scholarly journals Parallel Processing of Sound Dynamics across Mouse Auditory Cortex via Spatially Patterned Thalamic Inputs and Distinct Areal Intracortical Circuits

Cell Reports ◽  
2019 ◽  
Vol 27 (3) ◽  
pp. 872-885.e7 ◽  
Author(s):  
Ji Liu ◽  
Matthew R. Whiteway ◽  
Alireza Sheikhattar ◽  
Daniel A. Butts ◽  
Behtash Babadi ◽  
...  
Cell Reports ◽  
2015 ◽  
Vol 12 (6) ◽  
pp. 955-964 ◽  
Author(s):  
Xiangying Meng ◽  
Joseph P.Y. Kao ◽  
Hey-Kyoung Lee ◽  
Patrick O. Kanold

Author(s):  
Josef P. Rauschecker ◽  
Biao Tian ◽  
Timothy Pons ◽  
Mortimer Mishkin

1998 ◽  
Vol 3 (2-3) ◽  
pp. 86-103 ◽  
Author(s):  
Josef P. Rauschecker

2006 ◽  
Vol 96 (6) ◽  
pp. 2972-2983 ◽  
Author(s):  
Gabriel Soto ◽  
Nancy Kopell ◽  
Kamal Sen

Two fundamental issues in auditory cortical processing are the relative importance of thalamocortical versus intracortical circuits in shaping response properties in primary auditory cortex (ACx), and how the effects of neuromodulators on these circuits affect dynamic changes in network and receptive field properties that enhance signal processing and adaptive behavior. To investigate these issues, we developed a computational model of layers III and IV (LIII/IV) of AI, constrained by anatomical and physiological data. We focus on how the local and global cortical architecture shape receptive fields (RFs) of cortical cells and on how different well-established cholinergic effects on the cortical network reshape frequency-tuning properties of cells in ACx. We identify key thalamocortical and intracortical circuits that strongly affect tuning curves of model cortical neurons and are also sensitive to cholinergic modulation. We then study how differential cholinergic modulation of network parameters change the tuning properties of our model cells and propose two different mechanisms: one intracortical (involving muscarinic receptors) and one thalamocortical (involving nicotinic receptors), which may be involved in rapid plasticity in ACx, as recently reported in a study by Fritz and coworkers.


2012 ◽  
Vol 108 (1) ◽  
pp. 200-214 ◽  
Author(s):  
Daniel Stolzberg ◽  
Michael Chrostowski ◽  
Richard J. Salvi ◽  
Brian L. Allman

A high dose of sodium salicylate temporarily induces tinnitus, mild hearing loss, and possibly hyperacusis in humans and other animals. Salicylate has well-established effects on cochlear function, primarily resulting in the moderate reduction of auditory input to the brain. Despite decreased peripheral sensitivity and output, salicylate induces a paradoxical enhancement of the sound-evoked field potential at the level of the primary auditory cortex (A1). Previous electrophysiologic studies have begun to characterize changes in thalamorecipient layers of A1; however, A1 is a complex neural circuit with recurrent intracortical connections. To describe the effects of acute systemic salicylate treatment on both thalamic and intracortical sound-driven activity across layers of A1, we applied current-source density (CSD) analysis to field potentials sampled across cortical layers in the anesthetized rat. CSD maps were normally characterized by a large, short-latency, monosynaptic, thalamically driven sink in granular layers followed by a lower amplitude, longer latency, polysynaptic, intracortically driven sink in supragranular layers. Following systemic administration of salicylate, there was a near doubling of both granular and supragranular sink amplitudes at higher sound levels. The supragranular sink amplitude input/output function changed from becoming asymptotic at approximately 50 dB to sharply nonasymptotic, often dominating the granular sink amplitude at higher sound levels. The supragranular sink also exhibited a significant decrease in peak latency, reflecting an acceleration of intracortical processing of the sound-evoked response. Additionally, multiunit (MU) activity was altered by salicylate; the normally onset/sustained MU response type was transformed into a primarily onset response type in granular and infragranular layers. The results from CSD analysis indicate that salicylate significantly enhances sound-driven response via intracortical circuits.


