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.

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.