Physiological differences between histologically defined subdivisions in the mouse auditory thalamus

Anderson, Lucy A.; Linden, JF

doi:10.1016/j.heares.2010.12.016

Cited by 83 publications

(97 citation statements)

References 53 publications

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“…Surgical procedures were similar to those described previously (Anderson and Linden, 2011), except for the use of urethane (1.9 g/kg in a 20% solution, Sigma) for anesthesia and buprenorphine (0.1 mg/kg) for analgesia. All auditory stimuli were presented free-field to the left ear (contralateral to the thalamic recording site), using a speaker (FF1, Tucker-Davis Technologies) positioned at Ϫ45°in azimuth relative to the animal and at the same elevation as the left auditory canal.…”

Section: Methodsmentioning

confidence: 99%

“…As in Anderson and Linden (2011), discrete electrolytic lesions (5 A for 5-7 s) were created to indicate the region of recording within the thalamus. Once physiological recording at each rostrocaudal position had ceased (and before moving to a new rostrocaudal position), electrolytic lesions were made in the most lateral and most medial electrode tracks that had yielded data.…”

Section: Methodsmentioning

confidence: 99%

“…Procedures for histological processing were as described by Anderson et al (2007). Briefly, following an overdose of sodium pentobarbital (Euthatal, i.p.…”

Section: Methodsmentioning

confidence: 99%

“…Similar results were obtained in all cases from Kolmogorov-Smirnov tests for differences in distributions (all MGB and ventral MGB, p Ͻ 1 ϫ 10 Ϫ13 ; dorsal MGB, p ϭ 0.02; medial MGB, p Ͼ 0.2). The deficit in thalamic sensitivity to brief gaps in noise observed in ectopic mice therefore appeared to be subdivision-specific, affecting the lemniscal and perhaps nonlemniscal central auditory pathways but not the polysensory pathway (for further details on these pathways, see Anderson and Linden, 2011).…”

Section: Thalamic-subdivision-specific Deficit In Neural Sensitivity mentioning

confidence: 99%

“…We focused on the auditory thalamus because previous studies have suggested that both ectopia-like cortical abnormalities in animal models (Herman et al, 1997;Peiffer et al, 2002) and developmental disorders in humans (Galaburda et al, 1994;Díaz et al, 2012) cause abnormalities in the auditory thalamus. Furthermore, previous work had suggested that the abnormalities could be specific to particular central auditory pathways, and the three major ascending auditory pathways (lemniscal, nonlemniscal, and polysensory) are much more easily distinguished in the thalamus (Anderson and Linden, 2011) than in the cortex (Lee and Sherman, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Anderson

Linden

2016

J. Neurosci.

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High temporal acuity of auditory processing underlies perception of speech and other rapidly varying sounds. A common measure of auditory temporal acuity in humans is the threshold for detection of brief gaps in noise. Gap-detection deficits, observed in developmental disorders, are considered evidence for "sluggish" auditory processing. Here we show, in a mouse model of gap-detection deficits, that auditory brain sensitivity to brief gaps in noise can be impaired even without a general loss of central auditory temporal acuity. Extracellular recordings in three different subdivisions of the auditory thalamus in anesthetized mice revealed a stimulus-specific, subdivision-specific deficit in thalamic sensitivity to brief gaps in noise in experimental animals relative to controls. Neural responses to brief gaps in noise were reduced, but responses to other rapidly changing stimuli unaffected, in lemniscal and nonlemniscal (but not polysensory) subdivisions of the medial geniculate body. Through experiments and modeling, we demonstrate that the observed deficits in thalamic sensitivity to brief gaps in noise arise from reduced neural population activity following noise offsets, but not onsets. These results reveal dissociable sound-onset-sensitive and sound-offset-sensitive channels underlying auditory temporal processing, and suggest that gap-detection deficits can arise from specific impairment of the sound-offset-sensitive channel.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Procedures for histological processing were as described by Anderson et al (2007). Briefly, following an overdose of sodium pentobarbital (Euthatal, i.p.…”

Section: Methodsmentioning

confidence: 99%

Section: Thalamic-subdivision-specific Deficit In Neural Sensitivity mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Anderson

Linden

2016

J. Neurosci.

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Adenosine A₁ Receptor mRNA Expression by Neurons and Glia in the Auditory Forebrain

