The cardioprotective effect of brief acidic reperfusion after ischemia in perfused rat hearts is not mimicked by inhibition of the Na(+)/H(+) exchanger NHE1.

BACKGROUND: Ischemic postconditioning (PostC), i.e. brief ischemia-reperfusion cycles before full reperfusion, is protective against cardiac ischemia/reperfusion (I/R) injury. Inhibition of the Na(+)/H(+) exchanger NHE1 and delayed intracellular pH-normalization have been proposed to underlie protection by PostC. METHODS AND RESULTS: We used Langendorff perfused rat hearts exposed to 35 min global ischemia to show that 15 min acidic (pH 6.5) treatment at onset of reperfusion decreased infarct size and functional deterioration at least to the same extent as PostC. In contrast, NHE1 inhibition by EIPA was detrimental. To evaluate HL-1 atrial cardiomyocytes as a cellular model for PostC, we exposed the cells to simulated ischemia/reperfusion (I/R) mimicking that in perfused hearts. Necrosis and apoptosis induced by I/R were unaffected by 15 min of pH 6.0 at onset of reperfusion. I/R increased the activity of c-Jun N-terminal Kinase 1/2 (JNK1/2) and Akt, but not of p38 MAPK, with no further effect of acidic reperfusion or EIPA. CONCLUSION: In rat hearts, 15 min acidic reperfusion improves myocardial performance at least as much as does PostC, whereas NHE1 inhibition is detrimental. In contrast, in HL-1 cardiomyocytes, acidic reperfusion or NHE1 inhibition affect neither survival nor JNK1/2-, Akt-, and p38 MAPK activity after I/R, pointing to different mechanisms of damage and protection in these systems.

Binaural interaction in the frog dorsal medullary nucleus.

We have studied binaural and directional processing in cells in the frog dorsal medullary nucleus (DMN) stimulated with dichotic sound (couplers) and free-field sound. We present evidence that already at this stage of central processing the neural directionality is sharpened, probably by binaural interaction. Binaural interaction in the DMN was usually interpreted as inhibition, mostly driven from the contralateral side and dependent on a certain combination of interaural time differences (ITD) and interaural level differences (ILD). In free-field measurements, the strength and timing of the binaural inputs will depend on sound direction as processed by the auditory fibers. Thus, the directionality of DMN cells is caused by both monaural directional cues generated by acoustical coupling of the eardrums and non-tympanic pathways as well as binaural interaction. Most DMN cells show ovoidal directional characteristics and the directionality is sharpened compared to that of auditory nerve fibers. We suggest that the sharpening is due to the inhibitory interactions.

Dendritic spike back propagation in the electrosensory lobe of Gnathonemus petersii.

Spike timing-dependent plasticity that follows anti-Hebbian rules has been demonstrated at synapses between parallel fibers and inhibitory interneurons known as medium ganglionic layer (MG) neurons in the cerebellum-like electrosensory lobe of mormyrid fish. This plasticity is expressed when presynaptic activation is associated with a characteristically broad, postsynaptic action potential, lasting 7-15 ms, occurring within a window of up to 60-80 ms following synaptic activation. Since the site of plastic change is presumably in the apical dendrites, it is important to know where, when and how this broad spike is generated and the manner in which such events propagate within the intrinsic network of the electrosensory lobe. The electrosensory lobe has a strict layered organization that makes the preparation suitable for one dimension current source density analysis. Using this technique in an 'in vitro' interface slice preparation, we found that following either parallel fiber stimulation or an orthogonal field stimulus, a sink appeared in the ganglionic layer and propagated into the molecular layer. Intracellular records from MG somata showed these stimuli evoked broad action potentials whose timing corresponds to this sink. TTX application in the deep fiber layer blocked the synaptically evoked ganglionic layer field potential and the 'N3' wave of the outer molecular layer field potential simultaneously, while the molecular layer 'N1' and 'N2' waves corresponding to synaptic activation of the apical dendrites remained intact. These results confirm the hypothesis that the broad spikes of MG cells originate in the soma and propagate through the molecular layer in the apical dendritic tree, and suggest the possibility that this backpropagation may contribute to 'boosting' of the synaptic response in distal apical dendrites in certain circumstances.

Her odours make him deaf: crossmodal modulation of olfaction and hearing in a male moth.

All animals have to cope with sensory conflicts arising from simultaneous input of incongruent data to different sensory modalities. Nocturnal activity in moths includes mate-finding behaviour by odour detection and bat predator avoidance by acoustic detection. We studied male moths that were simultaneously exposed to female sex pheromones indicating the presence of a potential mate, and artificial bat cries simulating a predation risk. We show that stimulation of one sensory modality can modulate the response to information from another, suggesting that behavioural thresholds are dynamic and depend on the behavioural context. The tendency to respond to bat sounds decreased as the quality and/or the amount of sex pheromone increased. The behavioural threshold for artificial bat cries increased by up to 40 dB when male moths where simultaneously exposed to female sex pheromones. As a consequence, a male moth that has detected the pheromone plume from a female will not try to evade an approaching bat until the bat gets close, hence incurring increased predation risk. Our results suggest that male moths' reaction to sensory conflicts is a trade-off depending on the relative intensity of the input to CNS from the two sensory modalities.