Differential Dependence of LTD on Glutamate Receptors in the Auditory Cortical Synapses of Cortical and Thalamic Inputs

Kudoh, Masaharu; Sakai, Masashi; Shibuki, Katsuei

doi:10.1152/jn.00928.2001

Cited by 31 publications

(25 citation statements)

References 42 publications

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“…1-5) confirms previous reports on the induction of cortico-and thalamocortical LTP and LTD (13,15,43). The behavioral relevance of NMDA receptor-mediated plasticity in ACx has also been demonstrated in adult rats (44).…”

Section: Discussionsupporting

confidence: 85%

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: Discussionsupporting

confidence: 85%

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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“…Depression of synapses in A1 has been suggested to involve several distinct mechanisms, with LTD at thalamocortical and intracortical synapses in vitro depending on activation of metabotropic glutamate and NMDA receptors, respectively (Kudoh et al, 2002). In the present study, LTD was largely abolished by APV alone, even though there appeared to be some small, residual depression in the absence of NMDA activation.…”

Section: Discussioncontrasting

confidence: 41%

Continuous white noise exposure during and after auditory critical period differentially alters bidirectional thalamocortical plasticity in rat auditory cortex in vivo

Speechley¹,

Hogsden

Dringenberg

2007

Eur J of Neuroscience

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Long-term potentiation (LTP) and long-term depression are thought to mediate activity-dependent brain plasticity but their role in the development of the thalamocortical auditory system in vivo has not been investigated. In adult urethane-anaesthetized rats, theta-burst stimulation of the medial geniculate nucleus produced robust LTP (40% amplitude enhancement) of field post-synaptic evoked potentials recorded in the superficial layers of the primary auditory cortex. Low-frequency (1-Hz) stimulation resulted in transient depression ( approximately 40%) of field post-synaptic evoked potential amplitude. Both LTP and synaptic depression were found to be dependent on cortical N-methyl-d-aspartate receptors. Thalamocortical plasticity was also assessed after continuous white noise exposure, thought to arrest auditory cortex maturation when applied during the critical period of post-natal primary auditory cortex development. Rats housed in continuous white noise for the first 50 days of post-natal life exhibited greater LTP ( approximately 80%) than controls reared in unaltered acoustic environments. The protocol used to elicit depression also resulted in substantial LTP ( approximately 50%) in white noise-reared animals. Adults housed in white noise for the same length of time exhibited normal LTP but displayed greater and persistent levels of synaptic depression ( approximately 70%). Thus, the absence of patterned auditory stimulation during early post-natal life appears to retard sensory-dependent thalamocortical synaptic strengthening, as indicated by the preferential readiness for synaptic potentiation over depression. The fact that the same auditory manipulation in adults results in synapses favouring depression demonstrates the critical role of developmental stage in determining the direction of synaptic modification in the thalamocortical auditory system.

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“…Of the MDD subjects who were tested for the presence of alcohol postmortem, 7 were positive and 24 were negative. 6. Gene expression (y) = β0+β1PMI+β2Age+β3pH+β4RIN+β5Anti-depressant+β6X+β7Antidepressant*X with Antidepressant as a two-level factor in the MDD group, positive vs negative and X is Diagnosis (MDD vs controls) or Suicide (MDD-S vs MDD-NS).…”

Section: Gene Expression (Y) = β0+β1pmi+β2age+β3ph+β4rin+β5suicidementioning

confidence: 99%

“…4 Recent reports of a rapid antidepressant response in MDD patients after treatment with ketamine have led to increased scientific interest in the glutamate system and its possible dysfunction in MDD. [5][6][7] Unlike conventional antidepressant drugs, ketamine is an NMDA receptor (NMDAR) antagonist. It may exert its therapeutic effects after an acute low dose by increasing the synaptic release of glutamate.…”

Section: Introductionmentioning

confidence: 99%

Sex differences in glutamate receptor gene expression in major depression and suicide

et al. 2015

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Accumulating data indicate that the glutamate system is disrupted in major depressive disorder (MDD), and recent clinical research suggests that ketamine, an antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor (GluR), has rapid antidepressant efficacy. Here we report findings from gene expression studies of a large cohort of postmortem subjects, including subjects with MDD and controls. Our data reveal higher expression levels of the majority of glutamatergic genes tested in the dorsolateral prefrontal cortex (DLPFC) in MDD (F21,59=2.32, P=0.006). Posthoc data indicate that these gene expression differences occurred mostly in the female subjects. Higher expression levels of GRIN1, GRIN2A-D, GRIA2-4, GRIK1-2, GRM1, GRM4, GRM5 and GRM7 were detected in the female patients with MDD. In contrast, GRM5 expression was lower in male MDD patients relative to male controls. When MDD suicides were compared with MDD non-suicides, GRIN2B, GRIK3 and GRM2 were expressed at higher levels in the suicides. Higher expression levels were detected for several additional genes, but these were not statistically significant after correction for multiple comparisons. In summary, our analyses indicate a generalized disruption of the regulation of the GluRs in the DLPFC of females with MDD, with more specific GluR alterations in the suicides and in the male groups. These data reveal further evidence that, in addition to the NMDA receptor, the AMPA, kainate and the metabotropic GluRs may be targets for the development of rapidly acting antidepressant drugs.

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Differential Dependence of LTD on Glutamate Receptors in the Auditory Cortical Synapses of Cortical and Thalamic Inputs

Cited by 31 publications

References 42 publications

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

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

Continuous white noise exposure during and after auditory critical period differentially alters bidirectional thalamocortical plasticity in rat auditory cortex in vivo

Sex differences in glutamate receptor gene expression in major depression and suicide

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