Intrinsic electrophysiology of neurons in thalamorecipient layers of developing rat auditory cortex

Metherate, Raju; Aramakis, V B

doi:10.1016/s0165-3806(99)00058-9

Cited by 61 publications

(51 citation statements)

References 62 publications

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“…Consistent with previous reports (30,31), the recorded L5 neurons displayed three different firing patterns in response to suprathreshold depolarizing current pulses: intrinsic bursting (IB; Fig. 1 A), regular spiking (RS; Fig.…”

Section: Resultssupporting

confidence: 90%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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Severe hearing loss during early development is associated with deficits in speech and language acquisition. Although functional studies have shown a deafness-induced alteration of synaptic strength, it is not known whether long-term synaptic plasticity depends on auditory experience. In this study, sensorineural hearing loss (SNHL) was induced surgically in developing gerbils at postnatal day 10, and excitatory synaptic plasticity was examined subsequently in a brain slice preparation that preserves the thalamorecipient auditory cortex. Extracellular stimuli were applied at layer 6 (L6), whereas evoked excitatory synaptic potentials (EPSPs) were recorded from L5 neurons by using a whole-cell current clamp configuration. In control neurons, the conditioning stimulation of L6 significantly altered EPSP amplitude for at least 1 h. Approximately half of neurons displayed long-term potentiation (LTP), whereas the other half displayed long-term depression (LTD). In contrast, SNHL neurons displayed only LTD after the conditioning stimulation of L6. Finally, the vast majority of neurons recorded from control prehearing animals (postnatal days 9 -11) displayed LTD after L6 stimulation. Thus, normal auditory experience may be essential for the maturation of synaptic plasticity mechanisms.deafness ͉ long-term depression S evere hearing loss is known to affect auditory processing in humans. This loss includes impairments of signal detection in noise or in a multiple source environment, and disruption of intensity discrimination, frequency discrimination, and temporal resolution (1-4). Even transient bouts of conductive hearing loss can disrupt auditory processing, and months or years may be required for normal perception to resolve (5, 6). Because severe hearing loss during development is implicated in the deficient acquisition of auditory perceptual skills and language, which presumably require learning, we have examined whether synaptic plasticity is also affected.At a structural level, hearing impairments can lead to neuron death or atrophy and alter process outgrowth (7). Furthermore, direct examination of neuron function in brain slice preparations from deaf animals has revealed significant physiological changes to intrinsic and synaptic properties. In both the inferior colliculus and auditory cortex (ACx), early sensorineural hearing loss (SNHL) alters the balance of excitatory and inhibitory synaptic strength (8-10). A similar disruption in synaptic physiology and certain intrinsic properties also occurs in the auditory brainstem of the congenitally deaf mutant mouse (11,12).Both long-term potentiation (LTP) and depression (LTD) have been characterized in a series of studies on the rat ACx (13-18). For example, an NMDA receptor-mediated LTP in the ACx can be induced by stimulation of afferents innervating the ACx via the white matter (13), whereas thalamo-and corticocortical synapse activation can induce LTD (16). These cellular mechanisms may serve as a substrate for use-dependent alteration of coding properties in...

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Section: Resultssupporting

confidence: 90%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Timbre is a biologically significant feature of natural sounds. Also, sound transients appear to be of particular significance in the development of auditory cortex (Metherate & Aramakis, 1999) and A1 has a greater sensitivity to onset transients than other auditory cortical fields (Heil & Irvine, 1998).…”

