Intracellular Recording from the Giant Synapse of the Squid

Bullock, Theodore H.; Hagiwara, Susumu

doi:10.1007/978-1-4684-9427-3_8

Cited by 4 publications

(4 citation statements)

References 20 publications

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“…These results are in agreement with previous findings on the role of synaptic terminal polarization on synaptic strength, as presynaptic hyperpolarization increases presynaptic action potential size and modulates Ca 2+ current activation and driving force (Hubbard & Willis, 1962a;Takeuchi & Takeuchi, 1962;Miledi & Slater, 1966). Accordingly, release is enhanced by terminal hyperpolarization and decreased by terminal depolarization (Bullock & Hagiwara, 1957;Hubbard & Willis, 1962b, 1968Takeuchi & Takeuchi, 1962;Miledi & Slater, 1966;Dudel, 1971).…”

Section: Axon Terminal Polarization Mediates Modulation Of Synaptic Esupporting

confidence: 93%

Cellular effects of acute direct current stimulation: somatic and synaptic terminal effects

Rahman

Reato

Arlotti

et al. 2013

The Journal of Physiology

488

533

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Key points• The diversity of cellular targets of direct current stimulation (DCS), including somas, dendrites and axon terminals, determine the modulation of synaptic efficacy.• Axon terminals of cortical pyramidal neurons are two-three times more susceptible to polarization than somas.• DCS in humans results in current flow dominantly parallel to the cortical surface, which in animal models of cortical stimulation results in synaptic pathway-specific modulation of neuronal excitability.• These results suggest that somatic polarization together with axon terminal polarization may be important for synaptic pathway-specific modulation of DCS, which underlies modulation of neuronal excitability during transcranial DCS.Abstract Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique to modulate cortical excitability. Although increased/decreased excitability under the anode/cathode electrode is nominally associated with membrane depolarization/hyperpolarization, which cellular compartments (somas, dendrites, axons and their terminals) mediate changes in cortical excitability remains unaddressed. Here we consider the acute effects of DCS on excitatory synaptic efficacy. Using multi-scale computational models and rat cortical brain slices, we show the following. (1) Typical tDCS montages produce predominantly tangential (relative to the cortical surface) direction currents (4-12 times radial direction currents), even directly under electrodes. (2) Radial current flow (parallel to the somatodendritic axis) modulates synaptic efficacy consistent with somatic polarization, with depolarization facilitating synaptic efficacy. (3) Tangential current flow (perpendicular to the somatodendritic axis) modulates synaptic efficacy acutely (during stimulation) in an afferent pathway-specific manner that is consistent with terminal polarization, with hyperpolarization facilitating synaptic efficacy. (4) Maximal polarization during uniform DCS is expected at distal (the branch length is more than three times the membrane length constant) synaptic terminals, independent of and two-three times more susceptible than pyramidal neuron somas. We conclude that during acute DCS the cellular targets responsible for modulation of synaptic efficacy are concurrently somata and axon terminals, with the direction of cortical current flow determining the relative influence.

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Section: Axon Terminal Polarization Mediates Modulation Of Synaptic Esupporting

confidence: 93%

Cellular effects of acute direct current stimulation: somatic and synaptic terminal effects

Rahman

Reato

Arlotti

et al. 2013

The Journal of Physiology

488

533

View full text Add to dashboard Cite

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“…In principle, one might expect depolar-ization to reduce the size of the spike (through Na + channel inactivation) and to reduce Ca 2+ current activation, as well as the driving force for Ca 2+ flowing during the tail current on the falling edge of the spike. Accordingly, in the squid giant synapse, transmitter release is enhanced by preceding hyperpolarizing membrane currents (Bullock and Hagiwara, 1957;Takeuchi and Takeuchi, 1962). Similar results were reported for neuromuscular junctions (Dudel, 1971;Hubbard and Willis, 1968).…”

Section: Presynaptic Regulation At Other Synapsessupporting

confidence: 83%

Modulation of Transmitter Release by Presynaptic Resting Potential and Background Calcium Levels

