scholarly journals Effects of Multisession Anodal Electrical Stimulation of the Auditory Cortex on Temporary Noise-Induced Hearing Loss in the Rat

2021 ◽  
Vol 15 ◽  
Author(s):  
Iván Díaz ◽  
Ana Cecilia Colmenárez-Raga ◽  
David Pérez-González ◽  
Venezia G. Carmona ◽  
Ignacio Plaza Lopez ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Optical Density ◽  
Outer Hair Cell ◽  
Acoustic Trauma ◽  
Experimental Conditions ◽  
Compensatory Response ◽  
Epidural Stimulation ◽  
Efferent System ◽  
Efferent Neurons ◽  
Experimental Approaches

The protective effect of the efferent system against acoustic trauma (AT) has been shown by several experimental approaches, including damage to one ear, sectioning of the olivocochlear bundle (OCB) in the floor of the IV ventricle, and knock-in mice overexpressing outer hair cell (OHC) cholinergic receptors, among others. Such effects have been related to changes in the regulation of the cholinergic efferent system and in cochlear amplification, which ultimately reverse upon protective hearing suppression. In addition to well-known circuits of the brainstem, the descending corticofugal pathway also regulates efferent neurons of the olivary complex. In this study, we applied our recently developed experimental paradigm of multiple sessions of electrical stimulation (ES) to activate the efferent system in combination with noise overstimulation. ABR thresholds increased 1 and 2 days after AT (8–16 kHz bandpass noise at 107 dB for 90 min) recovering at AT + 14 days. However, after multiple sessions of epidural anodal stimulation, no changes in thresholds were observed following AT. Although an inflammatory response was also observed 1 day after AT in both groups, the counts of reactive macrophages in both experimental conditions suggest decreased inflammation in the epidural stimulation group. Quantitative immunocytochemistry for choline acetyltransferase (ChAT) showed a significant decrease in the size and optical density of the efferent terminals 1 day after AT and a rebound at 14 days, suggesting depletion of the terminals followed by a long-term compensatory response. Such a synthesis recovery was significantly higher upon cortical stimulation. No significant correlation was found between ChAT optical density and size of the buttons in sham controls (SC) and ES/AT + 1day animals; however, significant negative correlations were shown in all other experimental conditions. Therefore, our comparative analysis suggests that cochleotopic cholinergic neurotransmission is also better preserved after multisession epidural stimulation.

scholarly journals Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 77
Author(s):  
Kristin M. Barry ◽  
Donald Robertson ◽  
Wilhelmina H. A. M. Mulders
Keyword(s):  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Auditory System ◽  
Acoustic Trauma ◽  
Neuron Activity ◽  
Compensatory Mechanism ◽  
Efferent Connections ◽  
Medial Geniculate ◽  
Central Auditory Pathways ◽  
Stimulation Of

In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception.

Formation of sarcomeres in developing myotubes: role of mechanical stretch and contractile activation

2000 ◽  
Vol 279 (6) ◽  
pp. C1801-C1811 ◽  
Author(s):  
Patrick G. De Deyne
Keyword(s):  
Electrical Stimulation ◽  
Structural Alignment ◽  
Major Change ◽  
Mechanical Stretch ◽  
Experimental Conditions ◽  
Pharmacological Agents ◽  
Cultured Myotubes ◽  
Contractile Activation ◽  
Sarcomere Assembly ◽  
Passive Stretch

In a series of experiments, cultured myotubes were exposed to passive stretch or pharmacological agents that block contractile activation. Under these experimental conditions, the formation of Z lines and A bands (morphological structures, resulting from the specific structural alignment of sarcomeric proteins, necessary for contraction) was assessed by immunofluorescence. The addition of an antagonist of the voltage-gated Na+ channels [tetrodotoxin (TTX)] for 2 days in developing rat myotube cultures led to a nearly total absence of Z lines and A bands. When contractile activation was allowed to resume for 2 days, the Z lines and A bands reappeared in a significant way. The appearance of Z lines or A bands could not be inhibited nor facilitated by the application of a uniaxial passive stretch. Electrical stimulation of the cultures increased sarcomere assembly significantly. Antagonists of L-type Ca2+ channels (verapamil, nifedipine) combined with electrical stimulation led to the absence of Z lines and A bands to the same degree as the TTX treatment. Western blot analysis did not show a major change in the amount of sarcomeric α-actinin nor a shift in myosin heavy chain phenotype as a result of a 2-day passive stretch or TTX treatment. Results of experiments suggest that temporal Ca2+ transients play an important factor in the assembly and maintenance of sarcomeric structures during muscle fiber development.

