Synaptic action during and after repetitive stimulation

Curtis, D. R.; Eccles, John C.

doi:10.1113/jphysiol.1960.sp006393

Cited by 513 publications

(227 citation statements)

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“…These effects include increases in the discharge threshold of the Ia afferents and inhibition of Ia terminals (Hayward et al, 1986, Hultborn et al, 1987, Shinohara, 2005. Such vibration has been shown, in the ankle, to decrease the amplitude of H reflexes in both the stimulated and synergistic muscles (Curtis and Eccles, 1960, Hultborn et al, 1987, Shinohara, 2005. Such vibration exposure has been demonstrated to alter overall joint dynamics as well, with vibration of the ankle tendons, for example, altering center of pressure trajectories in standing sway after vibration exposure (Wierzbicka et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Whole-body vibration alters proprioception in the trunk

Li¹,

Lamis²,

Wilson³

2008

International Journal of Industrial Ergonomics

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Abstract:Occupational whole body vibration has long been associated with low back injuries.However, the mechanism of these injuries is not well understood. In this paper, the effect of whole body vibration on proprioception and dynamic stability was examined. Subjects exposed to 20 minutes of vertical, seated, whole body vibration were found to have a 1.58 fold increase in position sense errors after vibration relative to controls exposed to 20 minutes of the same seated posture without vibration exposure. To understand the potential effect of a sensory loss on dynamic low back stability a lumped parameter model of the trunk and neuromotor response was created. Using this model, an increase in the threshold of the sensory system was predicted to increase trunk flexion and delay neuromotor response with a sudden, unexpected perturbation. These predictions were demonstrated in a second experiment where subjects exhibited both an 11.9% increase in trunk flexion and an 11.2% increase in time to peak paraspinal muscle response (measured using integrated electromyographic activity) after exposure to 20 minutes of vertical, seated, whole body vibration.

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Section: Discussionmentioning

confidence: 99%

Whole-body vibration alters proprioception in the trunk

Li¹,

Lamis²,

Wilson³

2008

International Journal of Industrial Ergonomics

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“…Synaptic transmission at the inhibitory synapse per se, or at the excitatory synapses converging onto inhibitory interneurones may exhibit a frequencydependent depression. The latter may be inferred from the parallel decline of EPSPs and IPSPs in spinal cord (Curtis & Eccles, 1960). In neocortex the frequency R. A. DEISZ AND D. A.…”

Section: Frequency Dependence Of Local Circuitsmentioning

confidence: 99%

“…This attenuation occurs in a frequency range where no significant effects on EPSPs are detectable. rendering a causal link to EPSP depression unlikely (Curtis & Eccles, 1960;Miles, 1986). It is possible that EPSPs of inhibitory interneurones exhibit a more pronounced frequency dependence than those of pyramidal cells.…”

Section: Contribution Of Local Circuits To Frequency Dependence Of Ipspsmentioning

confidence: 99%

“…Inhibitory postsynaptic potentials (IPSPs) were also shown to be reduced at higher frequencies of stimulation in motoneurones (Curtis & Eccles, 1960), hippocampal pyramidal cells in vivo (Ben-Ari, Krnjevic & Reinhardt, 1979) and in vitro (McCarren & Alger, 1985) and in neocortical cells (Connors, Gutnick & Prince, 1982). Like drug-induced depression of lPSPs, frequency-dependent attenuation may facilitate the onset of abnormal neuronal discharges.…”

Section: Introductionmentioning

confidence: 99%

“…For example, the attenuation of EPSPs at higher stimulus frequencies (Curtis & Eccles, 1960;Miles, 1986) may also occur at inhibitory interneurones and result in reduced IPSPs. Alternatively, the ionic gradient underlying postsynaptic inhibition may exhibit a use-dependent decrease.…”

Section: Introductionmentioning

confidence: 99%

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Frequency‐dependent depression of inhibition in guinea‐pig neocortex in vitro by GABAB receptor feed‐back on GABA release.

