Spontaneous inhibitory post-synaptic potentials in hippocampus: Mechanism for tonic inhibition
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Modeling and simulation of organophosphate-induced neurotoxicity: Prediction and validation by experimental studies
2016, NeuroToxicologyCitation Excerpt :A number of pharmacological studies showed that ACh facilitates CA1 pyramidal cell discharges by blocking two distinct families of potassium channels, calcium-dependent potassium channels (SK, MK and BK) and the potassium channel responsible for the M current (KCNQ) that is functionally associated with the muscarinic ACh receptor type M1 (Biscoe and Straughan 1966; Benardo and Prince 1981; Dodd et al., 1981; Benardo et al., 1982; Halliwell and Adams, 1982; Krnjevic and Ropert 1982; Ropert and Krnjevic, 1982; Benardo and Prince, 1982a,b; Cole and Nicoll, 1983, 1984a,b; Muller and Misgeld, 1986). Calcium-dependent potassium channels are activated by increased intracellular calcium concentrations resulting from AP discharge and are responsible for the after-hyperpolarization (AHP) that follows AP production (Hotson and Prince, 1980; Alger and Nicoll, 1980a,b). The M current is blocked by activation of M1 receptor (Halliwell and Adams, 1982; Halliwell, 1990) and contributes to cell depolarization.
Spontaneous Spiking and Synaptic Depression Underlie Noradrenergic Control of Feed-Forward Inhibition
2011, NeuronCitation Excerpt :For example, multiple classes of inhibitory interneuron exhibit spontaneous spiking behavior in vivo (Gentet et al., 2010; Klausberger et al., 2003; Ruigrok et al., 2011) and in vitro (Parra et al., 1998). Postsynaptic targets of inhibitory neurons are therefore subject to constantly fluctuating inhibitory synaptic conductances which do not necessarily correspond to stimulus-evoked activity (Alger and Nicoll, 1980; Salin and Prince, 1996; Vincent and Marty, 1996). This background input may impose a tonic inhibition that shapes neuronal integration (Mitchell and Silver, 2003) and can even enhance stimulus encoding if its structure correlates with that of background excitatory inputs (Cafaro and Rieke, 2010).
Calcineurin-mediated LTD of GABAergic inhibition underlies the increased excitability of CA1 neurons associated with LTP
2000, NeuronCitation Excerpt :Therefore, the voltage threshold for firing measured in the soma does not reflect the actual threshold at distant synaptic loci. Second, a decreased threshold for neuronal firing can occur through the attenuation of feedforward inhibition (Andersen et al. 1987) as well as by the reduction of GABAA receptor–mediated tonic inhibitory currents (Alger and Nicoll 1980). The experiments of Chavez-Noriega et al. 1990 were performed in the absence of GABAA receptor blockers; therefore, a reduced threshold after tetanic stimulation could have resulted from the reduction in tonic inhibition via GABAA receptor channels.
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This work was supported by PHS Grant GM-23478, NIH Postdoctoral Fellowship 9 F32 NS05744-02 (B.E.A.) and RCDA NS 00287 (R.A.N.).