Photoacoustic effect invokes auditory response in infrared neuron stimulation

Infrared neuron stimulation is regarded as an innovative approach for stimulating cochleae in animals while the exact mechanism still remains unknown. In this paper, we studied compound action potentials of guinea pig cochleae with chronic or acute deafness. We recorded optical compound action potentials and analyzed stretched cochlear preparations by fluorescence microscopy. Photoacoustic signals were measured by hydrophone and microphone, respectively. In our experiment, we observed a switch response effect in vitro and in vivo experiments. Therefore, we proposed photoacoustic effect could invoke auditory response in infrared neuron stimulation.

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Stretch of mammalian nerve in vitro: Effect on compound action potentials

Journal of the Peripheral Nervous System ◽

10.1046/j.1529-8027.2000.00025.x ◽

2000 ◽

Vol 5 (4) ◽

pp. 227-235 ◽

Cited By ~ 13

Author(s):

Sidney Ochs ◽

Rahman Pourmand ◽

Kenan Si ◽

Richard N. Friedman

Keyword(s):

Action Potentials ◽

Compound Action Potentials ◽

Vitro Effect ◽

Mammalian Nerve ◽

Compound Action

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Neuroprotective Effects of Increased Extracellular Ca2+ During Aglycemia in White Matter

Journal of Neurophysiology ◽

10.1152/jn.2002.88.3.1302 ◽

2002 ◽

Vol 88 (3) ◽

pp. 1302-1307 ◽

Cited By ~ 8

Author(s):

Angus M. Brown ◽

Bruce R. Ransom

Keyword(s):

Action Potentials ◽

Divalent Cations ◽

Neuroprotective Effects ◽

Adult Rat ◽

Artificial Cerebrospinal Fluid ◽

Before And After ◽

Compound Action Potentials ◽

Compound Action

We investigated the effects of extracellular [Ca2+] ([Ca2+]o) on aglycemia-induced dysfunction and injury in adult rat optic nerves. Compound action potentials (CAPs) from adult rat optic nerve were recorded in vitro, and the area under the CAP was used to monitor nerve function before and after 1 h periods of aglycemia. In control artificial cerebrospinal fluid (ACSF) containing 2 mM Ca2+, CAP function fell after 29.9 ± 1.5 (SE) min and recovered to 48.8 ± 3.9% following aglycemia. Reducing bath [Ca2+] during aglycemia progressively improved recovery. For example, in Ca2+-free ACSF, the CAP recovered to 99.1 ± 3.8%. Paradoxically, increasing bath [Ca2+] also improved recovery from aglycemia. In 5 or 10 mM bath [Ca2+], CAP recovered to 78.8 ± 9.2 or 91.6 ± 5.2%, respectively. The latency to CAP failure during aglycemia increased as a function of bath [Ca2+] from 0 to 10 mM. Increasing bath [Mg2+] from 2 to 5 or 10 mM, with bath [Ca2+] held at 2 mM, increased latency to CAP failure with aglycemia and improved recovery from this insult. [Ca2+]o recorded with calcium-sensitive microelectrodes in control ACSF, dropped reversibly during aglycemia from 1.54 ± 0.03 to 0.45 ± 0.04 mM. In the presence of higher ambient levels of bath [Ca2+] (i.e., 5 or 10 mM), the aglycemia-induced decrease in [Ca2+]o declined, indicating that less Ca2+ left the extracellular space to enter an intracellular compartment. These results indicate that the role of [Ca2+], and divalent cations in general, during aglycemia is complex. While extracellular Ca2+ was required for irreversible aglycemic injury to occur, higher levels of [Ca2+] or [Mg2+] increased the latency to CAP failure and improved the extent of recovery, apparently by limiting Ca2+ influx. These effects are theorized to be mediated by divalent cation screening.

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