Plasticity of Bat's Central Auditory System Evoked by Focal Electric Stimulation of Auditory and/or Somatosensory Cortices

2001 ◽  
Vol 85 (3) ◽  
pp. 1078-1087 ◽  
Author(s):  
Xiaofeng Ma ◽  
Nobuo Suga
Keyword(s):  
Electrical Stimulation ◽  
Somatosensory Cortex ◽  
Cortical Neurons ◽  
Electric Stimulation ◽  
Time Course ◽  
Recovery Period ◽  
Acoustic Stimulus ◽  
Acoustic Parameter ◽  
Response Curves ◽  
Stimulation Of

Recent findings indicate that the corticofugal system would play an important role in cortical plasticity as well as collicular plasticity. To understand the role of the corticofugal system in plasticity, therefore, we studied the amount and the time course of plasticity in the inferior colliculus (IC) and auditory cortex (AC) evoked by focal electrical stimulation of the AC and also the effect of electrical stimulation of the somatosensory cortex on the plasticity evoked by the stimulation of the AC. In adult big brown bats ( Eptesicus fuscus), we made the following major findings. 1) Electric stimulation of the AC evokes best frequency (BF) shifts, i.e., shifts in frequency-response curves of collicular and cortical neurons. These BF shifts start to occur within 2 min, reach a maximum (or plateau) at 30 min, and then recover ∼180 min after a 30-min-long stimulus session. When the stimulus session is lengthened from 30 to 90 min, the plateau lasts ∼60 min, but BF shifts recover ∼180 min after the session. 2) The electric stimulation of the somatosensory cortex delivered immediately after that of the AC, as in fear conditioning, evokes a dramatic lengthening of the recovery period of the cortical BF shifts but not that of the collicular BF shift. The electric stimulation of the somatosensory cortex delivered before that of the AC, as in backward conditioning, has no effect on the collicular and cortical BF shifts. 3) Electric stimulation of the AC evokes BF shifts not only in the ipsilateral IC and AC but also in the contralateral IC and AC. BF shifts are smaller in amount and shorter in recovery time for contralateral collicular and cortical neurons than for ipsilateral ones. Our findings support the hypothesis that the AC and the corticofugal system have an intrinsic mechanism for reorganization of the IC and AC, that the reorganization is highly specific to a value of an acoustic parameter (frequency), and that the reorganization is augmented by excitation of nonauditory sensory cortex that makes the acoustic stimulus behaviorally relevant to the animal through associative learning.

scholarly journals Augmentation of Plasticity of the Central Auditory System by the Basal Forebrain and/or Somatosensory Cortex

2003 ◽  
Vol 89 (1) ◽  
pp. 90-103 ◽  
Author(s):  
Xiaofeng Ma ◽  
Nobuo Suga
Keyword(s):  
Somatosensory Cortex ◽  
Auditory System ◽  
Basal Forebrain ◽  
Cortical Neurons ◽  
Electric Stimulation ◽  
Cortical Plasticity ◽  
Frequency Tuning ◽  
Cortical Stimulation ◽  
Cholinergic Basal Forebrain ◽  
Stimulation Of

Auditory conditioning (associative learning) or focal electric stimulation of the primary auditory cortex (AC) evokes reorganization (plasticity) of the cochleotopic (frequency) map of the inferior colliculus (IC) as well as that of the AC. The reorganization results from shifts in the best frequencies (BFs) and frequency-tuning curves of single neurons. Since the importance of the cholinergic basal forebrain for cortical plasticity and the importance of the somatosensory cortex and the corticofugal auditory system for collicular and cortical plasticity have been demonstrated, Gao and Suga proposed a hypothesis that states that the AC and corticofugal system play an important role in evoking auditory collicular and cortical plasticity and that auditory and somatosensory signals from the cerebral cortex to the basal forebrain play an important role in augmenting collicular and cortical plasticity. To test their hypothesis, we studied whether the amount and the duration of plasticity of both collicular and cortical neurons evoked by electric stimulation of the AC or by acoustic stimulation were increased by electric stimulation of the basal forebrain and/or the somatosensory cortex. In adult big brown bats ( Eptesicus fuscus), we made the following major findings. 1) Collicular and cortical plasticity evoked by electric stimulation of the AC is augmented by electric stimulation of the basal forebrain. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 2) Collicular and cortical plasticity evoked by AC stimulation is augmented by somatosensory cortical stimulation mimicking fear conditioning. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 3) Collicular and cortical plasticity evoked by both AC and basal forebrain stimulations is further augmented by somatosensory cortical stimulation. 4) A lesion of the basal forebrain tends to reduce collicular and cortical plasticity evoked by AC stimulation. The reduction is small and statistically insignificant for collicular plasticity but significant for cortical plasticity. 5) The lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. 6) Collicular and cortical plasticity evoked by repetitive acoustic stimuli is augmented by basal forebrain and/or somatosensory cortical stimulation. However, the lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. These findings support the hypothesis proposed by Gao and Suga.

