Intracellular responses of primary auditory cortical neurons to tones of different frequencies and to electrical stimulation of spiral ganglion fibers in cat

1984 ◽  
Vol 16 (1) ◽  
pp. 112-118 ◽  
Author(s):  
F. N. Serkov ◽  
I. O. Volkov
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.


2001 ◽  
Vol 85 (3) ◽  
pp. 1078-1087 ◽  
Author(s):  
Xiaofeng Ma ◽  
Nobuo Suga

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.


1987 ◽  
Vol 58 (4) ◽  
pp. 765-780 ◽  
Author(s):  
H. Sato ◽  
Y. Hata ◽  
H. Masui ◽  
T. Tsumoto

1. Effects of microionophoretic application of acetylcholine (ACh) and its antagonists on neuronal responses to visual stimuli and to electrical stimulation of the lateral geniculate nucleus were studied in the cat striate cortex. 2. Responses elicited visually and electrically were facilitated by ACh in 74% of the cells tested, whereas the responses were suppressed in 16%. These ACh effects were blocked by a muscarinic antagonist, atropine, but not by a nicotinic antagonist, hexamethonium, indicating that the ACh effects are mediated through muscarinic receptors. A single application of atropine suppressed visual responses of cells facilitated by ACh, whereas it enhanced those of cells inhibited by ACh, suggesting that endogenous ACh may tonically modulate visual responsivity of cortical neurons. 3. In most cells with the facilitatory ACh effect, responses with single spikes to the electrical stimulation became more consistent, often with double spikes, during the ACh application. The suppressive effects of ACh were noted most often in cells with a longer response latency to electrical stimulation of lateral geniculate nucleus. 4. In most of the facilitated cells the spontaneous activity remained null or very low during ACh application, in spite of marked enhancement of visual responses, suggesting that ACh may improve the signal-to-noise ratio (S/N) of cortical neuron activity. To confirm this suggestion, we calculated a S/S + N index by counting the total number of spikes in the responses (S) and that in peristimulus time histogram (S + N) and found that it was improved during the ACh application in about a half of the cells, whereas it became worse in about one-fifth. 5. In most of the facilitated cells, ACh enhanced visual responses not only to optimal but also to nonoptimal stimuli, resulting in no improvement or even worsening of the orientation selectivity. This was also the case in the selectivity of direction of stimulus movement. 6. The laminar location of the facilitated cells was biased toward layers V and VI of the cortex, although they also made up the majority in layers II + III and about half the tested cells in layers IVab and IVc. 7. In the light of recent understanding of cortical circuitry, these results suggest that the cholinergic innervation to cortical neurons may play a role in improvement of the S/N ratio of information processing in the striate cortex and in facilitation of sending processed informations to other visual centers.


1973 ◽  
Vol 82 (4) ◽  
pp. 473-485 ◽  
Author(s):  
Richard Walloch ◽  
David DeWeese ◽  
Robert Brummett ◽  
Jack Vernon

In the guinea pig the effects of electrical stimulation of the inner ear were measured by recording the evoked potentials at the auditory cortex. The cortical evoked responses to electrical stimuli greatly resembled those resulting from auditory stimuli in the same ears. The similarity was in wave shape, latency, duration, sharpness of thresholds, etc. It was also possible to produce evoked cortical responses when the electrical stimuli were delivered to ears suffering from severe acoustic trauma. These ears were so traumatized by acoustic over-stimulation that they were totally unresponsive to sound. In addition, it was possible to produce electrically evoked cortical responses in ears suffering from drug induced damage. The damage was of sufficient long standing as to produce extensive degeneration in the spiral ganglion. The damage was verified histologically and was severe enough to produce a 90% loss of the spiral ganglion cells. Similar electrical stimulation has been carried out in one human subject with normal hearing. Using sinusoidal electrical currents of approximately 10–100 microamperes, hearing sensations were produced only for stimulus frequencies between 4,000 Hz and 10,000 Hz. The intent had been to place a chronic electrode on the round window membrane of a normal human ear. When the same electrode was used to record the alternating current (a.c.) cochlear potential the resulting data were so insensitive as to suggest that the electrode placement had been less than ideal. Exploration revealed the electrode to have been on the floor of the fossula of the cochlea fenestra. A repeat procedure, with improved visualization, located a new chronic electrode on the round window membrane. Recordings and stimulations are currently in progress with that electrode.


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