2012 ◽  
Vol 107 (10) ◽  
pp. 2782-2793 ◽  
Author(s):  
Irakli Intskirveli ◽  
Raju Metherate

Activation of nicotinic acetylcholine receptors (nAChRs) by systemic nicotine enhances sensory-cognitive function and sensory-evoked cortical responses. Although nAChRs mediate fast neurotransmission at many synapses in the nervous system, nicotinic regulation of cortical processing is neuromodulatory. To explore potential mechanisms of nicotinic neuromodulation, we examined whether intracellular signal transduction involving mitogen-activated protein kinase (MAPK) contributes to regulation of tone-evoked responses in primary auditory cortex (A1) in the mouse. Systemic nicotine enhanced characteristic frequency (CF) tone-evoked current-source density (CSD) profiles in A1, including the shortest-latency (presumed thalamocortical) current sink in layer 4 and longer-latency (presumed intracortical) sinks in layers 2–4, by increasing response amplitudes and decreasing response latencies. Microinjection of the MAPK kinase (MEK) inhibitor U0126 into the thalamus, targeting the auditory thalamocortical pathway, blocked the effect of nicotine on the initial (thalamocortical) CSD component but did not block enhancement of longer-latency (intracortical) responses. Conversely, microinjection of U0126 into supragranular layers of A1 blocked nicotine's effect on intracortical, but not thalamocortical, CSD components. Simultaneously with enhancement of CF-evoked responses, responses to spectrally distant (nonCF) stimuli were reduced, implying nicotinic “sharpening” of frequency receptive fields, an effect also blocked by MEK inhibition. Consistent with these physiological results, acoustic stimulation with nicotine produced immunolabel for activated MAPK in A1, primarily in layer 2/3 cell bodies. Immunolabel was blocked by intracortical microinjection of the nAChR antagonist dihydro-β-erythroidine, but not methyllycaconitine, implicating α4β2*, but not α7, nAChRs. Thus activation of MAPK in functionally distinct forebrain circuits—thalamocortical, local intracortical, and long-range intracortical—underlies nicotinic neuromodulation of A1.


eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Alexandre Hyafil ◽  
Lorenzo Fontolan ◽  
Claire Kabdebon ◽  
Boris Gutkin ◽  
Anne-Lise Giraud

Many environmental stimuli present a quasi-rhythmic structure at different timescales that the brain needs to decompose and integrate. Cortical oscillations have been proposed as instruments of sensory de-multiplexing, i.e., the parallel processing of different frequency streams in sensory signals. Yet their causal role in such a process has never been demonstrated. Here, we used a neural microcircuit model to address whether coupled theta–gamma oscillations, as observed in human auditory cortex, could underpin the multiscale sensory analysis of speech. We show that, in continuous speech, theta oscillations can flexibly track the syllabic rhythm and temporally organize the phoneme-level response of gamma neurons into a code that enables syllable identification. The tracking of slow speech fluctuations by theta oscillations, and its coupling to gamma-spiking activity both appeared as critical features for accurate speech encoding. These results demonstrate that cortical oscillations can be a key instrument of speech de-multiplexing, parsing, and encoding.


2010 ◽  
Vol 206 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Gregg H. Recanzone ◽  
Yale E. Cohen

eNeuro ◽  
2017 ◽  
Vol 4 (2) ◽  
pp. ENEURO.0092-17.2017 ◽  
Author(s):  
Xiangying Meng ◽  
Joseph P. Y. Kao ◽  
Hey-Kyoung Lee ◽  
Patrick O. Kanold

2005 ◽  
Vol 16 (1) ◽  
pp. 18-30 ◽  
Author(s):  
Koji Inui ◽  
Hidehiko Okamoto ◽  
Kensaku Miki ◽  
Atsuko Gunji ◽  
Ryusuke Kakigi

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