scholarly journals Electrical Stimulation of Injected Muscles to Boost Botulinum Toxin Effect on Spasticity: Rationale, Systematic Review and State of the Art

Toxins ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 303
Author(s):  
Alessandro Picelli ◽  
Mirko Filippetti ◽  
Giorgio Sandrini ◽  
Cristina Tassorelli ◽  
Roberto De Icco ◽  
...  
Keyword(s):  
Systematic Review ◽  
Electrical Stimulation ◽  
Botulinum Toxin ◽  
Current Literature ◽  
Electric Stimulation ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Botulinum Toxins ◽  
Stimulation Of

Botulinum toxin type A (BoNT-A) represents a first-line treatment for spasticity, a common disabling consequence of many neurological diseases. Electrical stimulation of motor nerve endings has been reported to boost the effect of BoNT-A. To date, a wide range of stimulation protocols has been proposed in the literature. We conducted a systematic review of current literature on the protocols of electrical stimulation to boost the effect of BoNT-A injection in patients with spasticity. A systematic search using the MeSH terms “electric stimulation”, “muscle spasticity” and “botulinum toxins” and strings “electric stimulation [mh] OR electrical stimulation AND muscle spasticity [mh] OR spasticity AND botulinum toxins [mh] OR botulinum toxin type A” was conducted on PubMed, Scopus, PEDro and Cochrane library electronic databases. Full-text articles written in English and published from database inception to March 2021 were included. Data on patient characteristics, electrical stimulation protocols and outcome measures were collected. This systematic review provides a complete overview of current literature on the role of electrical stimulation to boost the effect of BoNT-A injection for spasticity, together with a critical discussion on its rationale based on the neurobiology of BoNT-A uptake.

Activation of thalamic ventroposteriolateral neurons by phrenic nerve afferents in cats and rats

2003 ◽  
Vol 94 (1) ◽  
pp. 220-226 ◽  
Author(s):  
Weirong Zhang ◽  
Paul W. Davenport
Keyword(s):  
Electrical Stimulation ◽  
Somatosensory Cortex ◽  
Phrenic Nerve ◽  
Proprioceptive Information ◽  
Neural Responses ◽  
Afferent Stimulation ◽  
Physiological Conditions ◽  
Sensory Pathways ◽  
Increased Activity ◽  
Stimulation Of

It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex.

Electrical stimulation of the primary somatosensory cortex inhibits spinal dorsal horn neuron activity

2005 ◽  
Vol 1057 (1-2) ◽  
pp. 134-140 ◽  
Author(s):  
Arun K. Senapati ◽  
Paula J. Huntington ◽  
Stacey C. LaGraize ◽  
Hilary D. Wilson ◽  
Perry N. Fuchs ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Somatosensory Cortex ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Dorsal Horn Neuron ◽  
Neuron Activity ◽  
Spinal Dorsal ◽  
Spinal Dorsal Horn Neuron ◽  
Horn Neuron ◽  
Stimulation Of

Production of Threshold Levels of Conscious Sensation by Electrical Stimulation of Human Somatosensory Cortex

1993 ◽  
pp. 1-34 ◽  
Author(s):  
B. Libet ◽  
W. W. Alberts ◽  
E. W. Wright ◽  
L. D. Delattre ◽  
G. Levin ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Somatosensory Cortex ◽  
Threshold Levels ◽  
Stimulation Of

scholarly journals Utility of Periurethral Electric Stimulation to Reduce Voiding Frequency in Rats

2009 ◽  
Vol 3 (2) ◽  
Author(s):  
A. Forrest ◽  
Y. Zhang ◽  
A. Bicek ◽  
G. Timm
Keyword(s):  
Electrical Stimulation ◽  
Electric Stimulation ◽  
The United States ◽  
The Body ◽  
Bladder Pressure ◽  
Urinary Continence ◽  
Sprague Dawley ◽  
Promising Alternative ◽  
Surgical Interventions ◽  
Stimulation Of

