitude of the initial deflection, the remainder of the ventricular electrogram failed to follow and the complex stood alone. 7. Its polarity indicated its origin at the base of the ventricle, the interval separating it from the origin of P indicated that it was downstream from the AV conduction mechanism. 8. This deflection, now a local ventricular potential (LVP) then progressively declined in amplitude and disappeared. 9. The possibility has been discussed that the potential represents (a) a true action potential localized by block or (b) a local, nonpropagated potential akin to junctional potentials like: (1) end-plate potentials, (2) generator potentials, (3) excitatory postsynaptic potentials (EPSPs), or (c) a pacemaker potential. The experiments that have revealed the phenomenon have not provided other than suggestive but inconclusive information about its nature. 10. The observations are new or certainly not well known and further study should shed light on the problem of intracardial impulse formation and conduction.

Animals↗

PubMed1986

Amino acid receptor-mediated transmission at primary afferent synapses in rat spinal cord.

Intracellular recording techniques have been used to provide information on the identity of excitatory transmitters released at synapses formed between dorsal root ganglion (DRG) and spinal cord neurones in two in vitro preparations. Explants of embryonic rat DRG were added to dissociated cultures of embryonic dorsal horn neurones and synaptic potentials recorded intracellularly from dorsal horn neurones after DRG explant stimulation. More than 80% of dorsal horn neurones received at least one fast, DRG-evoked, monosynaptic input. In the presence of high divalent cation concentrations (5 mmol l-1 Ca2+, 3 mmol l-1 Mg2+) the acidic amino acid receptor agonists, L-glutamate, kainate (KA) and quisqualate (QUIS) excited all dorsal horn neurones which received a monosynaptic DRG neurone input, whereas L-aspartate and N-methyl-D-aspartate (NMDA) had little or no action. 2-Amino-5-phosphonovalerate (APV), a selective NMDA receptor antagonist, was relatively ineffective at antagonizing DRG-evoked synaptic potentials and L-glutamate-evoked responses. In contrast, kynurenate was found to be a potent antagonist of amino acid-evoked responses and of synaptic transmission at all DRG-dorsal horn synapses examined. The blockade of synaptic transmission by kynurenate appeared to result from a postsynaptic action on dorsal horn neurones. Intracellular recordings from motoneurones in new-born rat spinal cord were used to study the sensitivity of the Ia excitatory postsynaptic potential (EPSP) to antagonists of excitatory amino acids. Superfusion of the spinal cord with APV did not inhibit the Ia EPSP but did suppress later, polysynaptic components of the afferent-evoked response. Kynurenate was a potent and selective inhibitor of the Ia EPSP, acting via a postsynaptic mechanism. These findings indicate that L-glutamate, or a glutamate-like compound, but not L-aspartate, is likely to be the predominant excitatory transmitter that mediates fast excitatory postsynaptic potentials at primary afferent synapses with both dorsal horn neurones and motoneurones.

Afferent Pathways↗

PubMed1975

Molecular model of postsynaptic potential.

A molecular model of the excitatory postsynaptic membrane is given in terms of two biochemical cycles intimately associated: an acetylcholine cycle and a calcium cycle. The acetylcholine controls the Na ionophores while calcium ions control the tk ionophore. The two ionophores are spatially separated but interact in such a way that the variation in K conductance precedes that in Na conductance. Digital simulation shows that our model accounts quantitatively for both the evolution of excitatory postsynaptic potential and current in a variety of experimental conditions.

Acetylcholine↗

PubMed1986

Associative induction of posttetanic and long-term potentiation in CA1 neurons of rat hippocampus.

Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.

Action Potentials↗

PubMed1992

Alterations in the properties of hippocampal pyramidal neurons in the aged rat.

The electrophysiological and pharmacological properties of CA1 hippocampal pyramidal neurons were studied in slices from young (three to four months) and aged (25-32 months) Sprague-Dawley rats having previously performed two behavioral tasks. About 20% of the aged rats were impaired in either the spontaneous alternation task or the water maze task. Electrophysiological parameters were measured and compared in young and aged animals using intracellular recordings. No age-related differences were observed in membrane potential, input resistance, amplitude of action potentials or amplitude of calcium spikes. The amplitude and duration of individual afterhyperpolarizations following a single spike were unchanged. In contrast, the neuronal excitability was significantly decreased and the spike duration significantly enhanced in aged rats as compared to young rats. The comparison of afterhyperpolarizations (which follow a burst of spikes) between young and aged rats was more complex. An increase in the amplitude and duration of afterhyperpolarizations generally occurred in aged animals. However, this increase was not consistent among animals and was dependent on the holding potential of the neuron and on the number of action potentials used to trigger the afterhyperpolarization. The depolarizing effect of bath-applied carbachol, as well as the associated increase in membrane resistance were reduced in neurons from aged rats. In contrast, the effects of carbachol on the depression of synaptic events and the blockade of the afterhyperpolarizations were similar in young and aged animals. In addition, the amplitude of the slow cholinergic excitatory postsynaptic potential induced by stimulation of cholinergic afferents in the presence of physostigmine was also decreased in aged rats. Excitatory postsynaptic potentials and inhibitory postsynaptic potentials following electrical stimulation of stratum radiatum were compared. The amplitude and duration of excitatory postsynaptic potentials were increased in aged rats. The amplitude and duration of the fast inhibitory postsynaptic potential were not significantly affected in aged animals. In contrast, the duration of the slow inhibitory postsynaptic potential was decreased in aged rats. Since the mean baclofen-induced hyperpolarization was only slightly reduced in aged rats, the most likely explanation is a decrease in the release of GABA rather than an alteration in the postsynaptic response mediated by GABAB receptors. A statistically significant correlation was found between the degree of impairment in the spontaneous alternation task and the amplitude of the carbachol-induced depolarization.

