Cortical Intracellular Potentials During Augmenting and Recruiting Responses: Ii. Patterns of Synaptic Activities in Pyramidal and Nonpyramidal Tract Neurons

Purpura, Dominick P.; Shofer, Robert J.; Musgrave, F. Story

doi:10.1152/jn.1964.27.2.133

Cited by 155 publications

(23 citation statements)

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“…Note that the voltage dependence of the isolated late EPSP1 was similar to that of the isolated late EPSP2 ( Fig. 9Ba; al. 1964;Douglas & Martin, 1991;Ferster & Jagadeesh, 1992;Metherate & Ashe, 1993a, b;Nunez et al 1993) and in vitro (Connors et al 1982;Jones & Baughman, 1988;Sutor & Hablitz, 1989a;Higashi et al 1991;Cox et al 1992).…”

Section: Pharmacological Agentssupporting

confidence: 58%

Facilitation of an NMDA receptor‐mediated EPSP by paired‐pulse stimulation in rat neocortex via depression of GABAergic IPSPs.

Metherate

Ashe

1994

The Journal of Physiology

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1. Tight seal, whole-cell recordings from auditory cortex in vivo and in vitro were obtained to investigate modification of N-methyl-D-aspartate (NMDA) receptor-mediated synaptic activity by paired-pulse afferent stimulation. 2. In recordings from urethane-anaesthetized rats (at 37°C), or from cortical slices maintained in vitro (32°C), afferent stimulation elicited a monosynaptic early EPSP and polysynaptic early and late IPSPs. In addition, a late EPSP could be elicited when the stimulus was preceded by an identical priming stimulus (interval -200 ms). The late EPSP was attenuated by the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (APV, 50 SuM). 3. Bath application of the y-aminobutyric acid-B (GABAB) receptor antagonist 3-amino-2-(4-chlorophenyl)-2-hydroxy-propylsulphonic acid (2-OH-saclofen; 50/M) attenuated the late IPSP and clearly revealed a late EPSP. However, 2-OH-saclofen had lesser effects on the second late EPSP elicited during paired-pulse stimulation. Membrane depolarization in 2-OH-saclofen increased the magnitude of the early IPSP, which suppressed the late EPSP once again. Since pharmacological blockade of EPSPs revealed paired-pulse depression of monosynaptically elicited early and late IPSPs, these data indicate that (1) both early and late IPSPs were capable of suppressing the late EPSP, and (2) these effects were reduced during paired-pulse stimulation. 4. Pharmacological isolation of the late EPSP allowed testing of the direct effect of pairedpulse stimulation. Application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20 /tM), picrotoxin (10 ,uM) and 2-OH-saclofen (50 ,lM) isolated the late EPSP (onset, 3 ms; peak latency, 28 ms; peak amplitude, 7 mV; duration, 240 ms), which grew in magnitude with membrane depolarization and was largely (> 90%) blocked by APV. Paired-pulse stimulation depressed the isolated late EPSP by 30 %. 5. Thus, apparent paired-pulse facilitation of the late EPSP is attributable to release from GABAergic inhibition, and not to direct facilitation. Facilitation of the late EPSP is a functional consequence of IPSP depression. The results indicate the importance of inhibition in regulating synaptic activity mediated by NMDA receptors.

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Section: Pharmacological Agentssupporting

confidence: 58%

Facilitation of an NMDA receptor‐mediated EPSP by paired‐pulse stimulation in rat neocortex via depression of GABAergic IPSPs.

Metherate

Ashe

1994

The Journal of Physiology

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“…Morison and Dempsey originally proposed a thalamic system in parallel to that underlying the primary response but which receives substantial indirect excitation from cortical efferents as well as from lemniscal afferents. The state of increased excitation of the augmented response was suggested to involve 'mutual reinforcement' between thalamus and cortex, but the 'principal mechanism underlying augmentation ... lies in the thalamus' Grossman, Clark & Whiteside, 1967;Sasaki et al 1970;Matsuda et al 1972), others still have sought to explain the phenomenon in terms of a cortical mechanism (Purpura, Shofer & Musgrave, 1964;Morin & Steriade, 1981). While the pathway from the site of stimulation is said to be the same as that underlying the primary response, the intracortical effects of the input change dramatically with stimulus frequency.…”

Section: Source Of Incremental Responsementioning

confidence: 99%

Augmenting responses evoked in area 17 of the cat by intracortical axon collaterals of cortico‐geniculate cells.

