BOLD-fMRI in the mouse auditory pathway

Freches, Guilherme Blazquez; Chavarrías, Cristina; Shemesh, Noam

doi:10.1016/j.neuroimage.2017.10.027

Cited by 16 publications

(14 citation statements)

References 57 publications

(80 reference statements)

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“…Although normal vascular physiological condition can be achieved with mechanical ventilation, as was done with resting-state fMRI 38 , we chose not to intubate to limit possible arousal and the technical difficulty of mouse intubation. Furthermore, evoked sensory studies using medetomidine/isoflurane or ketamine/xylazine in mice have adopted self-breathing state which is closer to our experiment design 6 , 9 , 34 , 35 , 40 .…”

Section: Discussionmentioning

confidence: 99%

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Characterization of brain-wide somatosensory BOLD fMRI in mice under dexmedetomidine/isoflurane and ketamine/xylazine

You

Kim

2021

Sci Rep

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Mouse fMRI under anesthesia has become increasingly popular due to improvement in obtaining brain-wide BOLD response. Medetomidine with isoflurane has become well-accepted for resting-state fMRI, but whether this combination allows for stable, expected, and robust brain-wide evoked response in mice has yet to be validated. We thus utilized intravenous infusion of dexmedetomidine with inhaled isoflurane and intravenous infusion of ketamine/xylazine to elucidate whether stable mouse physiology and BOLD response are obtainable in response to simultaneous forepaw and whisker-pad stimulation throughout 8 h. We found both anesthetics result in hypercapnia with depressed heart rate and respiration due to self-breathing, but these values were stable throughout 8 h. Regardless of the mouse condition, brain-wide, robust, and stable BOLD response throughout the somatosensory axis was observed with differences in sensitivity and dynamics. Dexmedetomidine/isoflurane resulted in fast, boxcar-like, BOLD response with consistent hemodynamic shapes throughout the brain. Ketamine/xylazine response showed higher sensitivity, prolonged BOLD response, and evidence for cortical disinhibition as significant bilateral cortical response was observed. In addition, differing hemodynamic shapes were observed between cortical and subcortical areas. Overall, we found both anesthetics are applicable for evoked mouse fMRI studies.

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Section: Discussionmentioning

confidence: 99%

“…Similarly, improvements in coils, which detect the signal, such as the cryogenically cooled volume coil helps to increase the signal to noise ratio 4 , 5 . These improvements have led to a growth of successful rodent fMRI experiments that has supplemented translational brain research 6 – 11 .…”

Section: Introductionmentioning

confidence: 99%

Characterization of brain-wide somatosensory BOLD fMRI in mice under dexmedetomidine/isoflurane and ketamine/xylazine

You

Kim

2021

Sci Rep

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“…OPN3 is also expressed in the mouse retina ( Nissilä et al, 2012 ; Buhr et al, 2015 ), possibly explaining OPN3-mCh expression in the LGd of the thalamus, which is the terminal region of most retinal ganglion cells ( Szentagothai, 1963 ). OPN3-mCh is furthermore expressed in many regions essential for the relay and processing of auditory information: auditory cortex, medial geniculate complex of the thalamus, inferior colliculus and superior olivary complex of the midbrain and hindbrain, respectively ( Oh et al, 2014 ; Blazquez Freches et al, 2018 ). We also found OPN3-mCh in the motor nuclei of the thalamus, the motor area of the CTX, Purkinje cells, and other nuclei of the cerebellum and in ventral pontine nuclei.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Opsin 3 (OPN3) Protein Expression in the Adult Brain Using a Novel OPN3-mCherry Knock-In Mouse Model

Olinski

Tsuda

Kauer

et al. 2020

eNeuro

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The opsins have been studied extensively for their functions in visual phototransduction; however, the mechanisms underlying extraocular opsin signaling remain poorly understood. The first mammalian extraocular opsin to be discovered, opsin 3 (OPN3), was found in the brain more than two decades ago, yet its function remains unknown. A significant hindrance to studying OPN3 has been a lack of specific antibodies against mammalian OPN3, resulting in an incomplete understanding of its expression in the brain. Although Opn3 promoter-driven reporter mice have been generated to examine general OPN3 localization, they lack the regulated expression of the endogenous protein and the ability to study its subcellular localization. To circumvent these issues, we have created a knock-in OPN3-mCherry mouse model in which the fusion protein OPN3-mCherry is expressed Significance Statement Before the current report, there had been a significant lack of encephalic opsin 3 (OPN3) protein characterization, likely driven by the absence of murine OPN3 antibodies. This study describes a novel OPN3-mCherry knock-in mouse that we used to analyze endogenous OPN3 protein expression across the brain. We have uncovered new aspects of OPN3: localization to previously undocumented brain subregions, expression in GABAergic neurons and non-neuronal cells, and punctate subcellular localization in the soma. Our OPN3 expression map is an invaluable step toward discovering its elusive encephalic functions. The OPN3-mCherry mouse will facilitate investigation of OPN3 not only in the brain, but also across the entire organism, a useful feature as OPN3 is emerging as a possible mediator of phototransduction outside the brain.

