Transcranial photo-inactivation of neural activities in the mouse auditory cortex

Kubota, Yamato; Kamatani, Daiki; Tsukano, Hiroaki; Ohshima, Shinsuke; Takahashi, Kuniyuki; Hishida, Ryuichi; Kudoh, Masaharu; Takahashi, Sugata; Shibuki, Katsuei

doi:10.1016/j.neures.2007.12.013

Cited by 40 publications

(57 citation statements)

References 50 publications

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“…The close temporal correlation of the spinal AFI response to electrical input is in agreement with other in vivo AFI studies using direct electrical stimulation of the somatosensory cortex (Shibuki et al, 2003) or cerebellum (Reinert et al, 2004;Gao et al, 2006;Wang et al, 2009). The somatotopic distribution of the AFI response that we found after sciatic nerve stimulation is in agreement with in vivo AFI studies using tactile, auditory, and visual stimuli and AFI recordings from the somatosensory cortex (Shibuki et al, 2003;Murakami et al, 2004), barrel cortex (Weber et al, 2004), auditory cortex (Takahashi et al, 2006;Kubota et al, 2008), or visual cortex (Tohmi et al, 2006;Husson et al, 2007), respectively. Furthermore, the absence of an AFI response after electrical blockade of the sciatic nerve by lidocaine indicated that the AFI signal was indeed generated by sciatic nerve input.…”

Section: Discussionsupporting

confidence: 91%

Autofluorescent Flavoprotein Imaging of Spinal Nociceptive Activity

Jongen¹,

Pederzani²,

Koekkoek³

et al. 2010

J. Neurosci.

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Pain arises from activation of peripheral nociceptors, and strong noxious stimuli may cause an increase in spinal excitability called central sensitization, which is likely involved in many pathological pain states. So far, it has not been achieved to simultaneously visualize in vivo both the temporal and spatial aspects of spinal activity, including central sensitization. Using autofluorescent flavoprotein imaging (AFI), an optical technique suitable for mapping activity in nervous tissue, we demonstrate a close temporal and spatial correlation of electrically evoked nociceptive input with the spinal AFI signal, representing spinal neuronal activity. The AFI signal increases linearly with stimulation intensity. Furthermore, we found that the AFI signal was much larger in intensity and size when the same electrical stimulation was applied after the induction of central sensitization by a subcutaneous capsaicin injection. Finally, innocuous palpation of the hindpaw did not evoke an AFI response in naive animals, but after capsaicin injection a strong response was obtained. This is the first report demonstrating simultaneously the temporal and spatial propagation of spinal nociceptive activity in vivo.

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Section: Discussionsupporting

confidence: 91%

Autofluorescent Flavoprotein Imaging of Spinal Nociceptive Activity

Jongen¹,

Pederzani²,

Koekkoek³

et al. 2010

J. Neurosci.

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“…The surgical procedures and imaging experiments were performed as described previously (Tohmi et al, 2006;Kubota et al, 2008;Kitaura et al, 2010). Mice were anesthetized with urethane (1.65 g/kg, i.p.).…”

Section: Methodsmentioning

confidence: 99%

“…Activity-dependent fluorescence changes derived from mitochondrial flavoproteins have been used in vivo for visualizing brain activities (Shibuki et al, 2003;Reinert et al, 2004). Cortical fluorescence changes can be imaged through the intact skull without surgical damage to the brain in mice (Tohmi et al, 2006;Kubota et al, 2008;Kitaura et al, 2010). Flavoprotein signals are resistant to and spontaneously recover from photobleaching (Kubota et al, 2008) and quantitatively reflect neural activities (Tohmi et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Cortical fluorescence changes can be imaged through the intact skull without surgical damage to the brain in mice (Tohmi et al, 2006;Kubota et al, 2008;Kitaura et al, 2010). Flavoprotein signals are resistant to and spontaneously recover from photobleaching (Kubota et al, 2008) and quantitatively reflect neural activities (Tohmi et al, 2006). Therefore, we used this technique to quantify the cortical changes after peripheral nerve cutting.…”

Section: Introductionmentioning

confidence: 99%

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Initial Phase of Neuropathic Pain within a Few Hours after Nerve Injury in Mice

Komagata

Chen²,

Suzuki³

et al. 2011

J. Neurosci.

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We tested a hypothesis that the spinal plasticity induced within a few hours after nerve injury may produce changes in cortical activities and an initial phase of neuropathic pain. Somatosensory cortical responses elicited by vibratory stimulation were visualized by transcranial flavoprotein fluorescence imaging in mice. These responses were reduced immediately after cutting the sensory nerves. However, the remaining cortical responses mediated by nearby nerves were potentiated within a few hours after nerve cutting. Nerve injury induces neuropathic pain. In the present study, mice exhibited tactile allodynia 1-2 weeks after nerve injury. Lesioning of the ipsilateral dorsal column, mediating tactile cortical responses, abolished somatic cortical responses to tactile stimuli. However, nontactile cortical responses appeared in response to the same tactile stimuli within a few hours after nerve injury, indicating that tactile allodynia was acutely initiated. We investigated the trigger mechanisms underlying the cortical changes. Endogenous glial cell line-derived neurotrophic factor (GDNF), found in the Meissner corpuscles, induced basal firing ϳ0.

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“…Interestingly, localised and reversible inactivation of mitochondrial and neuronal function has been achieved in vivo by prolonged exposure to blue light, which can cause reversible inactivation of fl avoproteins [ 61 ]. This however also has implications on the reliability and effect of prolonged imaging of any autofl uorescent molecules, particularly fl avoproteins.…”

Section: Mitochondrial Redox Potentialmentioning

confidence: 99%

Mitochondrial Function and Dynamics Imaged In Vivo

Chisholm

Peters

Schiza

et al. 2016

Mitochondrial Dysfunction in Neurodegenerative Disorders

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The previous chapters have described the extraordinary depth of knowledge of mitochondrial biology revealed by in vitro observations where the environment can be closely controlled. However, in recent years there has been increased interest in the study of mitochondria in vivo, where their properties can be studied with high spatial and temporal resolution while ensuring that key factors such as the oxygen and glucose concentrations are physiologically accurate. Advances facilitating such in vivo research include improved microscope systems and mitochondrially targeted dyes, as well as a wide range of transgenic animals expressing fl uorescent proteins. Such in vivo observations provide a more realistic picture of mitochondrial involvement in health and disease and also offer the potential to reveal novel targets for therapeutic interventions. For example, loss of mitochondrial membrane potential and alterations in mitochondrial morphology and traffi cking have been reported in mouse models of multiple sclerosis and Alzheimer's disease, and redox potential changes have been reported during (patho)physiological changes in oxygen supply and demand.In this chapter we summarise some techniques used in imaging of mitochondria in vivo, followed by a summary of key fi ndings and recent advances in the study of mitochondrial function and dynamics. We aim to provide insight into the benefi ts and limitations of intravital imaging of mitochondria in the nervous system.

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Transcranial photo-inactivation of neural activities in the mouse auditory cortex

Cited by 40 publications

References 50 publications

Autofluorescent Flavoprotein Imaging of Spinal Nociceptive Activity

Autofluorescent Flavoprotein Imaging of Spinal Nociceptive Activity

Initial Phase of Neuropathic Pain within a Few Hours after Nerve Injury in Mice

Mitochondrial Function and Dynamics Imaged In Vivo

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