Urinary continence is maintained through coordination of electrical (nervous) and mechanical (muscles, ligaments and other structures) systems in the body. During micturition, the central nervous system sends a signal to the detrusor and sphincter muscles to coordinate voiding. Pathological problems can undermine either of the two systems and result in urinary incontinence (UI). Thirteen million people in the United States live with UI. Clinical treatments to date are largely mechanical in nature, restoring function through surgical interventions. However, electrically-based treatments, such as electric stimulation, offer a promising alternative. Here we investigate the utility of electrical stimulation of the periurethral neuromusculature to reduce voiding contractions in well-controlled animal experiments. Female Sprague Dawley rats were anesthetized with a ketamine/xylazine/acepromazine cocktail and the bladder was catheterized through a small incision in the bladder dome and was infused with saline. Continuous filling of the bladder triggered related cycles of voiding which was identified through bladder pressure increases and visual urination. The pubic symphysis bone was cut to expose the urethra and a stimulating electrode was placed in the periurethral region. The electrical stimulation parameters were 2.8 mA of current, 200 us pluses, and 20 Hz. The electrical stimulation was done in fifteen minute intervals. Statistically, the rats without electrical stimulation have an average contraction period of 63.1 sec (+/– 31.3 sec) and the rats with electrical stimulation have an average contraction period of 97.2 sec (+/– 43.0 sec). The results showed that the electrical stimulation of the periurethral neuromusculature in the group revealed 54.0% increase in average contraction period and decrease in voiding frequency. Electrical stimulation of the periurethral neuromusculature increases the voiding interval and void volume for the rats. This suggests the existence of an external urinary sphincter to the bladder inhibitory pathway and supports periurethral neuromusculature stimulation as an alternative to spinal nerve stimulation for the treatment of bladder overactivity.

Intrinsic discharge patterns and somatosensory inputs for neurons in raccoon primary somatosensory cortex

1994 ◽  
Vol 72 (6) ◽  
pp. 2827-2839 ◽  
Author(s):  
P. J. Istvan ◽  
P. Zarzecki
Keyword(s):  
Somatosensory Cortex ◽  
Cortical Neurons ◽  
Primary Somatosensory Cortex ◽  
Membrane Properties ◽  
Postsynaptic Potentials ◽  
Synaptic Inputs ◽  
Ionic Conductances ◽  
Discharge Patterns ◽  
Intrinsic Membrane Properties ◽  
Stimulation Of

1. Discharge patterns of neurons are regulated by synaptic inputs and by intrinsic membrane properties such as their complement of ionic conductances. Discharge patterns evoked by synaptic inputs are often used to identify the source and modality of sensory input. However, the interpretation of these discharge patterns may be complicated if different neurons respond to the same synaptic input with a variety of discharge patterns due to differences in intrinsic membrane properties. The purposes of this study were 1) to investigate intrinsic discharge patterns of neurons in primary somatosensory cortex of raccoon in vivo and 2) to use somatosensory postsynaptic potentials evoked by stimulation of forepaw digits to determine thalamocortical connectivity for the same neurons. 2. Conventional intracellular recordings with sharp electrodes were made from 121 neurons in the cortical representation of glabrous skin of digit four (d4). Intracellular injection of identical current pulses (100-120 ms in duration) elicited various patterns of discharge in different neurons. Neurons were classified on the basis of these intrinsic patterns of discharge, rates of spike adaptation, and characteristics of spike waveforms. Three main groups were identified: regular spiking (RS) neurons, intrinsic bursting (IB) neurons, and fast spiking (FS) neurons. Subclasses were identified for the RS and IB groups. 3. Neurons were tested for somatosensory inputs by stimulating electrically d3, d4, and d5. Excitatory postsynaptic potentials (EPSPs) were elicited in 100% of the neurons by electrical stimulation of d4, the "on-focus" digit. EPSPs were usually followed by inhibitory postsynaptic potentials (IPSPs). Many neurons (41%) responded with EPSP-IPSP sequences after stimulation of d3 or d5, the "off-focus" digits. 4. Latencies of somatosensory EPSPs and IPSPs were used to determine the synaptic order in the cortical circuitry of RS, IB, and FS neurons. EPSPs with monosynaptic thalamocortical latencies were recorded in RS, IB, and FS neurons. 5. We conclude that precise patterns of neural discharge in primary somatosensory cortex cannot be reliable estimates of sensory inputs reaching these neurons because patterns of discharge are so strongly influenced by intrinsic membrane properties. Ionic conductances governing patterns of neuronal discharge seem almost identical in intact cortex of raccoon, rat, and cat, and in slices of rodent cortex, because similar patterns of discharge are found. The consistency of patterns of discharge across species and types of preparation suggests that these intrinsic membrane properties are a general property of cerebral cortical neurons and should be considered when evaluation sensory coding by these neurons.

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