Ferster¹,

Lindström²

1985

The Journal of Physiology

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Evoked potentials were recorded in the visual cortex of the cat after electrical stimulation of the lateral geniculate nucleus (l.g.n.). The primary response, mediated by geniculo‐cortical fibres, was depressed at stimulation frequencies above 7 Hz and replaced by a late potential, the incremental response, which gradually increased in amplitude with successive stimuli. The incremental response was a negative‐positive potential in the depth of the cortex with the negative component having maximal amplitude in layer 4. The response reversed polarity in layer 1 to become a positive‐negative potential at the surface. The latency of the negative component of the incremental response was about 3.5‐4 ms in layer 4, compared to about 1.5 and 2.5 ms for the mono‐ and disynaptic components of the primary response. The incremental response could only be evoked from the l.g.n. and the optic radiation, not from the optic tract, superior colliculus or other surrounding structures. Within the l.g.n., the effect was only evoked from stimulation sites in approximate retinotopic register with the recording site in the cortex. Low threshold points were found in the A laminae, completely overlapping with the low threshold points for the primary response. Thresholds increased steeply when the stimulation electrode was lowered into the C laminae. The incremental response could still be evoked ten days after the destruction of all cells in the l.g.n. complex by kainic acid. It is concluded that the described incremental response is identical to the augmenting response of Dempsey & Morison (1943) and is mediated by intracortical axon collaterals of antidromically activated cortico‐geniculate neurones.

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“…Upon repetitive stimulation of specific or nonspecific thalamic nuclei, an augmenting or recruiting response, respectively, could be recorded from the cortical surface (10,11). Intracellular recordings re-608 B. SUTOR AND J. J. HABLITZ vealed significant changes in the EPSP amplitude and duration (20,22,35,36). The augmenting response, evoked by repetitive stimulation of the nucleus ventralis lateralis, was associated with the appearance of a delayed second EPSP (22).…”

Section: Introductionmentioning

confidence: 96%

EPSPs in rat neocortical neurons in vitro. I. Electrophysiological evidence for two distinct EPSPs

Sutor

Hablitz

1989

Journal of Neurophysiology

134

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1. To investigate excitatory postsynaptic potentials (EPSPs), intracellular recordings were performed in layer II/III neurons of the rat medial frontal cortex. The average resting membrane potential of the neurons was more than -75 mV and their average input resistance was greater than 20 M omega. The amplitudes of the action potentials evoked by injection of depolarizing current pulses were greater than 100 mV. The electrophysiological properties of the neurons recorded were similar to those of regular-spiking pyramidal cells. 2. Current-voltage relationships, determined by injecting inward and outward current pulses, displayed considerable inward rectification in both the depolarizing and hyperpolarizing directions. The steady-state input resistance increased with depolarization and decreased with hyperpolarization, concomitant with increases and decreases, respectively, in the membrane time constant. 3. Postsynaptic potentials were evoked by electrical stimulation via a bipolar electrode positioned in layer IV of the neocortex. Stimulus-response relationships, determined by gradually increasing the stimulus intensity, were consistent among the population of neurons examined. A short-latency EPSP [early EPSP (eEPSP)] was the response with the lowest threshold. Amplitudes of the eEPSP ranged from 4 to 8 mV. Following a hyperpolarization of the membrane potential, the amplitude of the eEPSP decreased. Upon depolarization, a slight increase in amplitude and duration was observed, accompanied by a significant increase in time to peak. 4. The membrane current underlying the eEPSP (eEPSC) was measured using the single-electrode voltage-clamp method. The amplitude of the eEPSC was apparently independent of the membrane potential in 8 of 12 neurons tested. In the other 4 neurons, the amplitude of the eEPSC increased with hyperpolarization and decreased with depolarization. 5. Higher stimulus intensities evoked, in addition to the eEPSP, a delayed EPSP [late EPSP (lEPSP)] in greater than 90% of the neurons tested. The amplitude of the lEPSP ranged from 12 to 20 mV, and the latency varied between 20 and 60 ms. The amplitude of the lEPSP varied with membrane potential, decreasing with depolarization and increasing following hyperpolarization. The membrane current underlying the lEPSP (lEPSC) displayed a similar voltage dependence. 6. At stimulus intensities that led to the activation of inhibitory postsynaptic potentials (IPSPs), the lEPSP was no longer observed.(ABSTRACT TRUNCATED AT 400 WORDS)

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Cortical Intracellular Potentials During Augmenting and Recruiting Responses: Ii. Patterns of Synaptic Activities in Pyramidal and Nonpyramidal Tract Neurons

Cited by 155 publications

References 0 publications

Facilitation of an NMDA receptor‐mediated EPSP by paired‐pulse stimulation in rat neocortex via depression of GABAergic IPSPs.

Facilitation of an NMDA receptor‐mediated EPSP by paired‐pulse stimulation in rat neocortex via depression of GABAergic IPSPs.

Augmenting responses evoked in area 17 of the cat by intracortical axon collaterals of cortico‐geniculate cells.

EPSPs in rat neocortical neurons in vitro. I. Electrophysiological evidence for two distinct EPSPs

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