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PubMed1996

Muscarine receptor activation in the substantia gelatinosa of the spinal trigeminal nucleus of the guinea pig.

1. Intracellular recordings were made from slices of guinea pig spinal trigeminal nucleus pars caudalis (SG). 2. Muscarine [0.3-30 microM; half maximally effective concentration (EC50) = 2.9 microM] hyperpolarized 61% of SG neurons. The effect was mimicked by carbachol (0.3-30 microM; EC50 = 3.9 microM) and antagonized by pirenzepine (1 microM). Thirty-four percent of the neurons were depolarized by muscarine and carbachol (1-30 microM: EC50 = 5.7 microM), and the effect was antagonized by pirenzepine (100 nM). 3. In approximately 80% of recordings, muscarine (10-30 microM) evoked repetitive spontaneous inhibitory postsynaptic potentials (IPSPs) that were sensitive to bicuculline (10 microM). 4. Muscarine (1-30 microM; EC50 = 3 microM) decreased the amplitude of the majority of evoked excitatory postsynaptic potentials (EPSPs), and the effect was mimicked by carbachol and antagonized by pirenzepine (100 nM). 5. These results indicate that there are at least three mechanisms by which muscarine inhibits SG neurons: 1) hyperpolarization through activation of non-M1 receptors; 2) activation of gamma-amino-butyric acid-containing interneurons that mediate IPSPs in a subset of neurons; and 3) a decrease in evoked EPSP amplitude. Muscarine can also activate SG neurons via interaction with an M1-type receptor.

Animals↗

PubMed1992

Pharmacological characterization of excitatory synaptic potentials in rat basolateral amygdaloid neurons.

The pharmacological properties of synaptic responses in rat basolateral amygdaloid (BLA) neurons were studied using intracellular recording techniques. Three distinct types of synaptic potential were evoked by stimulation of the adjacent ventral endopyriform nucleus: 1) a fast excitatory postsynaptic potential (f-EPSP); 2) a late EPSP (1-EPSP) following the f-EPSP; and 3) a multiphasic hyperpolarization following the initial depolarizing potential. Superfusion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a selective non-N-methyl-D-aspartate (non-NMDA) receptor antagonist, blocked the f-EPSP in a concentration-dependent manner. The ED50 for this effect was around 4 microM. In the presence of CNQX, however, a small depolarizing potential remained. This residual depolarizing component was markedly enhanced on removing Mg++ from the perfusing medium and could subsequently be abolished by DL-2-amino-5-phosphonovaleate (DL-APV, 50 microM) indicating its mediation via NMDA receptor-coupled ionophore. The l-EPSP was reversibly blocked by DL-APV. These results suggest that the pyriform cortex-amygdala pathway is mediated through excitatory amino acids acting on non-NMDA as well as NMDA receptors located on the BLA neurons.

2-Amino-5-phosphonovalerate↗

PubMed1988

Synaptic activation of N-methyl-D-aspartate receptors in the Schaffer collateral-commissural pathway of rat hippocampus.

