In acoustic communication, animals must extract biologically relevant signals that are embedded in noisy environment. The present study examines how weak noise may affect the auditory sensitivity of neurons in the central nucleus of themouse inferior colliculus (IC)which receives convergent excitatory and inhibitory inputs from both lower and higher auditory centers. Specifically, we studied the frequency sensitivity and minimum threshold of IC neurons using a pure tone probe and a weak white noise masker under forward masking paradigm. For most IC neurons, probe-elicited response was decreased by a weak white noise that was presented at a specific gap (i.e. time window). When presented within this time window, weak noise masking sharpened the frequency tuning curve and increased the minimum threshold of IC neurons. The degree of weak noise masking of these two measurements increased with noise duration. Sharpening of the frequency tuning curve and increasing of the minimum threshold of IC neurons during weak noise masking were mostly mediated through GABAergic inhibition. In addition, sharpening of frequency tuning curve by the weak noise masker was more effective at the high than at low frequency limb. These data indicate that in the real world the ambient noise may improve frequency sensitivity of IC neurons throughGABAergic inhibitionwhile inevitably decrease the frequency response range and sensitivity of IC neurons.

Using bats as a model auditory system, we studied corticofugal control of auditory sensitivity of neurons in the inferior colliculus. We demonstrate for the first time that the corticocollicular pathway continuously regulates acoustic signal processing in the inferior coiliculus by increasing the threshold, reducing the auditory spatial response area, and sharpening the frequency tuning curve of recorded inferior collicular neurons. Regulation of auditory sensitivity of recorded inferior collicular neurons was observed when the corticocollicular pathway was activated by electrical stimulation in the auditory cortex. The effect of this corticofugal regulation of auditory sensitivity in inferior collicular neurons can also be produced by ionophoretical application of GABA to the collicular recording site. This regulation of ascending acoustic information by commands originating from higher brain centers may provide the bat with a mechanism to actively control acoustic signal processing and thus optimize acoustic signal analysis.

为了探讨γ-氨基丁酸（γ-aminobutyric acid, GABA）能抑制对大棕蝠（Eptesicus fuscus）听皮层（auditory cortex，AC）神经元声反应特性的影响，采用多管微电极电泳方法，观察了8只大棕蝠AC神经元去GABA能抑制前后声刺激诱发的反应。结果显示，微电泳GABAa受体拮抗剂荷包牡丹碱（bicuculline，Bic）去GABA能抑制可改变声刺激诱发的反应模式；极大地增加神经元冲动发放率，缩短反应的潜伏期和降低反应的最小阈值；不同程度地改变强度-发放率和强度-潜伏期函数。结果提示：1、GABA能抑制对AC神经元声信号处理起重要作用；2、GABA能抑制可改变AC神经元兴奋性支配或输入的效应，并因此定型AC神经元的声反应性质，即发放模式、阈值、强度-发放率和强度-潜伏期函数；3、GABA能抑制为AC神经元的声诱发活动提供一种调制性抑制。

自由声场条件下，通过给予小鼠具有不同时程（10、40及100ms）、强度（最小阈值以上5、15、25、35及45dB SPPL）、呈现率（0.5、1、2、3.3、5、6.7、10和20Hz）的纯音短声刺激，分析探讨了昆明小鼠下丘神经元声刺激跟随力与声时程及强度的关系。结果发现：多数神经元的脉 冲发放数随声强增高而增加，随短声时程的延长而减少；随声强的增高，多数神经元的临界现率（CPR）和最大呈现率（MPR）变大，而随短声时程的延长，神经元的CPR、MPR变小为主要趋势；下丘神经元的声反应跟随力总体上随时程延长而下降，随声强加大而提高。推测当声时程延长、强度下降时，前次刺激对后继刺激声反应的抑制性影响增强，提示声时程适当缩短、声强增大可能有助于下丘神经元汇聚更多的声信息进行高级神经处理，从而提高听中枢表征高密度声信息的能力。

We recorded extracellular activity from 402 single units located in the inferior colliculus (IC) of barbiturate-anesthetized albino mice. The stimuli were pure tones at characteristic frequency (CF) with durations of 10, 40 and 100 ms and intensities ranged from 5 to 25 dB above unit’s minimum threshold (MT). The tones were presented with different repetition rates (RRs) ranging from 0.2 to 20.0 Hz. At low intensities (5 dB above MT, determined at RR of 0.5 Hz) the great majority of units exhibited a strong decline of their responses when the stimulus RR was increased. About one-half of the units did not respond to 40 ms tones when they were stimulated with the RR of 3.0 Hz. This effect was even more pronounced for 100 ms tones. Generally, the increase in stimulus intensity led to an increase in the high-frequency border of RR. Nevertheless, even at intensities of 20-30 dB above MT, some units showed no response when the RR exceeded 5.0 Hz. In many cases the band-pass or high-pass duration tuning of the single unit was transformed to low-pass or all-pass when the rate was low enough to guarantee the independence of successive presentations of the stimuli. Responses of a very small group of IC units, however, were enhanced when the RR was increased. Our data have shown that the changes in the RR radically modify many features of the neural response (number of spikes, latency, discharge pattern, duration selectivity). We suggest that long-lasting inhibitory processes may be induced by low intensity stimuli in many units of the IC.