Reflex Inhibition of Normal Cramp Following Electrical Stimulation of the Muscle Tendon

2007 ◽  
Vol 98 (3) ◽  
pp. 1102-1107 ◽  
Author(s):  
Serajul I. Khan ◽  
John A. Burne
Keyword(s):  
Electrical Stimulation ◽  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Muscle Cramp ◽  
Emg Activity ◽  
Reflex Inhibition ◽  
Experimental Conditions ◽  
Inhibitory Feedback ◽  
Two Phases ◽  
Stimulation Of

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I1, I2) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.

scholarly journals Distinct forms of synaptic plasticity during ascending vs descending control of medial olivocochlear efferent neurons

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Gabriel E Romero ◽  
Laurence O Trussell
Keyword(s):  
Dynamic Range ◽  
Short Term ◽  
Wide Dynamic Range ◽  
Efferent System ◽  
Short Term Plasticity ◽  
Ventral Cochlear Nucleus ◽  
Brainstem Nucleus ◽  
Reflex Arc ◽  
Efferent Neurons ◽  
Medial Olivocochlear

Activity in each brain region is shaped by the convergence of ascending and descending axonal pathways, and the balance and characteristics of these determine neural output. The medial olivocochlear (MOC) efferent system is part of a reflex arc that critically controls auditory sensitivity. Multiple central pathways contact MOC neurons, raising the question of how a reflex arc could be engaged by diverse inputs. We examined functional properties of synapses onto brainstem MOC neurons from ascending (ventral cochlear nucleus, VCN), and descending (inferior colliculus, IC) sources in mice using an optogenetic approach. We found that these pathways exhibited opposing forms of short-term plasticity, with VCN input showing depression and IC input showing marked facilitation. By using a conductance clamp approach, we found that combinations of facilitating and depressing inputs enabled firing of MOC neurons over a surprisingly wide dynamic range, suggesting an essential role for descending signaling to a brainstem nucleus.

scholarly journals The Cholinergic Lateral Line Efferent Synapse: Structural, Functional and Molecular Similarities With Those of the Cochlea

2021 ◽  
Vol 15 ◽  
Author(s):  
Paola V. Plazas ◽  
Ana Belén Elgoyhen
Keyword(s):  
Lateral Line ◽  
Sk Channels ◽  
Afferent Activity ◽  
Intact Specimen ◽  
Efferent System ◽  
Synaptic Physiology ◽  
Efferent Neurons ◽  
Medial Olivocochlear ◽  
Subsequent Activation ◽  
Mammalian Counterpart

Vertebrate hair cell (HC) systems are innervated by efferent fibers that modulate their response to external stimuli. In mammals, the best studied efferent-HC synapse, the cholinergic medial olivocochlear (MOC) efferent system, makes direct synaptic contacts with HCs. The net effect of MOC activity is to hyperpolarize HCs through the activation of α9α10 nicotinic cholinergic receptors (nAChRs) and the subsequent activation of Ca2+-dependent SK2 potassium channels. A serious obstacle in research on many mammalian sensory systems in their native context is that their constituent neurons are difficult to access even in newborn animals, hampering circuit observation, mapping, or controlled manipulation. By contrast, fishes and amphibians have a superficial and accessible mechanosensory system, the lateral line (LL), which circumvents many of these problems. LL responsiveness is modulated by efferent neurons which aid to distinguish between external and self-generated stimuli. One component of the LL efferent system is cholinergic and its activation inhibits LL afferent activity, similar to what has been described for MOC efferents. The zebrafish (Danio rerio) has emerged as a powerful model system for studying human hearing and balance disorders, since LL HC are structurally and functionally analogous to cochlear HCs, but are optically and pharmacologically accessible within an intact specimen. Complementing mammalian studies, zebrafish have been used to gain significant insights into many facets of HC biology, including mechanotransduction and synaptic physiology as well as mechanisms of both hereditary and acquired HC dysfunction. With the rise of the zebrafish LL as a model in which to study auditory system function and disease, there has been an increased interest in studying its efferent system and evaluate the similarity between mammalian and piscine efferent synapses. Advances derived from studies in zebrafish include understanding the effect of the LL efferent system on HC and afferent activity, and revealing that an α9-containing nAChR, functionally coupled to SK channels, operates at the LL efferent synapse. In this review, we discuss the tools and findings of these recent investigations into zebrafish efferent-HC synapse, their commonalities with the mammalian counterpart and discuss several emerging areas for future studies.

scholarly journals Evaluation of outer hair cell function and medial olivocochlear efferent system in patients with type II diabetes mellitus

2014 ◽  
Vol 44 ◽  
pp. 150-156 ◽  
Author(s):  
Hayriye KARABULUT ◽  
İsmail KARABULUT ◽  
Muharrem DAĞLI ◽  
Yıldırım Ahmet BAYAZIT ◽  
Şule BİLEN ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Hair Cell ◽  
Type Ii Diabetes ◽  
Outer Hair Cell ◽  
Cell Function ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Efferent System ◽  
Medial Olivocochlear ◽  
Medial Olivocochlear Efferent System

Avoidance and approach learning motivated by stimulation of identical hypothalamic loci

1959 ◽  
Vol 197 (1) ◽  
pp. 153-157 ◽  
Author(s):  
George W. Brown ◽  
Bertram D. Cohen
Keyword(s):  
Electrical Stimulation ◽  
Lateral Hypothalamus ◽  
Opportunity To Learn ◽  
Hypothalamic Stimulation ◽  
Experimental Conditions ◽  
Approach Response ◽  
Lateral Hypothalamic ◽  
Stimulating Electrodes ◽  
Second Procedure ◽  
Stimulation Of

