Effectiveness of Middle Ear Electrical Stimulation for Activating Central Auditory Pathways

1982 ◽  
Vol 91 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Ben M. Clopton ◽  
Martha M. Bosma

Electrical stimulation of afferent auditory elements through electrodes placed in the middle ear was investigated in acute guinea pig preparations. Thresholds for auditory activation were current-dependent for low frequencies (<1 kHz) and charge-dependent at higher frequencies. Threshold currents were 3–5 times those for intracochlear stimulation. Mechanisms of activation were examined with removal of cochlear fluids and injection of neomycin, Xylocaine, saline, and artificial perilymph with different calcium concentrations. Neurons of the spiral ganglion are indicated as mediators of this stimulation.

1980 ◽  
Vol 89 (2_suppl) ◽  
pp. 5-7 ◽  
Author(s):  
Ben M. Clopton ◽  
Francis A. Spelman ◽  
Josef M. Miller

Electrical stimulation of afferent auditory pathways through electrodes placed within and outside of the cochlea were used to study stimulation and design parameters relevant to a cochlear prosthesis. In the acute guinea pig preparation, the tract response evoked in brachium of the inferior colliculus by electrical stimulation to an ear provided estimates of the effectiveness of various electrode placements. Stimulation between an electrode in the cochlea and a site along the eighth nerve was characterized by the lowest thresholds Stimulation between intracochlear electrodes was somewhat less effective, and stimulation between external electrodes at the nerve, cochlear nucleus, or distant point was least effective. Thresholds, expressed as current, rose at approximately 6 dB per octave for stimulus frequencies from 1 kHz to 16 kHz. Thresholds below 10 μ A rms were seen for optimal placements. These observations suggest that the neural elements being stimulated are the cell bodies of the spiral ganglion cells.


1972 ◽  
Vol 36 (2) ◽  
pp. 350-361 ◽  
Author(s):  
Graeme M. Clark ◽  
J.M. Nathar ◽  
Howard G. Kranz ◽  
Johannes S. Maritz

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 77
Author(s):  
Kristin M. Barry ◽  
Donald Robertson ◽  
Wilhelmina H. A. M. Mulders

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.


1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall

1987 ◽  
Vol 65 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Sylvain Foucart ◽  
Réginald Nadeau ◽  
Jacques de Champlain

The adrenal nerve of anaesthetized and vagotomized dogs was electrically stimulated (10 V pulses of 2 ms duration for 10 min) at frequencies of 1, 3, 10, and 25 Hz. There was a correlation between the frequency of stimulation and the plasma concentrations of epinephrine, norepinephrine, and dopamine in the adrenal vein, mainly after the 1st min of stimulation and the maximal concentration was reached sooner with higher frequencies of stimulation. Moreover, the relative percentage of catecholamines released in response to the electrical stimulation was not changed by the frequency of stimulation. To test the hypothesis that a local negative feedback mechanism mediated by α2-adrenoceptors exists in the adrenal medulla, the effects of the systemic administration of clonidine (α2-agonist) and yohimbine (α2-antagonist) on the concentrations of catecholamines in the adrenal vein were evaluated during the electrical stimulation of the adrenal nerve (5 V pulses of 2 ms duration for 3 min) at 3 Hz. Moreover, the effects of the systemic injections of more specific α2-agonist and antagonist (oxymetazoline and idazoxan) were tested on the release of catecholamines in the adrenal vein in response to electrical stimulation of the splanchnic nerve at 1 and 3 Hz frequencies. The injection of 0.5 mg/kg of yohimbine caused a significant increase in the concentrations of epinephrine and norepinephrine in the adrenal vein induced by the electrical stimulation of the adrenal nerve and the injection of 15 μg/kg of clonidine had no effects. In the second series of experiments, the injection of 2 μg/kg of oxymetazoline caused a significant decrease in the release of epinephrine and norepinephrine at 1 Hz, but similarly to clonidine, there were no changes at 3 Hz. In contrast, the release of epinephrine and dopamine in response to electrical stimulation of the splanchnic nerve was increased at 3 Hz after the injection of idazoxan, but not at 1 Hz. It is concluded that the adrenal medulla catecholamines secretion appears to be partly modulated by a presynaptic inhibitory mechanism that involves α2-adrenoceptors. The observation that agonists appear to be more efficient at low frequencies of stimulation while antagonists appear to be more efficient at higher frequencies could be explained by the possibility that adrenal medullary α2-receptors would be saturated at higher frequencies of stimulation.


