An Over 90 dB Intra-Scene Single-Exposure Dynamic Range CMOS Image Sensor Using a 3.0 µm Triple-Gain Pixel Fabricated in a Standard BSI Process.

To respond to the high demand for high dynamic range imaging suitable for moving objects with few artifacts, we have developed a single-exposure dynamic range image sensor by introducing a triple-gain pixel and a low noise dual-gain readout circuit. The developed 3 µm pixel is capable of having three conversion gains. Introducing a new split-pinned photodiode structure, linear full well reaches 40 ke-. Readout noise under the highest pixel gain condition is 1 e- with a low noise readout circuit. Merging two signals, one with high pixel gain and high analog gain, and the other with low pixel gain and low analog gain, a single exposure dynamic rage (SEHDR) signal is obtained. Using this technology, a 1/2.7", 2M-pixel CMOS image sensor has been developed and characterized. The image sensor also employs an on-chip linearization function, yielding a 16-bit linear signal at 60 fps, and an intra-scene dynamic range of higher than 90 dB was successfully demonstrated. This SEHDR approach inherently mitigates the artifacts from moving objects or time-varying light sources that can appear in the multiple exposure high dynamic range (MEHDR) approach.

alpha 2-Adrenoceptor-mediated presynaptic modulation of GABAergic transmission in mechanically dissociated rat ventrolateral preoptic neurons.

The ventrolateral preoptic nucleus (VLPO) is a key nucleus involved in the homeostatic regulation of sleep-wakefulness. Little is known, however, about the cellular mechanisms underlying its role in sleep regulation and how the neurotransmitters, such as GABA and noradrenaline (NA), are involved. In the present study we investigated GABAergic transmission to acutely dissociated VLPO neurons using an enzyme-free, mechanical dissociation procedure in which functional terminals remained adherent and we investigated how this GABAergic transmission was modulated by NA. As previously reported in slices, NA hyperpolarized multipolar VLPO neurons and depolarized bipolar VLPO neurons. NA also inhibited the release of GABA onto multipolar VLPO neurons but had no effect on GABAergic transmission to bipolar neurons. The inhibition of release was mediated by presynaptic alpha(2) adrenoceptors coupled to N-ethylmaleimide (NEM)-sensitive G-proteins which appeared to act via inhibition of adenylate cyclase and subsequent decreases in protein kinase A activity. The inhibition of GABA release did not, however, involve an inhibition of external Ca(2+) influx. The results indicate that all VLPO neurons contain GABAergic inputs and that the different morphological subgroups of VLPO neurons are correlated not only to different postsynaptic responses to NA but also to different presynaptic NA responses. Furthermore our results demonstrate an additional mechanism by which NA can modulate the excitability of multipolar VLPO neurons which may have important implications for its role in regulating sleep/wakefulness.

Modification of NMDA responses by tri-n-butyltin in rat brain neurons.

1. The effects of the organotin, tri-n-butyltin (TBT), on N-methyl-D-aspartate (NMDA) induced membrane currents were investigated in order to evaluate possible neuronal actions of this toxic environmental pollutant. Experiments were conducted on neurons acutely dissociated from the rat dorsal motor nucleus of vagus (DMV) using the nystatin-perforated patch clamp recording technique. 2. In Mg(2+)-free physiological recording solutions, the application of NMDA to single DMV neurons held at a holding potential (V(H)) of -40 mV evoked an inward current which rapidly reached a peak before declining to a steady-state inward current. This was followed, immediately after NMDA washout, by a transient outward current. TBT (100 nM) reversibly caused a slight reduction in the inward currents and greatly increased the amplitude of the outward currents. 3. The reversal potential of the NMDA-induced outward current in the presence of TBT was -86.7 mV, close to the theoretical K(+) equilibrium potential of -85.7 mV. 4. The NMDA-induced outward current was completely blocked when the K(+) in the internal solution was replaced with equimolar Cs(+). Under these conditions, the NMDA induced current was more sustained and was unaffected by TBT. 5. The NMDA-induced outward current was markedly inhibited by 5 mM tetraethylammonium chloride and 300 nM charybdotoxin, and it was abolished by removal of extracellular Ca(2+), suggesting that the outward current was due to the activation of Ca(2+)-activated K(+) channels by Ca(2+) influx through NMDA receptors. 6. In conclusion, in rat DMV neurons, TBT potentiates the Ca(2+)-activated K(+) current induced by NMDA application without having any direct effects on the NMDA-induced inward current. Given the significant role of NMDA receptor mediated excitation in various physiological and pathological processes, the modulation of this response by TBT may have an important influence on neuronal function.