1. The involvement of N-methyl-D-aspartate (NMDA) receptors in the response to single-shock (0.033 Hz) stimulation of the Schaffer collateral-commissural pathway in hippocampal slices has been investigated using current- and voltage-clamp techniques. 2. In the presence of Mg2+ (1 or 2 mM) at membrane potentials near rest, the selective NMDA antagonist D-2-amino-5-phosphonovalerate (APV) had no effect on the excitatory postsynaptic potential (EPSP) and the biphasic inhibitory postsynaptic potential (IPSP) evoked by Schaffer collateral-commissural stimulation. The recurrent IPSP evoked by antidromic stimulation of alvear fibres was also unaffected by APV. 3. The introduction of a Mg2+-free perfusate led, at high stimulus intensity, to an orthodromically evoked epileptiform discharge but little change in the recurrent IPSP. APV suppressed a large proportion of the enhanced response in Mg2+-free perfusate. 4. EPSPs and excitatory postsynaptic currents (EPSCs) evoked in Mg2+-free perfusate invariably had both APV-resistant and APV-sensitive components. Both synaptic components had similar thresholds and latencies to onset. The APV-sensitive component had a long time to peak and long duration. 5. Under current-clamp conditions in Mg2+-containing medium, an APV-sensitive component was recorded at membrane potentials of between -30 and -10 mV, but not at potentials more negative than -55 mV. 6. Under voltage-clamp, but not current-clamp, conditions in Mg2+-containing medium, a small APV-sensitive component was recorded at resting membrane potentials and increased with membrane depolarization. The difference between the current- and voltage-clamp data is attributed to the hyperpolarizing influence of conjointly activated IPSPs. 7. In the presence of Mg2+ and picrotoxin, a dual-component EPSC was recorded between -30 and +30 mV in all cells examined. The APV-resistant and APV-sensitive components had similar latencies to onset. They both had reversal potentials of between -8 and 0 mV. The APV-sensitive component had a longer latency to peak and duration than the APV-resistant component. 8. It is suggested that NMDA receptors can contribute a low-threshold and long-duration monosynaptic component of the response evoked by low-frequency stimulation of the Schaffer collateral-commissural pathway. However, under physiological conditions significant expression of this component is prevented by concurrently activated IPSPs which rapidly hyperpolarize neurones into a region where Mg2+ substantially blocks NMDA channels.

2-Amino-5-phosphonovalerate↗

PubMed1993

Pairing of pre- and postsynaptic activities in hippocampal CA1 neurons induces long-term modifications of NMDA receptor-mediated synaptic potential.

An in vitro slice preparation of rat hippocampus was used to study the long-term modifications of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSPNMDA). Intracellular recordings were made from CA1 pyramidal cells in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and picrotoxin (50 microM) which block non-NMDA and GABAA receptors, respectively. Pairing of low-frequency EPSPNMDA with postsynaptic depolarization induced a long-term depression (LTD) of EPSPNMDA. The maximal reduction of EPSPNMDA amplitude amounted to 81.3% of the control 1 min after the pairing. When low-frequency synaptic stimulation was paired with strong postsynaptic depolarization, a long-term potentiation (LTP) of EPSPNMDA could be induced. These results suggest that the induction of long-term modifications of EPSPNMDA has at least a postsynaptic component.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1990

A reevaluation of excitatory amino acid-mediated synaptic transmission in rat dentate gyrus.

1. Intracellular recordings were made from granule cells in combined slices of the hippocampus and parahippocampal cortex from adult Wistar rats. The neurons had a mean resting membrane potential (EM) of -85.1 +/- 0.7 (SE) mV, input resistance (Rin) of 30.9 +/- 1.5 M omega and action potential (AP) amplitude of 79.9 +/- 1.06 mV measured from the threshold potential. The threshold for AP generation was approximately 40 mV positive to EM. 2. The passive current-voltage relationship showed anomalous rectification, with Rin increasing by 34% on average at modest depolarizations. With large excursions of the EM (by +/- 30 mV or more), there was a marked fall in Rin. 3. With extracellular recording, a monophasic, positive-going field potential of 5-15 mV was evoked by stimulation of the perforant path (PP). Intracellularly, an excitatory postsynaptic potential (EPSP) of up to 40 mV in size was recorded. It was unusual to evoke an AP on orthodromic stimulation. Perfusion with picrotoxin (PTX, up to 20 microM) had small and variable effects on the EPSP, which implies that GABAergic inhibition does not play a major role. 4. Tonic depolarization reduced the EPSP. Hyperpolarization either had no effect or again decreased the EPSP. 5. The role of excitatory amino acid (EAA) receptor subtypes in mediation of the EPSP was investigated. Perfusion with the non-N-methyl-D-aspartate (NMDA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) caused a dose-dependent reduction of the EPSP with a shift to the right of the input-output relationship. The ED50 for this effect was approximately 2 microM. 6. In the presence of 5-10 microM CNQX a small component of the EPSP usually remained, which could be blocked by the NMDA receptor antagonist +/- 2-amino-5-phosphonovaleric acid (APV, 20-50 microM). This depolarizing component was markedly enhanced during perfusion with Mg2(+)-free medium. It increased in size and duration when the membrane was depolarized and decreased with hyperpolarization. These properties are consistent with the mediation of this potential via NMDA receptors. 7. These results indicate that NMDA receptors contribute to transmission at the synapse between the PP and the granule cell. This was confirmed by demonstrating that APV caused a small reduction in the size of the untreated EPSP and a shortening of the recovery phase.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1987

Electroconvulsive treatment reduces long-term potentiation in rat hippocampus.

