{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T06:25:04Z","timestamp":1774506304722,"version":"3.50.1"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2002,4,1]],"date-time":"2002-04-01T00:00:00Z","timestamp":1017619200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2002,4]]},"abstract":"<jats:p>The <jats:italic>deafness (dn\/dn<\/jats:italic>) mutant mouse provides a valuable model of human congenital deafness. We investigated the properties of synaptic transmission in the anteroventral cochlear nucleus (AVCN) of normal and congenitally deaf <jats:italic>dn\/dn<\/jats:italic> mice. Excitatory postsynaptic currents (EPSCs) were evoked by focal stimulation of single auditory nerve fibres, and measured by whole\u2010cell recordings from neurones in AVCN slices (mean postnatal age = P13). Absolute amplitudes of both AMPA\u2010 and NMDA\u2010mediated components of evoked EPSCs were greater (170 %) in deaf <jats:italic>versus<\/jats:italic> control animals. Enhanced transmission in deaf mice was due to a presynaptic mechanism. Variance\u2010mean analysis revealed that the probability of transmitter release was significantly greater in deaf (<jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub>= 0.8) <jats:italic>versus<\/jats:italic> control animals (<jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub>= 0.5). Following high frequency stimulation, deaf mice showed a greater depression of evoked EPSCs, and a significant increase in the frequency of delayed\u2010release (asynchronous) miniature EPSCs (aEPSCs) (deaf 100 Hz <jats:italic>vs.<\/jats:italic> control 7 Hz). The acetoxymethyl ester of EGTA (EGTA\u2010AM) blocked the increase in miniature aEPSCs and returned tetanic depression to control values. In deaf mice, reduction of mean <jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub> using cadmium caused an expected increase in paired\u2010pulse ratio (PPR). However, in the same cells, a similar reduction in release by EGTA\u2010AM did not result in a change in PPR, demonstrating that a change may occur in <jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub> without a concomitant change in PPR. In many respects, transmission in deaf mice was found to be remarkably similar to control mice, implying that many parameters of synaptic transmission develop normally in these animals. The two significant differences (higher <jats:italic>P<\/jats:italic><jats:sub>r<\/jats:sub> and asynchronous release in deaf mice) could both be reversed by the addition of EGTA\u2010AM, suggesting that endogenous calcium buffering may be impaired or undeveloped in the presynaptic terminals of the auditory nerve in deaf mice.<\/jats:p>","DOI":"10.1113\/jphysiol.2001.013821","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:45:57Z","timestamp":1027773957000},"page":"447-455","source":"Crossref","is-referenced-by-count":148,"title":["Synaptic transmission in the auditory brainstem of normal and congenitally deaf mice"],"prefix":"10.1113","volume":"540","author":[{"given":"Sharon","family":"Oleskevich","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce","family":"Walmsley","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2002,4]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.861bg.x"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(82)90536-4"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901550302"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80441-9"},{"key":"e_1_2_5_6_1","doi-asserted-by":"crossref","first-page":"1857","DOI":"10.1523\/JNEUROSCI.21-06-01857.2001","article-title":"Minimizing synaptic depression by control of release probability","volume":"21","author":"Brenowitz S.","year":"2001","journal-title":"Journal of Neuroscience"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(79)90066-6"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0093m.x"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(97)78062-7"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(99)01520-9"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80555-3"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.63.1.847"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/0378-5955(89)90057-9"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-20-08721.1999"},{"key":"e_1_2_5_15_1","first-page":"2324","article-title":"Properties of synchronous and asynchronous release during pulse train depression in cultured hippocampal neurons","volume":"85","author":"Hagler D. 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