Sensorineural hearing loss during early childhood alters auditory cortical evoked potentials in humans and profoundly changes auditory processing in hearing-impaired animals. Multiple mechanisms underlie the early postnatal establishment of cortical circuits, but one important set of developmental mechanisms relies on the neuromodulator serotonin (5-hydroxytryptamine [5-HT]). On the other hand, early sensory activity may also regulate the establishment of adultlike 5-HT receptor expression and function. We examined the role of 5-HT in auditory cortex by first investigating how 5-HT neurotransmission and 5-HT(2) receptors influence the intrinsic excitability of layer II/III pyramidal neurons in brain slices of primary auditory cortex (A1). A brief application of 5-HT (50 μM) transiently and reversibly decreased firing rates, input resistance, and spike rate adaptation in normal postnatal day 12 (P12) to P21 rats. Compared with sham-operated animals, cochlear ablation increased excitability at P12-P21, but all the effects of 5-HT, except for the decrease in adaptation, were eliminated in both sham-operated and cochlear-ablated rats. At P30-P35, cochlear ablation did not increase intrinsic excitability compared with shams, but it did prevent a pronounced decrease in excitability that appeared 10 min after 5-HT application. We also tested whether the effects on excitability were mediated by 5-HT(2) receptors. In the presence of the 5-HT(2)-receptor antagonist, ketanserin, 5-HT significantly decreased excitability compared with 5-HT or ketanserin alone in both sham-operated and cochlear-ablated P12-P21 rats. However, at P30-P35, ketanserin had no effect in sham-operated and only a modest effect cochlear-ablated animals. The 5-HT(2)-specific agonist 5-methoxy-N,N-dimethyltryptamine also had no effect at P12-P21. These results suggest that 5-HT likely regulates pyramidal cell excitability via multiple receptor subtypes with opposing effects. These data also show that early sensorineural hearing loss affects the ability of 5-HT receptor activation to modulate A1 pyramidal cell excitability.

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Facial nerve is subject to injury at any point in the course from the cerebral cortex to the motor end plate in the face. Many etiologic varieties of facial nerve paralysis may be encountered, including idiopathic, trauma, viral infection and so on. Although much research has been done concerning facial nerve paralysis, almost none of this research studied the difference between adult and children. The aim of this study was to evaluate etiology and recovery rate between children and adults. METHODS: Between January 1986 and July 2005, 975 patients who presented with facial palsy in Kyung Hee University Hospital were examined. The patients ages ranged from 0 to 88. RESULTS: The highest age groups were 46-60 years old. The causes of facial palsy in adults were as follow in order of frequences: Bell's palsy (54.9%), infection (26.8%), trauma (5.9%), iatrogenic (2.0%), tumor (1.8%) and in childhood, Bell's palsy (66.2%), infection (14.6%), trauma (13.4%), birth trauma (3.2%), leukemia (1.3%). Recovery rates in adults were 91.4% in Bell' palsy, 89.0% in infection, 64.3% in trauma, and, in childhood, 93.1% in Bell' palsy, 90.9% in infection, 42.9% in trauma. CONCLUSIONS: Bell's palsy and infection were common causes in adults and children. There were no statistically significant differences between children and adults in recovery rate.

16Cholinergic systems contribute to the refinement of auditory cortical receptive fields by 17 activating muscarinic acetylcholine receptors (mAChRs). However, the specific cellular and 18 synaptic mechanisms underlying acetylcholine's effects on cortical circuits are not fully 19 understood. In this study, we investigate the effects of muscarinic receptor modulation on 20 spike-timing dependent plasticity (STDP) at synapses onto layer 2/3 pyramidal neurons in 21 mouse auditory cortex (AC). Synapses onto layer 2/3 pyramidal neurons exhibit a STDP 22 rule for pairing of postsynaptic spike bursts with single presynaptic stimuli. Pre-before-post 23 pairing at +10 ms results in a timing-dependent long-term potentiation (tLTP), whereas pre-24 before-post pairing at +50 ms intervals, and post-before-pre pairing at -10 to -20 ms 25 produce a timing-dependent long-term depression. We also characterize how mAChR 26 activation affects plasticity at these synapses, focusing on the induction of tLTP. During pre-27 before-post pairing at +10 ms, mAChR activation by either carbachol or oxotremorine-M 28 suppresses tLTP. mAChR activation also reduces the NMDA-receptor dependent 29 synaptically evoked increase in calcium in dendrites, apparently without affecting 30 presynaptic transmitter release. Pharmacological experiments suggest that M1 and M3 31 receptors are not involved in the mAChR-mediated suppression of tLTP. Taken together, 32 these results suggest activating mAChRs in layer 2/3 intracortical circuits can modify the 33 circuit dynamics of AC by depressing tLTP mediated by NMDA receptors, and depressing 34 calcium influx at excitatory synapses onto layer 2/3 pyramidal cells. 35 36 Rao, Kratz and Manis