The effect of repeated electroconvulsive treatment (ECT) was investigated on long-term potentiation (LTP) in the rat hippocampal slice. Extracellular, recordings of population spikes and excitatory postsynaptic potentials (EPSP) were made from the pyramidal cell layer of CA1 in response to stimulation of the stratum radiatum. LTP was induced by 5 high-frequency trains of stimuli. ECT (10 treatments, 1 treatment every day for 20 days) markedly inhibited LTP of the population spike and EPSP. Thus LTP of the 25% maximum population spike was 104% in control, and 20% in rats 24 h after ECT. LTP of the EPSP was 35% in control and 12% after ECT.

Animals↗

PubMed1995

Long-term potentiation in vivo in the intact mouse hippocampus.

We describe the characteristics of long-term potentiation (LTP) in the intact mouse. Perforant path stimulation evokes both a population excitatory postsynaptic potential (pop-EPSP) and a population spike potential (pop-spike) from the hippocampal dentate gyrus in urethane anesthetized animals. LTP, as measured by increased pop-spike amplitude and pop-EPSP slope, was successfully induced and reliably maintained at a stable level for at least 12 h, the longest time tested. The LTP-inducing stimulus (3 trains of 400 Hz, 8 0.4 ms pulses/train) used in two strains of mice was less by half than that used in rat. These parameters for inducing LTP were also successfully applied to obtain LTP in two different transgenic mouse strains: one bearing a F1/Gap-43 promoter-lacZ fusion gene and another which overexpresses the S100 beta gene. We also examined the effects of protein synthesis inhibitors, cycloheximide (CXM) and anisomycin (ANI). When CXM or ANI was given 30 min before LTP induction, there was no persistent loss of LTP at the 4 h time point. However, if CXM was given 4 h before LTP induction, significant decay of the potentiated responses occurred 90 min after induction. Half of the animals receiving CXM but not ANI showed a complete and sudden elimination of the entire response after the LTP-inducing stimulus. It was speculated that loss of a constitutively-expressed housekeeping protein, for example a calcium buffering protein, with an estimated half-life of 2 h would lead to an inability to buffer LTP-induced alterations, such as intracellular calcium elevation, increasing intracellular calcium to toxic levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

4-Aminopyridine-mediated increase in long-term potentiation in CA1 of the rat hippocampus.

The effect of 4-aminopyridine (4-AP) on long-term potentiation (LTP) was studied in the hippocampal slice preparation of the rat. Field excitatory postsynaptic potentials (EPSPs) were recorded and evoked in the stratum radiatum of the CA1. Both the low frequency EPSP and LTP of the EPSP were significantly increased by treatment with 4-AP. These effects were inhibited by increasing the magnesium concentration from 1 to 4 mM. Pretreatment with 20 microM DL-2-amino-5-phosphonovalerate antagonized only the increase in LTP produced by 4-AP. It is suggested that 4-AP enhances Ca influx either pre- or postsynaptically and thereby increases LTP.

4-Aminopyridine↗

PubMed1987

Temporal requirements of associative short-term potentiation in CA1 neurons of rat hippocampus.

Temporal separation and juxtaposition of stimulations for the induction of associative short-term potentiation in the rat hippocampus were examined. A series of stimulations of stratum radiatum during brief tetanic stimulations of stratum oriens resulted in a short-term potentiation (of about 3 min duration) of stratum radiatum-induced CA1 population excitatory postsynaptic potential. Potentiation was evident when the stratum radiatum stimulus preceded the onset of the conditioning tetanus by no more than 50 ms, or followed by no more than 80 ms. These parameters closely resemble those found for associative long-term potentiation, suggesting the possibility of shared mechanisms for the induction of these two forms of potentiation.

