Tonotopic-column-dependent variability of neural encoding in the auditory cortex of rats.

Neural computation could benefit from the heterogeneity of neurons to achieve energy efficiency. Beyond a single neuron level, adaptation to biologically important signals should also make functional columns heterogeneous. In the present study, we test a hypothesis that variability of neural response depends on tonotopic columns in the primary auditory cortex (A1) of rats. Mutual information (MI) was estimated from multi-unit responses in A1 of anesthetized rats, to quantify how spike count (SC) and the first spike latency (FSL) carried information about frequency and intensity of test tones. Consequently, for both SC and FSL, we found best frequency (BF)-dependent MI distributions with wide variances in high BF regions. These MI distributions were caused by BF-dependence of the amount of information that neurons conveyed, i.e., total entropy, rather than the transmission efficiency. In addition, the relationship between the transmission efficiency and the total entropy differentiated SC encoding and FSL encoding, suggesting that SC encoding and FSL encoding are not redundant but each plays a different role in intensity encoding. These results provide compelling evidence that BF columns are heterogeneous. Such heterogeneity of columns may make the global computation in A1 more efficient. Thus, the efficient coding in the neural system could be achieved by multiple-scale heterogeneity.

Blockade of ATP-sensitive K+ channels attenuates preconditioning effect on myocardial metabolism in swine: myocardial metabolism and ATP-sensitive K+ channels.

OBJECTIVE: We investigated if blockade of ATP-sensitive K+ channels (KATP) abolishes the protective effect of ischemic preconditioning (IP) on myocardial metabolism and ischemia-induced reactive hyperemia (RH) in pigs. METHODS: IP was elicited by a single cycle of 5 min occlusion and 5 min reperfusion of coronary artery, followed by 15 min of test ischemia and 120 min of reperfusion. Vehicle or the ATP-sensitive K+ channels (KATP) blocker, glibenclamide (3 or 6 mg/kg; G3 or G6) was administered before IP (groups; IP, G3+IP, G6+IP). As respective controls, the same treatment was performed in groups without IP (groups; C, G3, G6). Tissue levels of ATP, creatine phosphate (CP) and intracellular pH (pHi) in the area at risk were measured by 31P-nuclear magnetic resonance spectroscopy. RH after 5 min of preconditioning ischemia was assessed by regional myocardial blood flow. RESULTS: ATP and pHi were preserved after 15 min of ischemia in the IP group [C/IP; ATP=57+/-4/76+/-10% of baseline, pHi=6.18+/-0.08/6.66+/-0.03, P<0.05, C vs. IP]. Both doses of glibenclamide completely abolished the ATP sparing effect of IP. The high dose completely abolished pHi preservation (G6+IP=6.33+/-0.06), while the low dose showed only a partial effect (G3+IP=6.48+/-0.03). Glibenclamide did not adversely affect myocardial metabolism in groups without IP. Glibenclamide attenuated RH after 5 min of ischemia by 30% in both subendocardium and subepicardium. CONCLUSIONS: Blockade of KATP abolished the preconditioning effect on myocardial metabolism, and partially attenuated post-ischemic reactive hyperemia in pigs. These results indicate that KATP activation might be involved in the mechanisms of these phenomena, reactive hyperemia is not sufficient to induce IP protection.