scholarly journals Focused ultrasound transiently increases membrane conductance in isolated crayfish axon

2019 ◽  
Vol 121 (2) ◽  
pp. 480-489
Author(s):  
Jen-Wei Lin ◽  
Feiyuan Yu ◽  
Wolfgang S. Müller ◽  
Gösta Ehnholm ◽  
Yoshio Okada
Keyword(s):  
Neuronal Activity ◽  
Focused Ultrasound ◽  
Brain Activity ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Tone Burst ◽  
Motor Axon ◽  
Neuronal Membrane ◽  
Channel Blockers ◽  
The Us

We report a novel phenomenon produced by focused ultrasound (US) that may be important for understanding its effects on cell membranes. When a US burst (2.1 MHz, 1-mm focal diameter, 0.1–1 MPa) was focused on a motor axon of the crayfish neuromuscular junction, it consistently produced a fast hyperpolarization, which was followed or superseded by subthreshold depolarizations or action potentials in a stochastic manner. The depolarization persisted in the presence of voltage-gated channel blockers [1 µM TTX ( INa), 50 µM ZD7288 ( Ih), and 200 µM 4-aminopyridine ( IK)] and typically started shortly after the onset of a 5-ms US burst, with a mean latency of 3.35 ± 0.53 ms (SE). The duration and amplitude of depolarizations averaged 2.13 ± 0.87 s and 10.1 ± 2.09 mV, with a maximum of 200 s and 60 mV, respectively. The US-induced depolarization was always associated with a decrease in membrane resistance. By measuring membrane potential and resistance during the US-induced depolarization, the reversal potential of US-induced conductance ( gus) was estimated to be −8.4 ± 2.3 mV, suggesting a nonselective conductance. The increase in gus was 10–100 times larger than the leak conductance; thus it could significantly influence neuronal activity. This change in conductance may be due to stimulation of mechanoreceptors. Alternatively, US may perturb the lateral motion of phospholipids and produce nanopores, which then increase gus. These results may be important for understanding mechanisms underlying US-mediated modulation of neuronal activity and brain function. NEW & NOTEWORTHY We report a specific increase in membrane conductance produced by ultrasound (US) on neuronal membrane. When a 5-ms US tone burst was focused on a crayfish motor axon, it stochastically triggered either depolarization or a spike train. The depolarization was up to 60 mV in amplitude and 200 s in duration and therefore could significantly influence neuronal activity. Depolarization was still evoked by US burst in the presence of Na+ and Ca2+ channel blockers and had a reversal potential of −8.4 ± 2.3 mV, suggesting a nonselective permeability. US can be applied noninvasively in the form of a focused beam to deep brain areas through the skull and has been shown to modulate brain activity. Understanding the depolarization reported here should be helpful for improving the use of US for noninvasive modulation and stimulation in brain-related disease.

K+-channel blockers do not decrease acetylcholine depolarizations in canine trachealis

1992 ◽  
Vol 70 (1) ◽  
pp. 43-52 ◽  
Author(s):  
E. E. Daniel ◽  
J. Jury ◽  
R. Serio ◽  
L. P. Jager
Keyword(s):  
Chloride Channels ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Resting Potential ◽  
K Channel ◽  
Channel Blockers ◽  
Membrane Effects ◽  
Sucrose Gap ◽  
Time Courses