Animals↗

PubMed1993

Cyclic AMP and long-term potentiation in the CA1 region of rat hippocampus.

Bath application of dibutyryl cyclic AMP, 8-bromo cyclic AMP or forskolin to hippocampal slices caused a short-lasting decrease, followed after washout by a long-lasting increase in the amplitude of population spikes recorded in area CA1 in response to 0.05 Hz stimulation of the Schaffer collateral/commissural pathway. Population spike depression lasted only as long as the cyclic AMP analogues were present in the bath, while the potentiation lasted for at least 2 h after they were washed out. Population excitatory postsynaptic potential amplitude was depressed while dibutyryl cyclic AMP was present in the bath, but after washout it was not significantly different from baseline amplitude. The population spike depression caused by dibutyryl cyclic AMP was prevented by the adenosine antagonist 8-p-sulfophenyltheophylline, but the long-lasting potentiation was not. Thus the transient depression induced by dibutyryl cyclic AMP was probably caused by an action of the drug or its breakdown products as adenosine agonists. The long-lasting potentiation is caused by a different mechanism. Occlusion experiments were performed to examine the relationship of the long-lasting population spike potentiation caused by dibutyryl cyclic AMP to the population spike long-term potentiation caused by high-frequency stimulation. High-frequency stimulation delivered after the population spike potentiation caused by dibutyryl cyclic AMP was established did cause a further potentiation, but only up to the level caused by high-frequency stimulation alone. Dibutyryl cyclic AMP administered after high frequency stimulation-induced long-term potentiation was established had no further potentiating effect.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1997

The contrasting effects of dendrotoxins and other potassium channel blockers in the CA1 and dentate gyrus regions of rat hippocampal slices.

1. The effects of potassium channel blocking compounds on synaptic transmission in the CA1 and dentate gyrus regions of the rat hippocampus were examined by means of simultaneous field potential recording techniques in brain slices. 2. 4-Aminopyridine (4-AP) enhanced the excitatory postsynaptic potential (e.p.s.p.) and induced multiple population spike responses in both regions. EC50 values were 6.7 microM in the CAI (n = 5) and 161.7 microM (n = 5) in the dentate gyrus. 3. Tetraethylammonium (TEA) increased the amplitude and induced broadening of the population spike in both regions. In the dentate gyrus (n = 5) a single slow spike response was introduced (EC50 12.8 mM) and in the CA1 region (n = 5) the response was transformed into two wide spikes (EC50 2.6 mM). 4. In the CA1 region all of the dendrotoxins (toxin I, toxin K, alpha-Dtx and delta-Dtx) induced multiple population spikes and enlarged e.p.s.p. responses. Potentials recorded simultaneously in the dentate gyrus exhibited comparatively minor enhancements. The EC50 value for toxin 1 in the CA1 was calculated to be 237 nM (n = 4). Estimated EC50 values were obtained for alpha-Dtx (1.1 microM, n = 3), toxin K (411 nM, n = 4) and delta-Dtx (176 nM, n = 3). 5. In the presence of toxin 1, DL-2-amino-5-phosphonovaleric acid (APV) induced slight reduction of the late e.p.s.p. phase (n = 3). 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) abolished all population spikes leaving a late slow positive waveform (n = 3). Co-application of APV and CNQX abolished all postsynaptic responses. 6. Charybdotoxin (CbTx) was significantly less potent than the dendrotoxins and had mixed actions in the CA1 region (n = 3). Again the dentate gyrus exhibited reduced sensitivity (n = 3). 7. In the presence of mast cell degranulating peptide (MCDP), enhancement of the CA1 field potential response (n = 5) was greater than that observed in the dentate gyrus (n = 5). 8. The results show that some potassium channel modulators can profoundly enhance CA1 region synaptic responses in the absence of notable changes in dentate gyrus excitability. Selective enhancement of defined synaptic pathways by potassium channel modulators may prove to have considerable therapeutic potential.

