scholarly journals The Effect of Calcium Ions on Mechanosensation and Neuronal Activity in Proprioceptive Neurons

NeuroSci ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 353-371
Author(s):  
Devan E. Atkins ◽  
Kimberly L. Bosh ◽  
Grace W. Breakfield ◽  
Sydney E. Daniels ◽  
Makayla J. Devore ◽  
...  

Proprioception of all animals is important in being able to have coordinated locomotion. Stretch activated ion channels (SACs) transduce the mechanical force into electrical signals in the proprioceptive sensory endings. The types of SACs vary among sensory neurons in animals as defined by pharmacological, physiological and molecular identification. The chordotonal organs within insects and crustaceans offer a unique ability to investigate proprioceptive function. The effects of the extracellular environment on neuronal activity, as well as the function of associated SACs are easily accessible and viable in minimal saline for ease in experimentation. The effect of extracellular [Ca2+] on membrane properties which affect voltage-sensitivity of ion channels, threshold of action potentials and SACs can be readily addressed in the chordotonal organ in crab limbs. It is of interest to understand how low extracellular [Ca2+] enhances neural activity considering the SACs in the sensory endings could possibly be Ca2+ channels and that all neural activity is blocked with Mn2+. It is suggested that axonal excitability might be affected independent from the SAC activity due to potential presence of calcium activated potassium channels (K(Ca)) and the ability of Ca2+ to block voltage gated Na+ channels in the axons. Separating the role of Ca2+ on the function of the SACs and the excitability of the axons in the nerves associated with chordotonal organs is addressed. These experiments may aid in understanding the mechanisms of neuronal hyperexcitability during hypocalcemia within mammals.

1998 ◽  
Vol 80 (2) ◽  
pp. 771-784 ◽  
Author(s):  
Christian Walther ◽  
Klaus E. Zittlau ◽  
Harald Murck ◽  
Karlheinz Voigt

Walther, Christian, Klaus E. Zittlau, Harald Murck, and Karlheinz Voigt. Resting membrane properties of locust muscle and their modulation. I. Actions of the neuropeptides YGGFMRFamide and proctolin. J. Neurophysiol. 80: 771–784, 1998. The resting K+ conductance ( G K,r) of locust jumping muscle and its modulation by two neuropeptides, proctolin (Arg-Tyr-Leu-Pro-Thr) and YGGFMRFamide (Tyr-Gly-Gly-Phe-Met-Arg-Phe-NH2), were investigated using the two-electrode voltage clamp. At a physiological [K+]o of 10 mM, G K,r accounts for ∼90% of the membrane resting conductance, and the resting membrane potential differs by ≤1 mV from E K (mean: −74 mV). There is a K+ conductance that slowly activates on hyperpolarization ( G K,H) and that seems to be largely located in the transverse tubules. Steady-state activation of G K,H was analyzed by tail current measurements. G K,H is activated partially at E K but accounts for probably ≤50% of total resting K+ conductance. Raising [K+]o caused a large increase in G K,r and in maximal steady state G K,H without shifting the voltage sensitivity of G K,H. YGGFMRFamide and proctolin reduce G K,H, mainly affecting the maximal steady-state conductance. The voltage-insensitive component of the resting K+ conductance is also reduced. The conductance suppressed by the peptides exhibited an outwardly rectifying instantaneous current/voltage-characteristic that is quite similar to that of G K,H. The actions of the two peptides appeared to be identical, but proctolin was by some two orders of magnitude more potent than YGGFMRFamide. The effects of both peptides are mediated by G proteins. They are mimicked by phorbol esters but do not seem to be initiated by either branch of the phospholipase C-dependent intracellular pathways. The properties of the resting K+ conductance in locust muscle and other invertebrate muscles are compared. The biological significance of peptide-induced reduction in resting K+ conductance is discussed in view of the known property of proctolin to support tonic force as opposed to FMRFamide-peptides that support quick leg movements.


2017 ◽  
Vol 117 (2) ◽  
pp. 738-755 ◽  
Author(s):  
Nareg Berberian ◽  
Amanda MacPherson ◽  
Eloïse Giraud ◽  
Lydia Richardson ◽  
J.-P. Thivierge

In various regions of the brain, neurons discriminate sensory stimuli by decreasing the similarity between ambiguous input patterns. Here, we examine whether this process of pattern separation may drive the rapid discrimination of visual motion stimuli in the lateral intraparietal area (LIP). Starting with a simple mean-rate population model that captures neuronal activity in LIP, we show that overlapping input patterns can be reformatted dynamically to give rise to separated patterns of neuronal activity. The population model predicts that a key ingredient of pattern separation is the presence of heterogeneity in the response of individual units. Furthermore, the model proposes that pattern separation relies on heterogeneity in the temporal dynamics of neural activity and not merely in the mean firing rates of individual neurons over time. We confirm these predictions in recordings of macaque LIP neurons and show that the accuracy of pattern separation is a strong predictor of behavioral performance. Overall, results propose that LIP relies on neuronal pattern separation to facilitate decision-relevant discrimination of sensory stimuli. NEW & NOTEWORTHY A new hypothesis is proposed on the role of the lateral intraparietal (LIP) region of cortex during rapid decision making. This hypothesis suggests that LIP alters the representation of ambiguous inputs to reduce their overlap, thus improving sensory discrimination. A combination of computational modeling, theoretical analysis, and electrophysiological data shows that the pattern separation hypothesis links neural activity to behavior and offers novel predictions on the role of LIP during sensory discrimination.