Acetylcholine↗

PubMed1991

Neuropharmacology of the muscarinic antagonist telenzepine in myenteric ganglia of the guinea-pig small intestine.

Intracellular recording methods were used to investigate the actions of the putative M1 muscarinic receptor antagonist telenzepine on the electrical and synaptic behavior of myenteric neurons. Telenzepine had no effect on resting membrane potential, input resistance, excitability and antidromic potentials in both AH/type 2 and S/type 1 neurons, when applied in concentrations of 0.1-2000 nM, although higher concentrations (10-100 microM) did have a significant non-specific effect on the postsynaptic membrane. Micromolar concentrations of telenpzepine (1-2 microM) had no effect on excitatory responses to substance P, vasoactive intestinal peptide, the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium or the nicotinic action of acetylcholine. Nicotinic fast excitatory postsynaptic potentials were also unaffected by 2 microM telenzepine. In contrast, at submicromolar concentrations (100 nM), telenzepine abolished responses to either muscarine or the muscarinic component of the acetylcholine response. The excitatory effect of muscarine at postsynaptic M1 receptors was dose dependently inhibited by telenzepine (0.1-1000 nM) at concentrations which had no effect on the electrical properties of the cells. This effect was slowly reversible, usually requiring more than 60 min for significant recovery. The threshold dose of telenzepine as an antagonist of the muscarinic depolarization in AH/type 2 neurons was in the range of 0.1-1 nM. The IC50 concentration of telenzepine needed to abolish the response was 8.5 nM. A small proportion of stimulus-evoked slow excitatory postsynaptic potentials in both AH/type 2 and S/type 1 cells were abolished by 1 microM telenzepine, while the majority of them remained unaffected, indicating that some slow excitatory postsynaptic potentials are mediated by the muscarinic action of released acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗

PubMed1991

Persistent enhancement of transmitter release accompanying long-term potentiation in the guinea pig hippocampus.

In order to examine temporal changes in enhancement of transmitter release during long-term potentiation (LTP), we examined amplitude fluctuation of excitatory postsynaptic potentials (EPSPs) for longer periods than 2 h after tetanic stimulation (up to 4 h in the longest observation). The relative magnitude of excitatory postsynaptic potentiation (EPSP) fluctuation (coefficient of variation, CV) reduced throughout the observation periods in association with an increase in EPSP amplitude after tetanic stimulation. The reciprocals of squared CVs (= mean2/variance) were almost in proportion to the magnitude of LTP, and the ratio of 1/CV2 and the LTP magnitude did not change significantly for up to 4 h. These findings suggest that a prolonged enhancement of transmitter release from presynaptic terminals underlies LTP, and the relative contribution of this presynaptic enhancement does not change significantly for 2 h (maybe up to 4 h, or longer) after tetanic stimulation.

Animals↗

PubMed1987

Postsynaptic membrane shifts during frequency potentiation of the hippocampal EPSP.

1. In some classes of central neurons, repetitive synaptic stimulation induces substantial changes in the postsynaptic membrane, in conjunction with robust frequency potentiation of the excitatory postsynaptic potential (EPSP). However, the nature and time course of these postsynaptic membrane shifts, or their possible contributions to EPSP frequency potentiation (e.g., by altering driving force or current pathways), have not been examined extensively. We therefore studied the simultaneous patterns of change in composite EPSP amplitude, postsynaptic input resistance (Rin), and postsynaptic membrane potential during a 4-min train of 10-Hz monosynaptic stimulation in CA1 neurons of hippocampal slices. Slices were maintained in media containing either control (4 mM) or high (6.5 mM) concentrations of K+. 2. Potentiation of the EPSP, hyperpolarization of the membrane, and a decline of Rin, all developed rapidly during 10-Hz synaptic stimulation; these responses reached maximal levels by 5-15 s of the stimulation train. In most cells, a membrane depolarization phase occurred between 15 and 45 s of stimulation, followed by rehyperpolarization by 1 min of stimulation. During the depolarization phase, both EPSP potentiation and the decline in Rin remained near maximal. No significant differences were seen as a function of K+ concentrations. 3. These results show that hyperpolarization is not invariably associated temporally with EPSP frequency potentiation. Moreover, if driving force and membrane conductance changes are assumed to be approximately similar in large dendrites and soma, then the increase in driving force due to membrane hyperpolarization was not sufficient to account for the three- and fourfold increases in EPSP amplitude seen during frequency potentiation. Further, based on similar assumptions and on dendritic models of EPSP attenuation, the decline in Rin should reduce EPSP amplitude at the dendritic synaptic site and, to a proportionately greater extent, at the soma. 4. Studies in which the membrane was hyperpolarized with injected current to approximately the IPSP reversal potential, or in which bicuculline methiodide was applied to the slices, indicated that depression of the IPSP by repetitive stimulation did not account for frequency potentiation of EPSP amplitude. 5. These data are therefore consistent with the conclusion that the frequency potentiation of composite EPSPs in central neurons depends on presynaptic mechanisms, rather than on generalized postsynaptic changes. However, our findings do not rule out localized postsynaptic changes in receptors or spines as possible contributing factors.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