scholarly journals Visual Deprivation Causes Refinement of Intracortical Circuits in the Auditory Cortex

Cell Reports ◽  
2015 ◽  
Vol 12 (6) ◽  
pp. 955-964 ◽  
Author(s):  
Xiangying Meng ◽  
Joseph P.Y. Kao ◽  
Hey-Kyoung Lee ◽  
Patrick O. Kanold
Keyword(s):  
Auditory Cortex ◽  
Visual Deprivation ◽  
Intracortical Circuits

scholarly journals Intracortical Circuits in Thalamorecipient Layers of Auditory Cortex Refine after Visual Deprivation

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

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 ◽  
...  
Keyword(s):  
Parallel Processing ◽  
Auditory Cortex ◽  
Intracortical Circuits

scholarly journals Network Architecture, Receptive Fields, and Neuromodulation: Computational and Functional Implications of Cholinergic Modulation in Primary Auditory Cortex

2006 ◽  
Vol 96 (6) ◽  
pp. 2972-2983 ◽  
Author(s):  
Gabriel Soto ◽  
Nancy Kopell ◽  
Kamal Sen
Keyword(s):  
Auditory Cortex ◽  
Cortical Neurons ◽  
Network Architecture ◽  
Frequency Tuning ◽  
Receptive Fields ◽  
Primary Auditory Cortex ◽  
Physiological Data ◽  
Cholinergic Modulation ◽  
Tuning Curves ◽  
Intracortical Circuits

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.

scholarly journals Intracortical circuits amplify sound-evoked activity in primary auditory cortex following systemic injection of salicylate in the rat

2012 ◽  
Vol 108 (1) ◽  
pp. 200-214 ◽  
Author(s):  
Daniel Stolzberg ◽  
Michael Chrostowski ◽  
Richard J. Salvi ◽  
Brian L. Allman
Keyword(s):  
Auditory Cortex ◽  
Field Potential ◽  
Primary Auditory Cortex ◽  
High Dose ◽  
Response Type ◽  
Cochlear Function ◽  
Systemic Injection ◽  
Sound Levels ◽  
Intracortical Circuits ◽  
Lower Amplitude

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.

scholarly journals Nicotinic neuromodulation in auditory cortex requires MAPK activation in thalamocortical and intracortical circuits

2012 ◽  
Vol 107 (10) ◽  
pp. 2782-2793 ◽  
Author(s):  
Irakli Intskirveli ◽  
Raju Metherate
Keyword(s):  
Auditory Cortex ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Current Source ◽  
Primary Auditory Cortex ◽  
Mek Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Evoked Responses ◽  
Intracortical Circuits ◽  
Sensory Evoked

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.

scholarly journals Temporary Visual Deprivation Causes Decorrelation of Spatiotemporal Population Responses in Adult Mouse Auditory Cortex

eNeuro ◽  
2019 ◽  
Vol 6 (6) ◽  
pp. ENEURO.0269-19.2019 ◽  
Author(s):  
Krystyna Solarana ◽  
Ji Liu ◽  
Zac Bowen ◽  
Hey-Kyoung Lee ◽  
Patrick O. Kanold
Keyword(s):  
Auditory Cortex ◽  
Adult Mouse ◽  
Visual Deprivation ◽  
Population Responses

scholarly journals Muscarinic modulation of spike-timing dependent plasticity at recurrent layer 2/3 synapses in mouse auditory cortex

2019 ◽  
Author(s):  
Deepti Rao ◽  
Megan B. Kratz ◽  
Paul B. Manis
Keyword(s):  
Auditory Cortex ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Receptor Modulation ◽  
Intracortical Circuits ◽  
Layer 2

AbstractCholinergic systems contribute to the refinement of auditory cortical receptive fields by activating muscarinic acetylcholine receptors (mAChRs). However, the specific cellular and synaptic mechanisms underlying acetylcholine’s effects on cortical circuits are not fully understood. In this study, we investigate the effects of muscarinic receptor modulation on spike-timing dependent plasticity (STDP) at synapses onto layer 2/3 pyramidal neurons in mouse auditory cortex (AC). Synapses onto layer 2/3 pyramidal neurons exhibit a STDP rule for pairing of postsynaptic spike bursts with single presynaptic stimuli. Pre-before-post pairing at +10 ms results in a timing-dependent long-term potentiation (tLTP), whereas pre-before-post pairing at +50 ms intervals, and post-before-pre pairing at -10 to -20 ms produce a timing-dependent long-term depression. We also characterize how mAChR activation affects plasticity at these synapses, focusing on the induction of tLTP. During pre-before-post pairing at +10 ms, mAChR activation by either carbachol or oxotremorine-M suppresses tLTP. mAChR activation also reduces the NMDA-receptor dependent synaptically evoked increase in calcium in dendrites, apparently without affecting presynaptic transmitter release. Pharmacological experiments suggest that M1 and M3 receptors are not involved in the mAChR-mediated suppression of tLTP. Taken together, these results suggest activating mAChRs in layer 2/3 intracortical circuits can modify the circuit dynamics of AC by depressing tLTP mediated by NMDA receptors, and depressing calcium influx at excitatory synapses onto layer 2/3 pyramidal cells.

Influence of kainic acid and long-lasting intermitent hypoxia on auditory cortex

2005 ◽  
Vol 84 (01) ◽  
Author(s):  
P Benesová ◽  
M Langmeier ◽  
J Betka ◽  
S Trojan
Keyword(s):  
Auditory Cortex ◽  
Kainic Acid
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