Hackett

2018

The Anatomical Record

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In the brain, purines such as ATP and adenosine can function as neurotransmitters and co‐transmitters, or serve as signals in neuron–glial interactions. In thalamocortical (TC) projections to sensory cortex, adenosine functions as a negative regulator of glutamate release via activation of the presynaptic adenosine A1 receptor (A1R). In the auditory forebrain, restriction of A1R‐adenosine signaling in medial geniculate (MG) neurons is sufficient to extend LTP, LTD, and tonotopic map plasticity in adult mice for months beyond the critical period. Interfering with adenosine signaling in primary auditory cortex (A1) does not contribute to these forms of plasticity, suggesting regional differences in the roles of A1R‐mediated adenosine signaling in the forebrain. To advance understanding of the circuitry, in situ hybridization was used to localize neuronal and glial cell types in the auditory forebrain that express A1R transcripts (Adora1), based on co‐expression with cell‐specific markers for neuronal and glial subtypes. In A1, Adora1 transcripts were concentrated in L3/4 and L6 of glutamatergic neurons. Subpopulations of GABAergic neurons, astrocytes, oligodendrocytes, and microglia expressed lower levels of Adora1. In MG, Adora1 was expressed by glutamatergic neurons in all divisions, and subpopulations of all glial classes. The collective findings imply that A1R‐mediated signaling broadly extends to all subdivisions of auditory cortex and MG. Selective expression by neuronal and glial subpopulations suggests that experimental manipulations of A1R‐adenosine signaling could impact several cell types, depending on their location. Strategies to target Adora1 in specific cell types can be developed from the data generated here. Anat Rec, 301:1882–1905, 2018. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.

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Large GABAergic neurons form a distinct subclass within the mouse dorsal cortex of the inferior colliculus with respect to intrinsic properties, synaptic inputs, sound responses, and projections

Geis

Borst

2012

J of Comparative Neurology

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Neurons in the inferior colliculus (IC) show a remarkable diversity in their responses to sound, but it has been difficult to relate these responses to their morphology. Large cells, which are found in all subdivisions of the IC, may form an exception. We found that large neurons of the mouse dorsal cortex of the IC were GABAergic and were contacted by vesicular glutamate transporter 2-containing somatic terminals, as previously observed for the rat IC. Large cells, which were targeted under two-photon guidance, typically had a low input resistance in comparison with the other cells in the dorsal cortex of the IC. Large cells received short-latency excitatory inputs and had short first-spike latencies. These excitatory inputs were often followed by long-latency inhibitory postsynaptic potentials. In four cells, it was possible to reconstruct the ascending axon following labeling with biocytin. We found evidence that they projected to both the ventral and the dorsal divisions of the medial geniculate body of the thalamus, but they also branched off large collaterals while passing through the brachium of the IC. Our data indicate that, owing to their somatic glutamatergic inputs, large GABAergic tectothalamic projection neurons can generate short-latency, well-timed, feed-forward inhibition, which affects not only the thalamus, but also other ascending nuclei. Their remarkably homogeneous properties, which generally differed from those of the other cells in the dorsal cortex of the IC, suggest that large neurons form a distinct subclass within the dorsal cortex of the IC.

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Physiological differences between histologically defined subdivisions in the mouse auditory thalamus

Cited by 83 publications

References 53 publications

Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Adenosine A₁ Receptor mRNA Expression by Neurons and Glia in the Auditory Forebrain

Large GABAergic neurons form a distinct subclass within the mouse dorsal cortex of the inferior colliculus with respect to intrinsic properties, synaptic inputs, sound responses, and projections

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Physiological differences between histologically defined subdivisions in the mouse auditory thalamus

Cited by 83 publications

References 53 publications

Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Mind the Gap: Two Dissociable Mechanisms of Temporal Processing in the Auditory System

Adenosine A1 Receptor mRNA Expression by Neurons and Glia in the Auditory Forebrain

Large GABAergic neurons form a distinct subclass within the mouse dorsal cortex of the inferior colliculus with respect to intrinsic properties, synaptic inputs, sound responses, and projections

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Adenosine A₁ Receptor mRNA Expression by Neurons and Glia in the Auditory Forebrain