Activity‐dependent regulation of synaptic strength and neuronal excitability in central auditory pathways

Walmsley, Bruce; Berntson, Amy; Leão, Richardson N.; Fyffe, Robert E.W.

doi:10.1113/jphysiol.2006.104851

Cited by 53 publications

(46 citation statements)

References 83 publications

(84 reference statements)

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“…Although it is clear that deafferentation perturbs cellular properties throughout the central auditory system (Kotak and Sanes, 1996;Vale and Sanes, 2000;Kotak et al, 2005;Walmsley et al, 2006;Wang and Manis, 2006), the effect of sound attenuation has not been established. Because there is considerable debate about the behavioral impact of conductive hearing loss alone (Feagans et al, 1987;Teele et al, 1990;Mody et al, 1999;Psarommatis et al, 2001;Roberts et al, 2002;Paradise et al, 2005), it is essential to establish whether or not central deficits occur.…”

Section: Discussionmentioning

confidence: 99%

Conductive Hearing Loss Disrupts Synaptic and Spike Adaptation in Developing Auditory Cortex

Han¹,

Kotak²,

Sanes³

2007

J. Neurosci.

102

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Although sensorineural hearing loss (SNHL) is known to compromise central auditory structure and function, the impact of milder forms of hearing loss on cellular neurophysiology remains mostly undefined. We induced conductive hearing loss (CHL) in developing gerbils, reared the animals for 8 -13 d, and subsequently assessed the temporal features of auditory cortex layer 2/3 pyramidal neurons in a thalamocortical brain slice preparation with whole-cell recordings. Repetitive stimulation of the ventral medial geniculate nucleus (MGv) evoked robust short-term depression of the postsynaptic potentials in control neurons, and this depression increased monotonically at higher stimulation frequencies. In contrast, CHL neurons displayed a faster rate of synaptic depression and a smaller asymptotic amplitude. Moreover, the latency of MGv evoked potentials was consistently longer in CHL neurons for all stimulus rates. A separate assessment of spike frequency adaptation in response to trains of injected current pulses revealed that CHL neurons displayed less adaptation compared with controls, although there was an increase in temporal jitter. For each of these properties, nearly identical findings were observed for SNHL neurons. Together, these data show that CHL significantly alters the temporal properties of auditory cortex synapses and spikes, and this may contribute to processing deficits that attend mild to moderate hearing loss.

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Section: Discussionmentioning

confidence: 99%

Conductive Hearing Loss Disrupts Synaptic and Spike Adaptation in Developing Auditory Cortex

Han¹,

Kotak²,

Sanes³

2007

J. Neurosci.

102

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“…In congenitally deaf mice, the lack of afferent input causes disruption of the topographic gradient of voltage gated potassium conductance (also inducing increased excitability), and dysfunctional sodium channels (Leão et al, 2006a,b;Walmsley et al, 2006). Spontaneous afferent activity is also important for survival of the LSO neurons and development of physiological properties controlling AP firing, as shown recently in Ca v 1.3 Ϫ/Ϫ mice (Hirtz et al, 2011).…”

Section: Importance Of Neuronal Activity For Functional Development Imentioning

confidence: 99%

“…Spontaneous afferent activity is also important for survival of the LSO neurons and development of physiological properties controlling AP firing, as shown recently in Ca v 1.3 Ϫ/Ϫ mice (Hirtz et al, 2011). By enhancing the excitability of CN bushy cells, MNTB, and (selected) LSO neurons, the actions of P2XRs may critically contribute to the maintenance of synaptic contacts through Hebbian-like plasticity (Walmsley et al, 2006). Contrary to NMDAR, the activation of P2XRs can mediate substantial Ca 2ϩ influx at resting membrane potential.…”

Section: Importance Of Neuronal Activity For Functional Development Imentioning

confidence: 99%

“…Establishment of a precise tonotopic organization within the auditory circuitry requires two important steps: Genetically determined assembly of initial connectivity, which is controlled by guidance molecules (Rubel and Fritzsch, 2002;Cramer, 2005;Appler and Goodrich, 2011;Nakamura and Cramer, 2011) and activitydependent remodeling of axonal domains, which yields a more selective topographic restriction of synaptic inputs (Sanes and Takács, 1993;Friauf and Lohmann, 1999;Kandler, 2004;Walmsley et al, 2006). Moreover, early neuronal activity provides trophic signals, necessary for survival of second-and third-order neurons of the auditory brainstem (Parks, 1997;O'Neil et al, 2011).…”

Section: Importance Of Neuronal Activity For Functional Development Imentioning

confidence: 99%

“…Development of neuronal membrane properties in the MNTB principal neurons and regulation of synaptic strength depend on auditory nerve activity (Walmsley et al, 2006). In congenitally deaf mice, the lack of afferent input causes disruption of the topographic gradient of voltage gated potassium conductance (also inducing increased excitability), and dysfunctional sodium channels (Leão et al, 2006a,b;Walmsley et al, 2006).…”

Section: Importance Of Neuronal Activity For Functional Development Imentioning

confidence: 99%

See 2 more Smart Citations

Purinergic Modulation of Neuronal Activity in Developing Auditory Brainstem

Dietz

Jovanovic²,

Wielsch³

et al. 2012

Journal of Neuroscience

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In the developing nervous system, spontaneous neuronal activity arises independently of experience or any environmental input. This activity may play a major role in axonal pathfinding, refinement of topographic maps, dendritic morphogenesis, and the segregation of axonal terminal arbors. In the auditory system, endogenously released ATP in the cochlea activates inner hair cells to trigger bursts of action potentials (APs), which are transferred to the central auditory system. Here we show the modulatory role of purinergic signaling beyond the cochlea, i.e., the developmentally regulated and cell-type-specific depolarizing effects on auditory brainstem neurons of Mongolian gerbil. We assessed the effects of P2X receptors (P2XRs) on neuronal excitability from prehearing to early stages of auditory signal processing. Our results demonstrate that in neurons expressing P2XRs, extracellular ATP can evoke APs in sync with Ca 2ϩ signals. In cochlear nucleus (CN) bushy cells, ATP increases spontaneous and also acoustically evoked activity in vivo, but these effects diminish with maturity. Moreover, ATP not only augmented glutamate-driven firing, but it also evoked APs in the absence of glutamatergic transmission. In vivo recordings also revealed that endogenously released ATP in the CN contributes to neuronal firing activity by facilitating AP generation and prolonging AP duration. Given the enhancing effect of ATP on AP firing and confinement of P2XRs to certain auditory brainstem nuclei, and to distinct neurons within these nuclei, it is conceivable that purinergic signaling plays a specific role in the development of neuronal brainstem circuits.

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Memory: Mechanisms Other than LTP

Debanne¹,

Campanac²

2009

Encyclopedia of Life Sciences

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Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage. Long‐term changes in neuronal excitability have been reported in several brain areas following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Similarly to synaptic plasticity, long‐lasting intrinsic plasticity is bidirectional and expresses a certain level of input or cell specificity. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram. Key concepts: Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.

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Activity‐dependent regulation of synaptic strength and neuronal excitability in central auditory pathways

Cited by 53 publications

References 83 publications

Conductive Hearing Loss Disrupts Synaptic and Spike Adaptation in Developing Auditory Cortex

Conductive Hearing Loss Disrupts Synaptic and Spike Adaptation in Developing Auditory Cortex

Purinergic Modulation of Neuronal Activity in Developing Auditory Brainstem

Memory: Mechanisms Other than LTP

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