4-Aminopyridine↗

PubMed1994

Persistent increase of hippocampal presynaptic axon excitability after repetitive electrical stimulation: dependence on N-methyl-D-aspartate receptor activity, nitric-oxide synthase, and temperature.

The electrical excitability of Schaffer collateral axons and/or terminals was studied in hippocampal slices by monitoring single, CA3 pyramidal neurons activated antidromically from CA1 stratum radiatum. At 22 degrees C, weak, repetitive stimulation with as few as 10 impulses at 2 Hz led to a robust lowering of the antidromic activation threshold that lasted > 30 min. The effect was completely absent at 32 degrees C and was blocked by both the N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovalerate and the inhibitor of nitric-oxide synthase, L-nitro-arginine methyl ester. Such threshold lowering would alter the variance of synaptic responses from axons stimulated in the variable excitation region of their input-output functions. These results thus raise important doubts about the interpretation of experiments in which the so-called minimal-stimulation method has been used at reduced temperature to infer changes in quantal transmission during hippocampal long-term potentiation. In the present experiments, no changes were observed in the estimate of excitatory postsynaptic potential quantal content in long-term potentiation experiments at either temperature, which could not be accounted for by an artificial, temperature-dependent change in the responsiveness of presynaptic axons.

Amino Acid Oxidoreductases↗

PubMed1985

Frequency-dependent block of field potentials in the rat hippocampal slice caused by tricyclic antidepressants.

The effect of the tricyclic antidepressants imipramine and desipramine were studied on field potentials in the rat hippocampal slice. The electrically evoked stratum radiatum nerve volley, excitatory postsynaptic potential (e.p.s.p.) and pyramidal cell layer population spike (PS) were recorded in the CA1 region. At concentrations of 10(-6)M to 10(-5)M, impramine did not affect the amplitude of the nerve volley, e.p.s.p. or PS at low frequencies of stimulation (0.01 Hz). At higher frequencies of stimulation (1-100 Hz), imipramine caused a frequency-dependent block of the nerve volley, e.p.s.p. and PS. The time course of onset of the frequency-dependent block in the presence of imipramine was very slow. Maximum inhibition was reached after 3-4 h treatment with imipramine. Desipramine (10(-6)-10(-5)M) also caused a frequency-dependent block of the hippocampal field potentials. Only slight frequency-dependent block was observed in slices from rats injected in vivo with desipramine (10 mg kg-1) for 14 days.

Action Potentials↗

PubMed2004

Intracortical pathways determine breadth of subthreshold frequency receptive fields in primary auditory cortex.

To examine the basis of frequency receptive fields in auditory cortex (ACx), we have recorded intracellular (whole cell) and extracellular (local field potential, LFP) responses to tones in anesthetized rats. Frequency receptive fields derived from excitatory postsynaptic potentials (EPSPs) and LFPs from the same location resembled each other in terms of characteristic frequency (CF) and breadth of tuning, suggesting that LFPs reflect local synaptic (including subthreshold) activity. Subthreshold EPSP and LFP receptive fields were remarkably broad, often spanning five octaves (the maximum tested) at moderate intensities (40-50 dB above threshold). To identify receptive-field features that are generated intracortically, we microinjected the GABA(A) receptor agonist muscimol (0.2-5.1 mM, 1-5 microl) into ACx. Muscimol dramatically reduced LFP amplitude and reduced receptive-field bandwidth, implicating intracortical contributions to these features but had lesser effects on CF response threshold or onset latency, suggesting minimal loss of thalamocortical input. Reversal of muscimol's inhibition preferentially at the recording site by diffusion from the recording pipette of the GABA(A) receptor antagonist picrotoxin (0.01-100 microM) disinhibited responses to CF stimuli more than responses to spectrally distant, non-CF stimuli. We propose that thalamocortical and intracortical pathways preferentially contribute to responses evoked by CF and non-CF stimuli, respectively, and that intracortical projections linking frequency representations determine the breadth of receptive fields in primary ACx. Broad, subthreshold receptive fields may distinguish ACx from subcortical auditory relay nuclei, promote integrated responses to spectrotemporally complex stimuli, and provide a substrate for plasticity of cortical receptive fields and maps.