Cats with stimulating electrodes implanted in the lateral hypothalamus were subjected to two types of experimental procedures. In the first procedure the cats were given an opportunity to learn to avoid hypothalamic stimulation which produces a typical ‘hypothalamic rage’ response. The second procedure allows the same cats to learn to approach an area where the hypothalamic stimulus is administered. In both procedures, electrical stimulation was delivered through identical electrodes, yet each animal learned the appropriate avoidance or approach response, depending upon the experimental conditions. Therefore, lateral hypothalamic stimulation may act as an energizing, drive-arousing, operation to produce both avoidance and approach learning in cats.

Spike-Wave Complexes and Fast Components of Cortically Generated Seizures. IV. Paroxysmal Fast Runs in Cortical and Thalamic Neurons

1998 ◽  
Vol 80 (3) ◽  
pp. 1495-1513 ◽  
Author(s):  
Igor Timofeev ◽  
François Grenier ◽  
Mircea Steriade
Keyword(s):  
Electrical Stimulation ◽  
High Frequency ◽  
Cortical Neurons ◽  
Field Potential ◽  
Thalamic Nuclei ◽  
Experimental Conditions ◽  
Thalamic Neurons ◽  
Single Action ◽  
Spike Bursts ◽  
Spike Wave

Timofeev, Igor, François Grenier, and Mircea Steriade. Spike-wave complexes and fast components of cortically generated seizures. IV. Paroxysmal fast runs in cortical and thalamic neurons. J. Neurophysiol. 80: 1495–1513, 1998. In the preceding papers of this series, we have analyzed the cellular patterns and synchronization of neocortical seizures occurring spontaneously or induced by electrical stimulation or cortical infusion of bicuculline under a variety of experimental conditions, including natural states of vigilance in behaving animals and acute preparations under different anesthetics. The seizures consisted of two distinct components: spike-wave (SW) or polyspike-wave (PSW) at 2–3 Hz and fast runs at 10–15 Hz. Because the thalamus is an input source and target of cortical neurons, we investigated here the seizure behavior of thalamic reticular (RE) and thalamocortical (TC) neurons, two major cellular classes that have often been implicated in the generation of paroxysmal episodes. We performed single and dual simultaneous intracellular recordings, in conjunction with multisite field potential and extracellular unit recordings, from neocortical areas and RE and/or dorsal thalamic nuclei under ketamine-xylazine and barbiturate anesthesia. Both components of seizures were analyzed, but emphasis was placed on the fast runs because of their recent investigation at the cellular level. 1) The fast runs occurred at slightly different frequencies and, therefore, were asynchronous in various cortical neuronal pools. Consequently, dorsal thalamic nuclei, although receiving convergent inputs from different neocortical areas involved in seizure, did not express strongly synchronized fast runs. 2) Both RE and TC cells were hyperpolarized during seizure episodes with SW/PSW complexes and relatively depolarized during the fast runs. As known, hyperpolarization of thalamic neurons deinactivates a low-threshold conductance that generates high-frequency spike bursts. Accordingly, RE neurons discharged prolonged high-frequency spike bursts in close time relation with the spiky component of cortical SW/PSW complexes, whereas they fired single action potentials, spike doublets, or triplets during the fast runs. In TC cells, the cortical fast runs were reflected as excitatory postsynaptic potentials appearing after short latencies that were compatible with monosynaptic activation through corticothalamic pathways. 3) The above data suggested the cortical origin of these seizures. To further test this hypothesis, we performed experiments on completely isolated cortical slabs from suprasylvian areas 5 or 7 and demonstrated that electrical stimulation within the slab induces seizures with fast runs and SW/PSW complexes, virtually identical to those elicited in intact-brain animals. The conclusion of all papers in this series is that complex seizure patterns, resembling those described at the electroencephalogram level in different forms of clinical seizures with SW/PSW complexes and, particularly, in the Lennox-Gastaut syndrome of humans, are generated in neocortex. Thalamic neurons reflect cortical events as a function of membrane potential in RE/TC cells and degree of synchronization in cortical neuronal networks.

scholarly journals Hsp70/Bmi1-FoxO1-SOD Signaling Pathway Contributes to the Protective Effect of Sound Conditioning against Acute Acoustic Trauma in a Rat Model

2020 ◽  
Vol 2020 ◽  
pp. 1-22
Author(s):  
Guoxia Zhu ◽  
Yongxiang Wu ◽  
Yang Qiu ◽  
Keyong Tian ◽  
Wenjuan Mi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Rat Model ◽  
Molecular Mechanisms ◽  
Outer Hair Cell ◽  
Acoustic Trauma ◽  
Auditory Brainstem Responses ◽  
Ultrastructural Changes ◽  
Ganglion Neurons ◽  
Acute Acoustic Trauma

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.

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