Mechanisms of presynaptic inhibition studied using paired-pulse facilitation
References (22)
- et al.
Facilitation as a tool to study the entry of calcium and the mechanism of neurotransmitter release
Prog. Neurobiol.
(1989) Composite nature of the monosynaptic excitatory postsynaptic potential
J. Neurophysiol.
(1967)- et al.
Post-synaptic conductance increase associated with presynaptic inhibition in cat lumbar motoneurones
J. Physiol.
(1980) - et al.
Statistical factors involved in neuromuscular facilitation and depression
J. Physiol.
(1954) - et al.
Presynaptic inhibition of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia axons
J. Physiol.
(1987) - et al.
Presynaptic and postsynaptic inhibition of spinal motoneurones
J. Neurophysiol.
(1972) - et al.
Spinal inhibition
Twin pulse facilitation in dependence on pulse duration and calcium concentration at motor nerve terminals of crayfish and frogs
Pflügers Arch.
(1989)- et al.
Central inhibitory action attributable to presynaptic depolarization produced by muscle afferent volleys
J. Physiol.
(1961) - et al.
Presynaptic and postsynaptic inhibition of monosynaptic reflexes
Post-tetanic potentiation and facilitation of synaptic potentials evoked in cat spinal motoneurones
J. Physiol.
Cited by (29)
Modulation of glycinergic synaptic transmission in the trigeminal and hypoglossal motor nuclei by the nitric oxide-cyclicGMP signaling pathway
2014, NeuroscienceCitation Excerpt :8BrcGMP did not modify the response to exogenous glycine application which suggests that postsynaptic receptors are not being modulated. The observed increase in the PPF and the increase in the number of failures are indicative of a reduced probability of neurotransmitter release (Stuart and Redman, 1991; Stevens and Wang, 1994). These data lead us to favor the notion that NO was acting to reduce glycine release in the trigeminal motor nucleus.
Inhibition of excitatory synaptic transmission in the trigeminal motor nucleus by the nitric oxide-cyclicGMP signaling pathway
2011, Brain ResearchCitation Excerpt :Second, the NO donor increased the PPF. It is accepted that a change in PPF indicates a presynaptic site of action (Stuart and Redman, 1991; Zucker, 1989). An increase in PPF indicates a decrease in the probability of neurotransmitter release (ibid).
John Eccles' studies of spinal cord presynaptic inhibition
2006, Progress in NeurobiologyDeficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: A model of Down syndrome
2005, Neuroscience LettersDual effect of GABA on descending monosynaptic excitatory postsynaptic potential in frog lumbar motoneurons
2004, NeuroscienceCitation Excerpt :Here, we used another independent approach to assess the site for (−)-baclofen action on VLC EPSP. Since the changes of the PPF are considered to be of presynaptic origin (Creager et al., 1980; Stuart and Redman, 1991; Clark et al., 1994; Kuhnt and Voronin, 1994; Schulz, 1997) we assessed the PPF value of VLC EPSP with 40 ms inter-impulse time intervals before and during (−)-baclofen (0.05 mM) and GABA (0.5 mM) application. The mean amplitude of R1 was 4.4±2.1 mV and that of R2 was 5.6±1.9 mV in control conditions (n=5).