Acoustic Stimulation↗

PubMed1982

Reversibility of Ia EPSP investigated with intracellularly iontophoresed QX-222.

1. Cat lumbosacral motoneurons were impaled by two individually advanced microelectrodes: one to record membrane potential (EM), the second to pass depolarizing currents. 2. During the passage of depolarizing current ramps the repetitive action-potential firing and the later high conductance (GM) state obscured and distorted Ia excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of hindlimb muscle afferents. 3. Intracellular iontophoresis of QX-222 (a trimethyl analogue of lignocaine) or methylxylocholine, prevented action-potential generation and reduced the GM increase during current depolarization so that positive levels of EM could be reached. 4. Following QX-222 treatment it was possible to demonstrate a reversal of the Ia EPSP including its first part, at EM values between -13 and +32 mV. Reversal was seen in 13 of the 22 motoneurons tested. 5. Reversal was easiest to obtain in motoneurons of the deep peroneal group. More positive levels of EM were needed to show a reversal in neurons of the gastrocnemius-so-leus group. (The 10-90% rise times of the EPSPs were rather similar for both groups.) 6. In a few motoneurons the initial part of the Ia EPSP reversed at a more negative EM than a later part. This was best seen after subtraction of the extracellular field potentials from the records.

Animals↗

PubMed1989

Monosynaptic excitatory amino acid transmission from the posterior rhombencephalic reticular nucleus to spinal neurons involved in the control of locomotion in lamprey.

1. The reticulospinal neurons in the lamprey posterior rhombencephalic reticular nucleus (PRRN) and their projections to different types of spinal neurons have been investigated by the use of simultaneous paired intracellular recordings from one pre- and one postsynaptic cell. PRRN is of particular importance for the initiation of locomotion. 2. Intracellular stimulation of single PRRN neurons produced monosynaptic excitatory postsynaptic potentials (EPSPs) in simultaneously recorded motoneurons and spinal premotor interneurons of both the excitatory and inhibitory type. Individual PRRN neurons produced EPSPs in several different types of target cells, as revealed by signal averaging. Each single PRRN neuron had extensive monosynaptic connections to approximately 73% of the motoneuronal population. Conversely, several PRRN neurons converge on individual spinal neurons. The average amplitude of the EPSPs was 0.43 +/- 0.40 (SD) mV. The EPSPs varied in time course (time to peak = 7.5 +/- 2.8 ms; duration at one-half peak amplitude = 21.9 +/- 18.1 ms). 3. The EPSPs produced by reticulospinal cells were composed of either exclusively chemical, exclusively electrical, or mixed chemical and electrical components. The electrical EPSPs remained when the ordinary physiological solution was substituted for one without Ca2+ but with Mn2+. The chemical component of the EPSPs was always depressed when a broad-spectrum excitatory amino acid (EAA) antagonist, such as kynurenic acid, was applied, suggesting that the chemical component was because of EAA transmission. The chemical EPSP could have two components, one late, suppressed by N-methyl-D-aspartate (NMDA) antagonists, and one early because of activation of kainate/quisqualate receptors. 4. Three-dimensional reconstructions of Lucifer yellow-filled PRRN neurons were performed with a confocal laser scanning microscope. PRRN neurons producing monosynaptic excitatory amino acid EPSPs were found to have a fusiform cell body located near the surface of the fourth ventricle and an extensive fanlike dendritic tree extending to the ventral and lateral margin of the brain stem within the basal plate. The axons descend in the lateral funiculi of the spinal cord. 5. PRRN neurons utilizing EAA transmission are active during fictive locomotion. They presumably initiate and reinforce ongoing spinal locomotor activity by monosynaptically increasing the general excitability of the spinal premotor interneurons of the spinal locomotor networks by means of their extensive divergent and convergent monosynaptic connections.