Deisz

Prince

1989

The Journal of Physiology

330

208

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SUMMARY1. The mechanisms involved in the lability of inhibition at higher frequencies of stimulation were investigated in the guinea-pig in vitro neocortical slice preparation by intracellular recording techniques. We attempted to test the possibility of a feedback depression of GABA on subsequent release.2. At resting membrane potential (Em, -75-8 + 5-2 mV) stimulation of either the pial surface or subcortical white matter evoked a sequence of depolarizing and hyperpolarizing synaptic components in most neurones. An early hyperpolarizing component (IPSPA) was usually only obvious as a pronounced termination of the EPSP. followed by a later hyperpolarizing event (IPSPB). Current-voltage relationships revealed two different conductances of about 200 and 20 nS and reversal potentials of -73-0+444 and -88-6+6 1 mV for the early and late component. respectively.3. The conductances of IPSPA and IPSPB were fairly stable at a stimulus frequency of 0-1 Hz. At frequencies between 0-5 and 2 Hz both IPSPs were attenuated with the second stimulus and after about five stimuli a steady state was reached. Concomitantly IPSPs were shortened. The average decrease in synaptic conductance between 0-1 and 1 Hz was 80% for the IPSPA and 60% for the IPSPB. At these frequencies the reversal potentials decreased by 5 and 2 mV, respectively; Em and input resistance (Rin) were not consistently affected.4. The amplitudes of field potentials, action potentials and EPSPs of pyramidal cells were attenuated less than 10% at stimulus frequencies up to 1 Hz, suggesting that alterations in local circuits between the stimulation site and excitatory input onto inhibitory interneurones may play only a minor role in the frequency-dependent decav of IPSPs.5. Localized application of GABA produced multiphasic responses. With low concentrations and application near the soma an early hyperpolarization prevailed followed by a depolarizing late component. Brief application of GABA at low frequencies induced constant responses; at higher frequencies, the responses sometimes declined. were similar to each other and to the early IPSP. An apparently fivefold higher conductance was estimated at lower Ems, suggesting that the GABA response had a voltage sensitivity. The slope conductance of IPSPs was decreased by up to 50 % for tens of seconds after postsynaptically detectable effects of GABA had dissipated. 6. Application of the GABA uptake inhibitor nipecotic acid (50-500 JLM) reduced the conductance of both components of orthodromically evoked inhibition and shortened the IPSP at low frequencies, but had no additional effects at higher stimulation rates. Em and Rin were not consistently affected. Application of nipecotic acid usually decreased the latency and increased the slope conductance of GABA responses. Depression of IPSPs by nipecotic acid at low frequencies, in the face of enhanced GABA responses, is probably presynaptically mediated. The prolonged time course of synaptically liberated GABA by nipecotic acid may cause extended presynaptic effects.7. ...

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Presynaptic and postsynaptic GABAB receptors of neocortical neurons of the rat in vitro: Differences in pharmacology and ionic mechanisms

Deisz¹,

Billard²,

Zieglgänsberger³

1997

Synapse

109

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The properties of pre- and postsynaptic GABAB receptors were investigated with intracellular recordings from rat neocortical neurons in vitro. An antagonist of the GABAB receptor (CGP 35348) and ions or drugs interfering with GABAB receptor-mediated K+ conductance (Ba2+, QX 314) were employed to delineate possible differences. CGP 35348 reduced the conductance of the late inhibitory postsynaptic potential (IPSPB) in a dose-dependent manner. Neither the early GABAA receptor-mediated inhibitory postsynaptic potential (IPSPA), nor resting membrane potential or direct excitability, were consistently affected by CGP 35348. Bath application of 100 mumol/l Ba2+ decreased IPSPB conductance to about 40% and increased IPSPA conductance to 130% of control. The depression of a second IPSP by a pair of stimuli (paired pulse depression, or PPD) was used as an index for presynaptic GABAB receptor activation. Neither CGP 35348 nor Ba2+ exerted significant effects on the PPD at intervals of 400 msec. The dependence of PPD on the latency of the interval of the stimulus pair was investigated after intracellular applicatio of QX 314 had virtually abolished the IPSPB. Decreasing the stimulus interval from 500 msec to 100 msec revealed a stronger depression of the second IPSPA. Application of CGP 35348 alleviated PPD for stimulus intervals below 300 msec. The data indicate a distinct pharmacological difference between pre- and postsynaptic GABAB receptors. Moreover, we suggest that two temporally distinct presynaptic GABAB receptor effects contribute to PPD: a short-lasting effect, sensitive to CGP 35348, and a long-lasting effect, insensitive to CGP 35348. The latter is insensitive to Ba2+, implying that this component is not associated with a K+ conductance mechanism.

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Synaptic action during and after repetitive stimulation

Cited by 513 publications

References 56 publications

Whole-body vibration alters proprioception in the trunk

Whole-body vibration alters proprioception in the trunk

Frequency‐dependent depression of inhibition in guinea‐pig neocortex in vitro by GABAB receptor feed‐back on GABA release.

Presynaptic and postsynaptic GABAB receptors of neocortical neurons of the rat in vitro: Differences in pharmacology and ionic mechanisms

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