Anomalous rectification in the metacerebral giant cells and its consequences for synaptic transmission

Kandel, Eric R.; Tauc, L

doi:10.1113/jphysiol.1966.sp007867

Cited by 211 publications

(73 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The strength of electrical transmission depends not only on the conductance of the gap junction channels but also on the electrical and geometrical characteristics of the coupled cells (Bennett, 1966(Bennett, , 1977, which are determined to a large extent by their morphology and membrane properties. Thus, in addition to the control of gap junctional conductance itself (Furshpan and Potter, 1959;Auerbach and Bennett, 1969;Piccolino et al, 1982;Lasater and Dowling, 1985;Yang et al, 1990;Pereda et al, 1992Pereda et al, , 1998, changes in the conductance of the nonjunctional membrane are known to have a profound impact on electrical coupling (Kandel and Tauc, 1966;Spira et al, 1976;Zipser, 1979). In the mammalian CNS, neuronal gap junctions are often localized between small dendritic processes of dissimilar size and shape (Llinás et al, 1974;De Zeeuw et al, 1995;Fukuda and Kosaka, 2000;Fukuda and Kosaka, 2003) where geometry may favor transmission in one direction or the other.…”

Section: Introductionmentioning

confidence: 99%

Voltage-Dependent Enhancement of Electrical Coupling by a Subthreshold Sodium Current

Curti¹,

Pereda²

2004

J. Neurosci.

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Voltage-Dependent Enhancement of Electrical Coupling by a Subthreshold Sodium Current

Curti¹,

Pereda²

2004

J. Neurosci.

View full text Add to dashboard Cite

“…The term anomalous rectification has been used to describe the increase and decrease in slope conductance that occur close to the resting potential in a number of vertebrate and invertebrate neurones as the membrane potential is either hyperpolarized or depolarized (metacerebral giant neurones of Helix aspersa: Kandel & Tauc, 1966;motoneurones: Nelson & Frank, 1967; hippocampal pyramidal cells in vivo: Purpura, Prelevic & Santini, 1968; hippocampal pyramidal cells in vitro: Hotson, Prince & Schwartzkroin, 1979). As noted by Nelson & Lux (1970) slopeconductance measurements provide little information on the nature or ionic mechanism of the rectifying process.…”

Section: Introductionmentioning

confidence: 99%

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

Mayer

Westbrook

1983

The Journal of Physiology

426

320

View full text Add to dashboard Cite

SUMMARY1. Mouse embryo dorsal root ganglion neurones were grown in tissue culture and voltage-clamped with two micro-electrodes. Hyperpolarizing voltage commands from holding potentials of -50 to -60 mV evoked slow inward current relaxations which were followed by inward tail currents on repolarization to the holding potential. These relaxations are due to the presence of a time-and voltage-dependent conductance provisionally termed Gh.2. Gh activates over the membrane potential range -60 to -120 mV. The presence of Gh causes time-dependent rectification in the current-voltage relationship measured between -60 and --120 mV. Gh does not inactivate within this range and thus generates a steady inward current at hyperpolarized membrane potentials.3. The current carried by Gh increases when the extracellular K+ concentration is raised, and is greatly reduced in Na+-free solutions. Current-voltage plots show considerably less inward rectification in Na+-free solution; conversely inward rectification is markedly enhanced when the extracellular K+ concentration is raised. The reversal potential of 'h is close to -30 mV in media of physiological composition.Tail-current measurement suggests that Ih is a mixed Na+-K+ current.4. Low concentrations ofCs+ reversibly block Ih and produce outward rectification in the steady-state current-voltage relationship recorded between membrane potentials of -60 and -120 mV. Cs+ also reversibly abolishes the sag and depolarizing overshoot that distort hyperpolarizing electrotonic potentials recorded in currentclamp experiments.5. Impermeant anion substitutes reversibly block Ih; this block is different from that produced by Cs+ or Na+-free solutions: Cs+ produces outward rectification in the steady-state current-voltage relationship recorded over the Ih activation range; in Na+-free solutions inward rectification, of reduced amplitude, can still be recorded since Ih is a mixed Na+-K+ current; in anion-substituted solutions the current-voltage relationship becomes approximately linear.6. It is concluded that in dorsal root ganglion neurones anomalous rectification is generated by the time-and voltage-dependent current Ih. The possible function of Ih in sensory neurones is discussed.

show abstract

“…Instead, they increase MCC excitability so that responses to afferent (i.e., C2 mediated) input are enhanced. Notably, the CC9 -10 induced depolarization may act in concert with the intrinsic anomalous rectification of the MCC (Kandel and Tauc, 1966;Weiss and Kupfermann, 1976) to further enhance the EPSPs that C2 evokes. C2 (Weiss et al, 1986b) is activated when food contacts the mouth and remains active as feeding progresses.…”

Section: Discussionmentioning

confidence: 99%

Neural Analog of Arousal: Persistent Conditional Activation of a Feeding Modulator by Serotonergic Initiators of Locomotion

Jing

Vilim²,

Cropper³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

We investigated how a neural analog of a form of arousal induced by a mildly noxious stimulus can promote two antagonistic responses, locomotion and feeding. Two pairs of cerebral serotonergic interneurons in Aplysia, CC9 and CC10, were persistently activated by transient noxious stimuli. Direct stimulation of CC9 -10 activated locomotor activity that outlasted the stimulation and enhanced subsequent nerve-evoked locomotor programs. Thus, CC9 -10 function both as initiators and as modulators of the locomotor network. CC9 -10 also interacted with the feeding circuit but in a fundamentally different manner. CC9 -10 did not directly trigger feeding activity or activate feeding command or pattern generating interneurons. CC9 -10 did, however, elicit slow EPSPs in serotonergic cells that modulate feeding responses, the metacerebral cells (MCCs). CC9 -10 persistently enhanced MCC excitability, but did not activate the MCCs directly. Previous work has demonstrated that the MCCs are activated during food ingestion via a sensory neuron C2. Interestingly, we found that CC9 -10 stimulation converted subthreshold C2 mediated excitation of the MCC into suprathreshold excitation. Transient noxious stimuli also enhanced MCC excitability, and this was largely mediated by CC9 -10. To summarize, CC9 -10 exert actions on the feeding network, but their functional effects appear to be conditional on the presence of food-related inputs to the MCCs. A potential advantage of this arrangement is that it may prevent conflicting responses from being directly evoked by noxious stimuli while also facilitating the ability of food-related stimuli to generate feeding responses in the aftermath of noxious stimulation.

show abstract

Anomalous rectification in the metacerebral giant cells and its consequences for synaptic transmission

Cited by 211 publications

References 15 publications

Voltage-Dependent Enhancement of Electrical Coupling by a Subthreshold Sodium Current

Voltage-Dependent Enhancement of Electrical Coupling by a Subthreshold Sodium Current

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

Neural Analog of Arousal: Persistent Conditional Activation of a Feeding Modulator by Serotonergic Initiators of Locomotion

Contact Info

Product

Resources

About