1999 ◽  
Vol 202 (12) ◽  
pp. 1579-1587 ◽  
Author(s):  
M.C. Göpfert ◽  
L.T. Wasserthal

The labral pilifers are thought to contain auditory sensory cells in hawkmoths of two distantly related subtribes, the Choerocampina and the Acherontiina. We identified and analysed these cells using neurophysiological and neuroanatomical techniques. In the death's head hawkmoth Acherontia atropos, we found that the labral nerve carries the auditory afferent responses of a single auditory unit. This unit responds to ultrasonic stimulation with minimum thresholds of 49–57 dB SPL around 25 kHz. Ablation experiments and analyses of the neuronal activity in different regions of the pilifer revealed that the auditory afferent response originates in the basal pilifer region. The sensory organ was identified as a chordotonal organ that attaches to the base of the pilifer. This organ is the only sensory structure in the basal pilifer region and consists of a single mononematic scolopidium and a single sensory cell. In Choerocampina, a homologous scolopidium was also found and is probably the only sensory structure of the pilifer that might serve an auditory function. Since a pilifer chordotonal organ with only a single scolopidium has also been detected in a non-hearing hawkmoth species, hearing in the distantly related choerocampine and acherontiine hawkmoths presumably evolved from a single proprioceptive mechanoreceptor cell that is present in all hawkmoths.


2019 ◽  
Vol 122 (3) ◽  
pp. 1123-1135 ◽  
Author(s):  
C. J. Scavuzzo ◽  
M. J. LeBlancq ◽  
F. Nargang ◽  
H. Lemieux ◽  
T. J. Hamilton ◽  
...  

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.


2012 ◽  
Vol 102 (8) ◽  
pp. 1815-1825 ◽  
Author(s):  
Huaiyu Yang ◽  
Zhaobing Gao ◽  
Ping Li ◽  
Kunqian Yu ◽  
Ye Yu ◽  
...  

2012 ◽  
Vol 24 (7) ◽  
pp. 1634-1644 ◽  
Author(s):  
Liping Wang ◽  
Xianchun Li ◽  
Steven S. Hsiao ◽  
Mark Bodner ◽  
Fred Lenz ◽  
...  

The neuronal activity in the primary somatosensory cortex was collected when monkeys performed a haptic–haptic DMS task. We found that, in trials with correct task performance, a substantial number of cells showed significant differential neural activity only when the monkeys had to make a choice between two different haptic objects. Such a difference in neural activity was significantly reduced in incorrect response trials. However, very few cells showed the choice-only differential neural activity in monkeys who performed a control task that was identical to the haptic–haptic task but did not require the animal to either actively memorize the sample or make a choice between two objects at the end of a trial. From these results, we infer that the differential activity recorded from cells in the primary somatosensory cortex in correct performance reflects the neural process of behavioral choice, and therefore, it is a neural correlate of decision-making when the animal has to make a haptic choice.


2013 ◽  
Vol 30 (5-6) ◽  
pp. 331-342 ◽  
Author(s):  
BENJAMIN HAYDEN ◽  
TATIANA PASTERNAK

AbstractIn the 1990s, seminal work from Newsome and colleagues made it possible to study the neuronal mechanisms of simple perceptual decisions. The key strength of this work was the clear and direct link between neuronal activity and choice processes. Since then, a great deal of research has extended these initial discoveries to more complex forms of decision making, with the goal of bringing the same strength of linkage between neural and psychological processes. Here, we discuss the progress of two such research programs, namely our own, that are aimed at understanding memory-guided decisions and reward-guided decisions. These problems differ in the relevant brain areas, in the progress that has been achieved, and in the extent of broader understanding achieved so far. However, they are unified by the use of theoretical insights about how to link neuronal activity to decisions.


2014 ◽  
pp. S205-S213 ◽  
Author(s):  
S. BOUKALOVA ◽  
F. TOUSKA ◽  
L. MARSAKOVA ◽  
A. HYNKOVA ◽  
L. SURA ◽  
...  

Gain-of-function (GOF) mutations in ion channels are rare events, which lead to increased agonist sensitivity or altered gating properties, and may render the channel constitutively active. Uncovering and following characterization of such mutants contribute substantially to the understanding of the molecular basis of ion channel functioning. Here we give an overview of some GOF mutants in polymodal ion channels specifically involved in transduction of painful stimuli – TRPV1 and TRPA1, which are scrutinized by scientists due to their important role in development of some pathological pain states. Remarkably, a substitution of single amino acid in the S4-S5 region of TRPA1 (N855S) has been recently associated with familial episodic pain syndrome. This mutation increases chemical sensitivity of TRPA1, but leaves the voltage sensitivity unchanged. On the other hand, mutations in the analogous region of TRPV1 (R557K and G563S) severely affect all aspects of channel activation and lead to spontaneous activity. Comparison of the effects induced by mutations in homologous positions in different TRP receptors (or more generally in other distantly related ion channels) may elucidate the gating mechanisms conserved during evolution.


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