Using the double sucrose gap, we have examined the role of K+ channels in the cholinergic depolarizations in response to field stimulation and acetylcholine (Ach) in canine trachealis. Acetylcholine-like depolarization per se decreased electrotonic potentials from hyperpolarizing currents. The net effect of acetylcholine (10−6 M) depolarization on membrane conductance was a small increase after the depolarization was compensated by current clamp. Reversal potentials for acetylcholine depolarization and for the excitatory junction potential (EJP) were determined by extrapolation to be 20–30 mV positive to the resting potential, previously shown to be approximately −55 mV. They were shifted positively by tetraethylammonium ion (TEA) at 20 mM or Ba2+ at 1 mM. TEA or Ba2+ initially depolarized the membrane and increased membrane resistance. Repolarization of the membrane restored any reductions in EJP amplitudes associated with depolarization. After 15 min, the membrane potential partially repolarized, and acetylcholine-induced depolarization and contractions were then increased by TEA. 4-Aminopyridine depolarized the membrane but decreased membrane resistance. Apamin (10−6 M), charybdotoxin (10−7 M), and glybenclamide (10−5 M) each failed to significantly depolarize membranes, increase membrane resistance, or reduce EJP amplitudes or depolarization to 10−6 M Ach. Glybenclamide reduced depolarizations to added acetylcholine slightly. TEA occasionally reduced the EJP markedly, but this was shown to be most likely a prejunctional effect mediated by norepinephrine release. TEA alone among K+-channel blockers slowed the onset and the time courses of the EJP as well as the acetylcholine-induced depolarization. K+-channel closure cannot be a complete explanation of acetylcholine-induced membrane effects on this tissue. Acetylcholine must have increased the conductance of an ion with a reversal potential positive to the resting potential in addition to any effect to close K+ channels.Key words: acetylcholine, tracheal smooth muscle, trachea, chloride channels, sucrose gap, potassium channels, tetraethylammonium, Ba2+.

Acetylcholine potentiates acetylcholine-induced increases in K+ current in cat atrial myocytes

1995 ◽  
Vol 268 (3) ◽  
pp. H1313-H1321 ◽  
Author(s):  
Y. G. Wang ◽  
S. L. Lipsius
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
K Channel ◽  
Channel Blockers ◽  
Atrial Myocytes ◽  
Initial Exposure ◽  
Recovery Interval ◽  
Cell Recording ◽  
K Current ◽  
K Currents

A nystatin-perforated patch whole cell recording method was used to study the effects of acetylcholine (ACh) on ACh-induced K+ currents in atrial myocytes isolated from cat hearts. The general protocol involved an initial 4-min exposure to ACh (ACh1), followed by a 4-min washout in ACh-free Tyrode solution and then a second 4-min ACh exposure (ACh2). Voltage ramps (40 mV/s) between -130 and +30 mV were used to assess changes in total membrane conductance. ACh2 (10 microM) induced an increase in K+ conductance that was significantly larger than that induced by ACh1 (10 microM) at voltages both negative and positive to the reversal potential. The potentiated current induced by ACh2 reversed at about -80 mV and inwardly rectified at voltages positive to the reversal potential. External Ba2+ (5 mM) or tetraethylammonium (10 mM) abolished all ACh2-induced increases in membrane conductance. The sensitivity to K+ channel blockers, reversal potential, and the rectifying properties indicate that the current potentiated by ACh2 is a K+ current. Atropine (1 microM) blocked all effects of ACh on K+ currents. Potentiation of K+ current by ACh2 required 1) ACh1 concentrations > or = 1 microM, 2) ACh1 duration > or = 2 min, and 3) recovery interval > or = 2 min. We conclude that an initial exposure to ACh potentiates subsequent ACh-induced increases in K+ current. ACh-induced potentiation depends on the concentration and duration of the initial ACh exposure and the recovery interval between consecutive ACh exposures.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Light Response of a Giant Aplysia Neuron

1973 ◽  
Vol 62 (3) ◽  
pp. 239-254 ◽  
Author(s):  
Arthur M. Brown ◽  
H. Mack Brown
Keyword(s):  
Reversal Potential ◽  
Outward Current ◽  
Membrane Conductance ◽  
Light Response ◽  
Resting Potential ◽  
Neuronal Membrane ◽  
Giant Neuron ◽  
Membrane Hyperpolarization ◽  
Pressure Injection ◽  
External K

