Effects of afferent firing frequency on the amplitude of the monosynaptic EPSP elicited by trigeminal spindle afferents on trigeminal motoneurones

Grimwood, Paul; Appenteng, Kwabena

doi:10.1016/0006-8993(95)00606-q

Cited by 11 publications

(5 citation statements)

References 13 publications

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“…Using multi-pulse stimulation to activate the group1A monosynaptic circuit, brief post-activation facilitation (<25ms) is superimposed on a more prolonged post-activation depression at longer intervals (Curtis and Eccles, 1960; Wolpaw and Carp, 2006). Similar processes have been reported in motoneurons and in the intermediate zone (Collins et al, 1986; Collins et al, 1988; Grimwood and Appenteng, 1995). Normally, short-term modifications of the 1A response are thought to reflect the size of the readily releasable vesicular pool (Nielsen et al, 2007).…”

Section: Discussionsupporting

confidence: 85%

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

et al. 2012

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The corticospinal tract (CST) has dense contralateral and sparse ipsilateral spinal cord projections that converge with proprioceptive afferents on common spinal targets. Previous studies in adult rats indicate that the loss of dense contralateral spinal CST connections after unilateral pyramidal tract section (PTX), which models CST loss after stroke or spinal cord injury, leads to outgrowth from the spared side into the affected, ipsilateral, spinal cord. The reaction of proprioceptive afferents after this CST injury, however, is not known. Knowledge of proprioceptive afferent responses after loss of the CST could inform mechanisms of maladaptive plasticity in spinal sensorimotor circuits after injury. Here we hypothesize that the loss of the contralateral CST results in a reactive increase in muscle afferents from the impaired limb and enhancement of their physiological actions within the cervical spinal cord. We found that ten days after PTX, proprioceptive afferents sprout into cervical gray matter regions denervated by the loss of CST terminations. Further, VGlut1 positive boutons, indicative of group 1A afferent terminals, increased on motoneurons. PTX also produced an increase in microglial density within the gray matter regions where CST terminations were lost. These anatomical changes were paralleled by reduction in frequency-dependent depression of the H-reflex, suggesting hyperreflexia. Our data demonstrate for the first time that selective CST injury induces maladaptive afferent fiber plasticity remote from the lesion. Our findings suggest a novel structural reaction of proprioceptive afferents to the loss of CST terminations and provide insight into mechanisms underlying spasticity.

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Section: Discussionsupporting

confidence: 85%

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

et al. 2012

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“…The frequency‐dependent depression of I a EPSPs observed here is similar to that described before (Curtis & Eccles, 1960; Hirst et al 1981; Honig et al 1983; Collins et al 1984; Grimwood & Appenteng, 1995). Most relevant are the studies by Mendell and colleagues (reviewed in Mendell et al 1990) of frequency‐dependent changes in EPSPs produced by single I a afferents in motoneurones.…”

Section: Discussionsupporting

confidence: 89%

“…This study provides the first evidence that PSTH primary peaks for single I a‐motoneurone synapses change with stimulation frequency, and that this modulation parallels that of the corresponding synaptic potentials. Although prior workers demonstrated a frequency dependence of the amplitude of EPSPs at the I a‐motoneurone synapse (Curtis & Eccles, 1960; Hirst et al 1981; Honig et al 1983; Grimwood & Appenteng, 1995), they measured only resting membranes, leaving open the question of whether the observed modulation was sufficient to alter motoneurone discharge. Although other workers found dependence of motoneurone discharge rate on the frequency of intracellular current pulses (Powers & Binder, 1996) or of group I stimulation (Redman et al 1968; Chaplain & Schaupp, 1973), they do not identify the possible contributions of frequency‐dependent changes in the synaptic potentials.…”

Section: Discussionmentioning

confidence: 99%

Frequency‐dependent synaptic depression modifies postsynaptic firing probability in cats

Clark

Cope

1998

The Journal of Physiology

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The influence of stimulus trains applied to single I a axons on the firing behaviour of single motoneurones was assessed in anaesthetized cats. The change in motoneurone firing probability associated with a single I a afferent spike was measured from short‐latency peaks in peristimulus time histograms or cross‐correlograms. Some synapses showed frequency‐dependent depression of the short‐latency peak, which is consonant with the frequency‐dependent depression reported for the I a‐motoneurone excitatory postsynaptic potential (EPSP). Where they could be measured, EPSPs superimposed on the depolarizing ramps of potential recorded from motoneurones as they fired repetitively showed frequency‐dependent changes in amplitude that parallelled those of the simultaneously recorded histograms. Thus it appears that at synapses with small EPSPs, which are typical in the mammalian CNS, modulation of the EPSP should result in similar modulation of cell firing.

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“…We found in preliminary experiments that intervals of 20-30 ms produced maximum facilitation, but that intervals of less than 10 ms produced depression. This pattern is consistent with the finding that Grimwood and Appenteng [16] made in vivo with trigeminal motoneurons, although their optimal interval was 10-20 ms. PPF was evoked in 4 motoneurons by recording the response to two stimuli separated by 20-30 ms. Alternate sweeps of the response to single and paired stimuli were sampled at 0.1 Hz. They were then assigned to different buffers, averaged off-line, and the averages subtracted to yield the response to the second stimulus pulse (fig.…”

Section: Effect Of Baclofen On Ppfsupporting

confidence: 80%

Role of GABA<sub>B</sub> Receptor in the Regulation of Excitatory Synaptic Transmission in Trigeminal Motoneurons

Min¹,

Appenteng²,

Yang³

2002

J Biomed Sci

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The aim of the present study was to determine if excitatory synaptic transmission onto trigeminal motoneurons is subject to a presynaptic modulation by γ-aminobutyric acid (GABA) via GABA_B receptor in this system. Whole cell recordings were made from trigeminal motoneurons in longitudinal brain stem slices taken from 8-day-old rats. Monosynaptic excitatory postsynaptic potential (EPSP) activity was evoked by placing bipolar stainless steel electrodes dorsal-caudal to the trigeminal motor nucleus. Bath application of the GABA_B receptor agonist, baclofen, produced a marked reduction in the mean amplitude and variance of evoked EPSPs and also increased the portion of transmission failures. It also produced a decrease in the frequency, but not in the mean amplitude, of spontaneous miniature EPSPs. Bath application of GABA_B receptor antagonists 6-hydroxy-saclofen and CGP35348 increased both the amplitude and frequency of miniature EPSP activity. Taken together the above results suggest that the excitatory synaptic inputs onto trigeminal motoneurons are controlled by tonic presynaptic modulation by GABA_B receptor.

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Effects of afferent firing frequency on the amplitude of the monosynaptic EPSP elicited by trigeminal spindle afferents on trigeminal motoneurones

Cited by 11 publications

References 13 publications

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

Frequency‐dependent synaptic depression modifies postsynaptic firing probability in cats

Role of GABA<sub>B</sub> Receptor in the Regulation of Excitatory Synaptic Transmission in Trigeminal Motoneurons

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