2014 ◽  
Vol 307 (7) ◽  
pp. G719-G731 ◽  
Author(s):  
Guo-Du Wang ◽  
Xi-Yu Wang ◽  
Sumei Liu ◽  
Meihua Qu ◽  
Yun Xia ◽  
...  

Mast cells express the substance P (SP) neurokinin 1 receptor and the calcitonin gene-related peptide (CGRP) receptor in guinea pig and human small intestine. Enzyme-linked immunoassay showed that activation of intramural afferents by antidromic electrical stimulation or by capsaicin released SP and CGRP from human and guinea pig intestinal segments. Electrical stimulation of the afferents evoked slow excitatory postsynaptic potentials (EPSPs) in the enteric nervous system. The slow EPSPs were mediated by tachykinin neurokinin 1 and CGRP receptors. Capsaicin evoked slow EPSP-like responses that were suppressed by antagonists for protease-activated receptor 2. Afferent stimulation evoked slow EPSP-like excitation that was suppressed by mast cell-stabilizing drugs. Histamine and mast cell protease II were released by 1) exposure to SP or CGRP, 2) capsaicin, 3) compound 48/80, 4) elevation of mast cell Ca2+ by ionophore A23187, and 5) antidromic electrical stimulation of afferents. The mast cell stabilizers cromolyn and doxantrazole suppressed release of protease II and histamine when evoked by SP, CGRP, capsaicin, A23187, electrical stimulation of afferents, or compound 48/80. Neural blockade by tetrodotoxin prevented mast cell protease II release in response to antidromic electrical stimulation of mesenteric afferents. The results support a hypothesis that afferent innervation of enteric mast cells releases histamine and mast cell protease II, both of which are known to act in a diffuse paracrine manner to influence the behavior of enteric nervous system neurons and to elevate the sensitivity of spinal afferent terminals.


1995 ◽  
Vol 73 (7) ◽  
pp. 903-907 ◽  
Author(s):  
M. Qtsuka ◽  
K. Yoshioka ◽  
M. Yanagisawa ◽  
H. Suzuki ◽  
F.-Y. Zhao ◽  
...  

Tachykinin NK1 receptor antagonists were used to explore the physiological functions of substance P (SP) and neurokinin A (NKA). Pharmacological profiles of three NK1 receptor antagonists, GR71251, GR82334, and RP 67580, were examined in the isolated spinal cord preparation of the neonatal rat. These tachykinin receptor antagonists exhibited considerable specificities and antagonized the actions of both SP and NKA to induce the depolarization of ventral roots. Electrical stimulation of the saphenous nerve with C-fiber strength evoked a depolarization lasting about 30 s of the ipsilateral L3 ventral root. This response, which is referred to as saphenous-nerve-evoked slow ventral root potential (VRP), was depressed by these NK1 receptor antagonists. In contrast, the saphenous-nerve-evoked slow VRP was potentiated by application of a mixture of peptidase inhibitors, including thiorphan, actinonin, and captopril in the presence of naloxone, but not after further addition of GR71251. Likewise, in the isolated coeliac ganglion of the guinea pig, electrical stimulation of the mesenteric nerves evoked in some ganglionic cells slow excitatory postsynaptic potentials (EPSPs), which were depressed by GR71251 and potentiated by peptidase inhibitors. These results further support the notion that SP and NKA serve as neurotransmitters producing slow EPSPs in the neonatal rat spinal cord and guinea pig prevertebral ganglia.Key words: substance P, neurokinin A, neurotransmitter, tachykinin antagonist, spinal cord.


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