Illumination of an Aplysia giant neuron evokes a membrane hyperpolarization which is associated with a membrane conductance increase of 15%. The light response is best elicited at 490 nM: the neuron also has an absorption peak at this wavelength. At the resting potential (-50 to -60 mV) illumination evokes an outward current in a voltage-clamped cell. This current reverses sign very close to EK calculated from direct measurements of internal and external K+ activity. Increases in external K+ concentration shift the reversal potential of the light-evoked response by the same amount as the change in EK. Decreases in external Na+ or Cl- do not affect the response. Therefore, the response is attributed to an increase in K+ conductance. Pressure injection of Ca2+ into this neuron also hyperpolarizes the cell membrane. This effect is also due largely to an increase in K+ conductance. The light response after Ca2+ injection does not appear to be altered. Pressure injection of EGTA abolished or greatly reduced the light response. The effect was reversible. We suggest that light acts upon a single pigment in this neuron, releasing Ca2+ which in turn increases K+ conductance, thereby hyperpolarizing the neuronal membrane.

scholarly journals Bidirectional and state-dependent modulation of brain activity by transcranial focused ultrasound in non-human primates

2021 ◽  
Vol 14 (2) ◽  
pp. 261-272
Author(s):  
Pai-Feng Yang ◽  
M. Anthony Phipps ◽  
Sumeeth Jonathan ◽  
Allen T. Newton ◽  
Nellie Byun ◽  
...  
Keyword(s):  
Focused Ultrasound ◽  
Brain Activity ◽  
State Dependent ◽  
Transcranial Focused Ultrasound

BICUCULLINE/BACLOFEN-INSENSITIVE GABA RESPONSE IN CRUSTACEAN NEURONES IN CULTURE

1994 ◽  
Vol 191 (1) ◽  
pp. 167-193
Author(s):  
C Jackel ◽  
W Krenz ◽  
F Nagy
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gamma Aminobutyric Acid ◽  
Action Potential Firing ◽  
Patch Clamp Technique ◽  
Conformationally Restricted ◽  
Whole Cell Patch Clamp ◽  
Gabac Receptor ◽  
Potential Firing ◽  
Sr 95531

Neurones were dissociated from thoracic ganglia of embryonic and adult lobsters and kept in primary culture. When gamma-aminobutyric acid (GABA) was applied by pressure ejection, depolarizing or hyperpolarizing responses were produced, depending on the membrane potential. They were accompanied by an increase in membrane conductance. When they were present, action potential firing was inhibited. The pharmacological profile and ionic mechanism of GABA-evoked current were investigated under voltage-clamp with the whole-cell patch-clamp technique. The reversal potential of GABA-evoked current depended on the intracellular and extracellular Cl- concentration but not on extracellular Na+ and K+. Blockade of Ca2+ channels by Mn2+ was also without effect. The GABA-evoked current was mimicked by application of the GABAA agonists muscimol and isoguvacine with an order of potency muscimol>GABA>isoguvacine. cis-4-aminocrotonic acid (CACA), a folded and conformationally restricted GABA analogue, supposed to be diagnostic for the vertebrate GABAC receptor, also induced a bicuculline-resistant chloride current, although with a potency about 10 times lower than that of GABA. The GABA-evoked current was largely blocked by picrotoxin, but was insensitive to the GABAA antagonists bicuculline, bicuculline methiodide and SR 95531 at concentrations of up to 100 µmol l-1. Diazepam and phenobarbital did not exert modulatory effects. The GABAB antagonist phaclophen did not affect the GABA-induced current, while the GABAB agonists baclophen and 3-aminopropylphosphonic acid (3-APA) never evoked any response. Our results suggest that lobster thoracic neurones in culture express a chloride-conducting GABA-receptor channel which conforms to neither the GABAA nor the GABAB types of vertebrates but shows a pharmacology close to that of the novel GABAC receptor described in the vertebrate retina.

Whole cell current analyses of pancreatic acinar AR42J cells. I. Voltage- and Ca(2+)-activated currents

1991 ◽  
Vol 260 (5) ◽  
pp. C934-C948 ◽  
Author(s):  
K. Kusano ◽  
H. Gainer
Keyword(s):  
Reversal Potential ◽  
Outward Current ◽  
Pancreatic Acinar Cells ◽  
Equilibrium Potential ◽  
Channel Blockers ◽  
Whole Cell ◽  
Inward Current ◽  
Tail Current ◽  
Ar42j Cells ◽  
Conductance Increase