Amino Acids↗

PubMed1990

Mormyromast electroreceptor organs and their afferent fibers in mormyrid fish. II. Intra-axonal recordings show initial stages of central processing.

1. Physiologically and morphologically identified primary afferent fibers from mormyromast electroreceptor organs were recorded intracellularly. The fiber recordings were made from the nerve root of the posterior lateral line nerve, where the fibers enter the brain, and from the electrosensory lateral line lobe (ELL), near the central terminals of the fibers. 2. The intracellular recordings reveal a variety of potentials, synaptic and nonsynaptic, in addition to the large orthodromic action potentials from the periphery. The goal of the present study was to describe and interpret these various potentials in mormyromast afferent fibers as a first step in understanding the processing of electrosensory information in ELL. 3. Three types of synaptic potentials were recorded inside mormyromast afferent fibers: 1) electric organ corollary discharge (EOCD) excitatory postsynaptic potentials (EPSPs), driven by the motor command that elicits the electric organ discharge (EOD); 2) EPSPs evoked by electrosensory stimulation of electroreceptors in the skin near the electroreceptor from which the recorded fiber originates or by direct stimulation of an electrosensory nerve; and 3) inhibitory postsynaptic potentials (IPSPs) evoked by electrosensory stimulation of more distant electroreceptors. These synaptic potentials can be attributed to synaptic input to postsynaptic cells in ELL that is observed inside the afferent fibers because of electrical synapses between the fibers and the postsynaptic cells. 4. The peripherally evoked EPSPs could frequently be shown to be unitary. The unitary EPSPs were identical to the orthodromic spikes in originating from a single electroreceptor, in threshold, and in latency shift with increasing stimulus intensity. These similarities suggest that the unitary EPSPs are electrotonic EPSPs caused by impulses in other mormyromast afferent fibers that terminate on some of the same postsynaptic cells as the recorded fiber. The peripherally evoked IPSPs had a longer latency than the EPSPs or orthodromic spikes, requiring the presence of an inhibitory interneuron. 5. The peripherally evoked EPSPs, both unitary and nonunitary, show absolute refractory periods of 3-8 ms, followed by relative refractory periods of approximately 8 ms, when tested with two identical stimuli to a nerve. These refractory periods are interpreted as because of refractoriness in the fine preterminal branches of the axonal arbor. 6. A depolarizing afterpotential is commonly associated with the orthodromic spike and probably results from the successful propagation of the spike into the entire terminal arbor. The depolarizing afterpotential has a refractory period that is similar to that of the peripherally evoked EPSPs and that is also interpreted as refractoriness in the fine preterminal branches.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Mechanisms underlying induction of long-term potentiation in rat medial and lateral perforant paths in vitro.

1. The mechanisms underlying the induction of long-term potentiation (LTP) in the medial and lateral perforant paths were studied by recording excitatory postsynaptic potentials (EPSPs) from rat dentate granule cells in vitro using extracellular and whole-cell recording techniques. 2. Paired stimuli (interstimulus interval, 50-1,000 ms) resulted in facilitation of the lateral and depression of the medial perforant path-evoked EPSPs, respectively. This physiological difference was used to isolate responses evoked by stimulation of a single path. 3. Tetanic stimulation induced LTP in both pathways, although the magnitude of LTP in the lateral perforant path was significantly less than that in the medial perforant path. Both forms of LTP were blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 4. Buffering intracellular calcium by loading granule cells with the calcium chelator bis (O-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid prevented LTP in both pathways. 5. Pairing of low-frequency (0.25 Hz) afferent stimulation with postsynaptic depolarization induced LTP in the medial but not the lateral perforant path. However, pairing of higher-frequency stimulation (1-4 Hz) with postsynaptic depolarization did potentiate the lateral perforant path-evoked EPSP in some cells. 6. Both the medial and lateral perforant path-evoked EPSPs had two components; a fast component blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and a slower, voltage-dependent component blocked by D-APV. 7. The results indicate that the induction of LTP in both the medial and lateral perforant paths requires activation of postsynaptic NMDA receptors and a rise in intracellular calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