Awatramani

Price

Trussell

2005

Neuron

243

248

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Activation of presynaptic ion channels alters the membrane potential of nerve terminals, leading to changes in transmitter release. To study the relationship between resting potential and exocytosis, we combined pre- and postsynaptic electrophysiological recordings with presynaptic Ca(2+) measurements at the calyx of Held. Depolarization of the membrane potential to between -60 mV and -65 mV elicited P/Q-type Ca(2+) currents of < 1 pA and increased intraterminal Ca(2+) by < 100 nM. These small Ca(2+) elevations were sufficient to enhance the probability of transmitter release up to 2-fold, with no effect on the readily releasable pool of vesicles. Moreover, the effects of mild depolarization on release had slow kinetics and were abolished by 1 mM intraterminal EGTA, suggesting that Ca(2+) acted through a high-affinity binding site. Together, these studies suggest that control of resting potential is a powerful means for regulating synaptic function at mammalian synapses.

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“…This involved giving a formal lecture, but also provided lab facilities for a research project. Ricardo and Clarke Slater (also supported by a Grass Fellowship) confirmed earlier work at Woods Hole (Bullock & Hagiwara 1957; Hagiwara & Tasaki 1958; Takeuchi & Takeuchi 1962), showing that, as in the frog NMJ, transmission in the giant synapse in calcium-free medium could be restored locally by application of calcium from a pipette (12). Ricardo recalled that ‘I thought, if all I need is the calcium inside, that should release neurotransmitter … But when I injected calcium, I didn't see any response’ (Jeng 2002).…”

Section: Synaptic Transmission At the Neuromuscular Junctionsupporting

confidence: 62%

Ricardo Miledi. 15 September 1927—18 December 2017

Parker

Slater

Cull-Candy

et al. 2021

Biogr. Mems Fell. R. Soc.

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For nearly five decades, Ricardo Miledi was among the foremost researchers in elucidating how nerves transmit signals across synapses. Born in Chihuahua, Mexico, he qualified as a medical doctor, obtained a PhD with Arturo Rosenblueth and then, while in Canberra with John Eccles FRS, was invited by Bernard Katz FRS to join the Biophysics department at University College London, where he stayed from 1958 to 1984. Both independently and with Katz, he demonstrated that influx of calcium into the presynaptic nerve terminal is the essential trigger for the release of the neurotransmitter that carries signals across to the postsynaptic cell. He found that cutting the nerve to a frog's muscle increased the number and distribution of its muscle acetylcholine (ACh) receptors, which he purified and established as membrane proteins. Together with Katz, he introduced the technique of membrane noise analysis to determine the properties of the individual ion channels opened by ACh, providing the first functional characterization of a single receptor with integral ion channel. With Eric Barnard (FRS 1981), he pioneered a new approach facilitating the study of neurotransmitter receptors and ion channels by ‘transplanting’ them from brain and other tissues into large Xenopus oocyte cells by injection of messenger RNA. After moving to the University of California, Irvine, in 1984, he helped to establish the Mexican Institute for Neurobiology at Querétaro. Working in Irvine and Mexico he extended this oocyte expression technique to incorporate transplanted brain membranes, particularly from patients with epilepsy or other neurological disorders. He received many honours for his work, including the Royal Medal (1998), but was happiest working in his lab applying his extraordinary technical skills and imagination to study synaptic transmission and inspiring a generation of neuroscientists.

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Intracellular Recording from the Giant Synapse of the Squid

Abstract: Several authors have described intracellular recording from the post-junctional cell in synaptic regions, for example, in the neuromuscular junction Katz, 1951, 1953), in the brain and spinal cord (

Cited by 4 publications

References 20 publications

Cellular effects of acute direct current stimulation: somatic and synaptic terminal effects

Cellular effects of acute direct current stimulation: somatic and synaptic terminal effects

Modulation of Transmitter Release by Presynaptic Resting Potential and Background Calcium Levels

Ricardo Miledi. 15 September 1927—18 December 2017

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