Section: Learning Strategies and Cortical Plasticitymentioning

confidence: 98%

Learning strategy determines auditory cortical plasticity

Berlau

Weinberger

2008

Neurobiology of Learning and Memory

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Learning modifies the primary auditory cortex (A1) to emphasize the processing and representation of behaviorally relevant sounds. However, the factors that determine cortical plasticity are poorly understood. While the type and amount of learning are assumed to be important, the actual strategies used to solve learning problems might be critical. To investigate this possibility, we trained two groups of adult male Sprague-Dawley rats to bar-press (BP) for water contingent on the presence of a 5.0 kHz tone using two different strategies: BP during tone presence or BP from tone-onset until receiving an error signal after tone cessation. Both groups achieved the same high levels of correct performance and both groups revealed equivalent learning of absolute frequency during training. Post-training terminal "mapping" of A1 showed no change in representational area of the tone signal frequency but revealed other substantial cuespecific plasticity that developed only in the tone-onset-to-error strategy group. Threshold was decreased ~10 dB and tuning bandwidth was narrowed by ~0.7 octaves. As sound onsets have greater perceptual weighting and cortical discharge efficacy than continual sound presence, the induction of specific learning-induced cortical plasticity may depend on the use of learning strategies that best exploit cortical proclivities. The present results also suggest a general principle for the induction and storage of plasticity in learning, viz., that the representation of specific acquired information may be selected by neurons according to a match between behaviorally selected stimulus features and circuit/network response properties.

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“…With postnatal age, there is increased ability to spike, decreased AP threshold, increased AP amplitude, and decreased spike width Christophe et al 2005;Kasper et al 1994b;Kriegstein et al 1987;Lorenzon and Foehring 1993;Maravall et al 2004b;McCormick and Prince 1987;Metherate and Aramakis 1999;Oswald and Reyes 2008). Spontaneous firing also increases with development .…”

Section: Development Of Excitability and Firing Patternsmentioning

confidence: 99%

“…The greatest changes occur between weeks 1 and 3 Lorenzon and Foehring 1993;Locke and Nerbonne 1997a;Maravall et al 2004b;Metherate and Aramakis 1999). Both Kv1 (Guan et al 2006b)-and Kv2 (Foehring et al 2009)-mediated currents regulate interspike intervals in these cells.…”

Section: Development Of Excitability and Firing Patternsmentioning

confidence: 99%

Postnatal development of A-type and Kv1- and Kv2-mediated potassium channel currents in neocortical pyramidal neurons

Guan

Horton

Armstrong

et al. 2011

Journal of Neurophysiology

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Guan D, Horton LR, Armstrong WE, Foehring RC. Postnatal development of A-type and Kv1-and Kv2-mediated potassium channel currents in neocortical pyramidal neurons. J Neurophysiol 105: 2976-2988, 2011. First published March 30, 2011 doi:10.1152/jn.00758.2010.-Potassium channels regulate numerous aspects of neuronal excitability, and several voltage-gated K ϩ channel subunits have been identified in pyramidal neurons of rat neocortex. Previous studies have either considered the development of outward current as a whole or divided currents into transient, A-type and persistent, delayed rectifier components but did not differentiate between current components defined by ␣-subunit type. To facilitate comparisons of studies reporting K ϩ currents from animals of different ages and to understand the functional roles of specific current components, we characterized the postnatal development of identified Kv channel-mediated currents in pyramidal neurons from layers II/III from rat somatosensory cortex. Both the persistent/slowly inactivating and transient components of the total K ϩ current increased in density with postnatal age. We used specific pharmacological agents to test the relative contributions of putative Kv1-and Kv2-mediated currents (100 nM ␣-dendrotoxin and 600 nM stromatoxin, respectively). A combination of voltage protocol, pharmacology, and curve fitting was used to isolate the rapidly inactivating A-type current. We found that the density of all identified current components increased with postnatal age, approaching a plateau at 3-5 wk. We found no significant changes in the relative proportions or kinetics of any component between postnatal weeks 1 and 5, except that the activation time constant for A-type current was longer at 1 wk. The putative Kv2-mediated component was the largest at all ages. Immunocytochemistry indicated that protein expression for Kv4.2, Kv4.3, Kv1.4, and Kv2.1 increased between 1 wk and 4 -5 wk of age. Kv channel; somatosensory cortex; voltage clamp; A current; delayed rectifier AT BIRTH, the rodent somatosensory system is immature, and somatosensory cortex undergoes dramatic changes over the first postnatal month. Neocortical pyramidal cells are generated prenatally in an "inside-out" laminar pattern (Caviness 1982; Caviness et al.

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Intrinsic electrophysiology of neurons in thalamorecipient layers of developing rat auditory cortex

Cited by 61 publications

References 62 publications

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Learning strategy determines auditory cortical plasticity

Postnatal development of A-type and Kv1- and Kv2-mediated potassium channel currents in neocortical pyramidal neurons

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