Voltage- and Ca(2+)-activated whole cell currents were studied in AR42J cells, a clonal cell line derived from rat pancreatic acinar cells, using a patch electrode voltage-clamp technique. Four kinds of ionic currents were identified by their ionic dependencies, pharmacological properties, and kinetic parameters: 1) an outward current flow due mainly to a voltage-dependent K(+)-conductance increase, 2) an initial transient inward current due to an Na(+)-conductance increase, 3) transient and long-duration inward current due to a Ca(2+)-conductance increase, and 4) a slowly activating inward current that persists over the duration of the depolarizing pulse and deactivates slowly upon repolarization, producing a slow inward tail current. The slow inward tail current was particularly robust and was interpreted as due to a Ca(2+)-activated Cl(-)-conductance increase, since 1) the generation of this current was blocked by removing the extracellular Ca2+, applying Ca(2+)-channel blockers (Cd2+, nifedipine), or by lowering the intracellular Ca2+ concentration [( Ca2+]i) with EGTA; and 2) the reversal potential (Erev) of the slow inward tail current was close to 0 mV in the control condition (152 mM [Cl-]o/154 mM [Cl-]i), and changes of the [Cl-]o/[Cl )i ratio shifted the Erev toward the predicted Cl- equilibrium potential.

scholarly journals Using experience to improve: how errors shape behavior and brain activity in monkeys

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5395
Author(s):  
Jose L. Pardo-Vazquez ◽  
Carlos Acuña
Keyword(s):  
Neuronal Activity ◽  
Decision Process ◽  
Brain Activity ◽  
Single Cells ◽  
Premotor Cortex ◽  
Strong Support ◽  
Behavioral Performance ◽  
Previous Trial ◽  
Current Trial ◽  
Future Behavior

Previous works have shown that neurons from the ventral premotor cortex (PMv) represent several elements of perceptual decisions. One of the most striking findings was that, after the outcome of the choice is known, neurons from PMv encode all the information necessary for evaluating the decision process. These results prompted us to suggest that this cortical area could be involved in shaping future behavior. In this work, we have characterized neuronal activity and behavioral performance as a function of the outcome of the previous trial. We found that the outcome of the immediately previous trial (n−1) significantly changes, in the current trial (n), the activity of single cells and behavioral performance. The outcome of trial n−2, however, does not affect either behavior or neuronal activity. Moreover, the outcome of difficult trials had a greater impact on performance and recruited more PMv neurons than the outcome of easy trials. These results give strong support to our suggestion that PMv neurons evaluate the decision process and use this information to modify future behavior.

scholarly journals Transcranial focused ultrasound modulates cortical and thalamic motor activity in awake sheep

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hyun-Chul Kim ◽  
Wonhye Lee ◽  
Jennifer Kunes ◽  
Kyungho Yoon ◽  
Ji Eun Lee ◽  
...  
Keyword(s):  
Focused Ultrasound ◽  
Brain Activity ◽  
Response Rates ◽  
Behavioral Observation ◽  
Acoustic Stimulation ◽  
Motion Artifacts ◽  
Experimental Conditions ◽  
Low Intensity ◽  
Hind Limbs ◽  
Brain Tissue Damage

AbstractTranscranial application of pulsed low-intensity focused ultrasound (FUS) modulates the excitability of region-specific brain areas, and anesthetic confounders on brain activity warrant the evaluation of the technique in awake animals. We examined the neuromodulatory effects of FUS in unanesthetized sheep by developing a custom-fit headgear capable of reproducibly placing an acoustic focus on the unilateral motor cortex (M1) and corresponding thalamic area. The efferent responses to sonication, based on the acoustic parameters previously identified in anesthetized sheep, were measured using electromyography (EMG) from both hind limbs across three experimental conditions: on-target sonication, off-target sonication, and without sonication. Excitatory sonication yielded greater amplitude of EMG signals obtained from the hind limb contralateral to sonication than that from the ipsilateral limb. Spurious appearance of motion-related EMG signals limited the amount of analyzed data (~ 10% selection of acquired data) during excitatory sonication, and the averaged EMG response rates elicited by the M1 and thalamic stimulations were 7.5 ± 1.4% and 6.7 ± 1.5%, respectively. Suppressive sonication, while sheep walked on the treadmill, temporarily reduced the EMG amplitude from the limb contralateral to sonication. No significant change was found in the EMG amplitudes during the off-target sonication. Behavioral observation throughout the study and histological analysis showed no sign of brain tissue damage caused by the acoustic stimulation. Marginal response rates observed during excitatory sonication call for technical refinement to reduce motion artifacts during EMG acquisitions as well as acoustic aberration correction schemes to improve spatial accuracy of sonication. Yet, our results indicate that low-intensity FUS modulated the excitability of regional brain tissues reversibly and safely in awake sheep, supporting its potential in theragnostic applications.