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“…Reducing voxel size increases spatial resolution, but also decreases BOLD signal per voxel and, hence, signal-to-noise ratio (SNR) as well 53 . Since higher magnetic field can enhance BOLD signals 54,55 , ultra-high field MRI has been used in some studies 39,56 . We used Spin Echo-Echo Planar Imaging (SE-EPI) sequence for high-resolution fMRI at ultra-high magnetic fields 55,57 .…”

Section: Discussionmentioning

confidence: 99%

Hyper BOLD Activation in Dorsal Raphe Nucleus of APP/PS1 Alzheimer’s Disease Mouse during Reward-Oriented Drinking Test under Thirsty Conditions

Sakurai

Shintani

Jomura

et al. 2020

Sci Rep

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Alzheimer's disease (AD), a neurodegenerative disease, causes behavioural abnormalities such as disinhibition, impulsivity, and hyperphagia. preclinical studies using AD model mice have investigated these phenotypes by measuring brain activity in awake, behaving mice. in this study, we monitored the behavioural alterations of impulsivity and hyperphagia in middle-aged AD model mice. As a behavioural readout, we trained the mice to accept a water-reward under thirsty conditions. to analyse brain activity, we developed a measure for licking behaviour combined with visualisation of whole brain activity using awake fMRI. In a water-reward learning task, the AD model mice showed significant hyperactivity of the dorsal raphe nucleus in thirsty conditions. in summary, we successfully visualised altered brain activity in AD model mice during reward-oriented behaviour for the first time using awake fMRi. this may help in understanding the causes of behavioural alterations in AD patients.Fifty million people worldwide currently suffer from dementia. This number is estimated to reach 130 million by 2050. Alzheimer's disease (AD) is a neurodegenerative disease accounting for 60-70% of dementia cases 1 . AD develops through amnestic mild cognitive impairment (MCI), in which a decrease of memory function is the only symptom can be recognised. Once dementia develops, memory and various cognitive functions decrease, behavioural and psychological symptoms of dementia (BPSP) are also exhibited 1-3 . As these symptoms progress, it becomes impossible to maintain an independent daily life. Dementia patients mostly need medical care due to BPSP rather than reducing of memory and cognitive functions. BPSP includes depression, anxiety, and apathy. Although research on these BPSP symptoms has progressed, however, most symptoms such as disinhibition, impulsivity and hyperphagia have not been analysed in the way of pathology.AD significantly impairs reward-based behaviour (by 15-20%) in patients. A typical example is hyperphagia, which stems from a lack of satiety control, similar to disorders of impulsivity and compulsivity 4,5 . The Urgency, lack of Perseverance, lack of Premeditation, Sensation Seeking (UPPS) Scale or Barrat's Impulsiveness Scale (BIS) are now used to test for impulsivity in AD patients 3 . Overeating and impulsivity have also recently been reported in AD model mice 6,7 . These observations suggest that AD mice models may be useful in studying hyperphagia and early changes in impulsive behaviour. It has also been suggested that the brainstem serotonergic system, including the dorsal raphe nucleus 8,9 and ventral temporal lobe (hippocampus, parahippocampus, amygdala), are involved in such alterations. However, the neurological mechanisms behind these phenotypes have not yet been identified. In order to elucidate these mechanistic underpinnings, direct evaluation of brain activity associated with abnormal behaviour phenotypes is required 10 .Functional magnetic resonance imaging (fMRI) is widely used in neuroscience resea...

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BOLD-fMRI in the mouse auditory pathway

Cited by 16 publications

References 57 publications

Characterization of brain-wide somatosensory BOLD fMRI in mice under dexmedetomidine/isoflurane and ketamine/xylazine

Characterization of brain-wide somatosensory BOLD fMRI in mice under dexmedetomidine/isoflurane and ketamine/xylazine

Endogenous Opsin 3 (OPN3) Protein Expression in the Adult Brain Using a Novel OPN3-mCherry Knock-In Mouse Model

Hyper BOLD Activation in Dorsal Raphe Nucleus of APP/PS1 Alzheimer’s Disease Mouse during Reward-Oriented Drinking Test under Thirsty Conditions

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