scholarly journals Fiber photometry does not reflect spiking activity in the striatum

2021 ◽  
Author(s):  
Alex A. Legaria ◽  
Julia A. Licholai ◽  
Alexxai V. Kravitz
Keyword(s):  
Neuronal Activity ◽  
Calcium Imaging ◽  
Brain Activity ◽  
Neural Population ◽  
Fluorescence Signal ◽  
Calcium Signals ◽  
Cellular Events ◽  
Neural Populations ◽  
Spiking Activity

AbstractFiber photometry recordings are commonly used as a proxy for neuronal activity, based on the assumption that increases in bulk calcium fluorescence reflect increases in spiking of the underlying neural population. However, this assumption has not been adequately tested. Here, using endoscopic calcium imaging in the striatum we report that the bulk fluorescence signal correlates weakly with somatic calcium signals, suggesting that this signal does not reflect spiking activity, but may instead reflect subthreshold changes in neuropil calcium. Consistent with this suggestion, the bulk fluorescence photometry signal correlated strongly with neuropil calcium signals extracted from these same endoscopic recordings. We further confirmed that photometry did not reflect striatal spiking activity with simultaneous in vivo extracellular electrophysiology and fiber photometry recordings in awake behaving mice. We conclude that the fiber photometry signal should not be considered a proxy for spiking activity in neural populations in the striatum.Significance statementFiber photometry is a technique for recording brain activity that has gained popularity in recent years due to it being an efficient and robust way to record the activity of genetically defined populations of neurons. However, it remains unclear what cellular events are reflected in the photometry signal. While it is often assumed that the photometry signal reflects changes in spiking of the underlying cell population, this has not been adequately tested. Here, we processed calcium imaging recordings to extract both somatic and non-somatic components of the imaging field, as well as a photometry signal from the whole field. Surprisingly, we found that the photometry signal correlated much more strongly with the non-somatic than the somatic signals. This suggests that the photometry signal most strongly reflects subthreshold changes in calcium, and not spiking. We confirmed this point with simultaneous fiber photometry and extracellular spiking recordings, again finding that photometry signals relate poorly to spiking in the striatum. Our results may change interpretations of studies that use fiber photometry as an index of spiking output of neural populations.

Hodgkin–Huxley neurons with defective and blocked ion channels

2015 ◽  
Vol 26 (10) ◽  
pp. 1550112 ◽  
Author(s):  
James Christopher S. Pang ◽  
Johnrob Y. Bantang
Keyword(s):  
Ion Channels ◽  
Action Potentials ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Potassium Ions ◽  
Temporal Response ◽  
Constant Input ◽  
Control Drug ◽  
Channel Control ◽  
Sodium And Potassium

We utilize the original Hodgkin–Huxley (HH) model to consider the effects of defective ion channels to the temporal response of neurons. Statistics of firing rate and inter-spike interval (ISI) reveal that production of action potentials (APs) in neurons is not sensitive to changes in membrane conductance for sodium and potassium ions, as well as to the reversal potential for sodium ions, as long as the relevant parameters do not exceed 13% from their normal levels. We also found that blockage of a critical fraction of either sodium or potassium channels (dependent on constant input current) respectively limits the firing activity or increases spontaneous spiking activity of neurons. Our model may be used to guide experiment designs related to ion channel control drug development.

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