Thalamo-hippocampal pathway regulates incidental memory capacity in mice.

Incidental memory can be challenged by increasing either the retention delay or the memory load. The dorsal hippocampus (dHP) appears to help with both consolidation from short-term (STM) to long-term memory (LTM), and higher memory loads, but the mechanism is not fully understood. Here we find that female mice, despite having the same STM capacity of 6 objects and higher resistance to distraction in our different object recognition task (DOT), when tested over 1 h or 24 h delays appear to transfer to LTM only 4 objects, whereas male mice have an STM capacity of 6 objects in this task. In male mice the dHP shows greater activation (as measured by c-Fos expression), whereas female mice show greater activation of the ventral midline thalamus (VMT). Optogenetic inhibition of the VMT-dHP pathway during off-line memory consolidation enables 6-object LTM retention in females, while chemogenetic VMT-activation impairs it in males. Thus, removing or enhancing sub-cortical inhibitory control over the hippocampus leads to differences in incidental memory.

Influence of protein kinases on the osmosensitive release of taurine from cerebellar granule neurons.

The role of phosphorylation events on the activation and modulation of the osmosensitive (3)H-taurine release (OTR) was examined in cultured cerebellar granule neurons (CGN) stimulated with 30% hyposmotic solutions. OTR was not decreased when [Ca(2+)](i) rise evoked by hyposmolarity was prevented by EGTA-AM (50 microM) or depleted by treatment with 1 microM ionomycin in Ca(2+)-free medium. Accordingly, OTR was not inhibited by Ca(2+)-dependent signaling events. The calmodulin (CAM) blocker W-7 (50 microM) potentiated OTR while the Ca(2+)/CAM kinase blocker KN-93 (10 microM) was without effect. Blockade of PKC by H-7, H-8 (50 microM) and Gö6976 (1 microM), as well as activation by phorbol myristate acetate (PMA) (100 nM) did not influence OTR, but chronic treatment to down regulate PKC decreased it by 30%. Forskolin (20 microM) and 8-BrcAMP (10 microM) did not change OTR. Protein tyrosine phosphorylation seems to be of crucial importance in the activation and modulation of OTR, as it was markedly inhibited (90%) by tyrphostine A23 (50 microM) and potentiated by the tyrosine phosphatase inhibitor ortho-vanadate (100 microM). The PI3 kinase blocker wortmannin 100 nM essentially abolished OTR but LY294002 (10-100 microM) was without effect. This difference may be accounted for PI3K isoforms in neurons with different sensitivity to the blockers. Alternatively, the effect of wortmannin may be exerted not in PI3 kinase but instead on phospholipases, which are also sensitive to this blocker. The hyposmotic stimulus induced activation of Erk1/Erk2, but blockade of this effect by PD 98059 (50 microM) only marginally decreased OTR suggesting that the Erk1/Erk2 is an epiphenomenon, not directly involved in OTR activation.

Role of Digestive Gland in the Energetic Metabolism of Penaeus setiferus.

We determined the role of the digestive gland in the respiratory metabolism of Penaeus setiferus adult males as a step toward proposing a feeding schedule based on the cycle of activity in the digestive gland. We measured pre- and postprandial values for oxygen consumption rate and hemolymph glucose concentrations in live animals, and oxygen consumption rate and glycogen concentration in excised digestive gland. After the animals were fed, which enhanced general metabolic activity, these indices changed. There was a high correlation between the oxygen consumption rate of the animal and the glucose concentration in the hemolymph, and between the oxygen consumption rate by the digestive gland and the glycogen concentration in the digestive gland, all in relation to time after feeding. Correlations support the hypothesis that the energy demand depends upon the metabolic substrate concentration. In this theory, glucose sustains muscle activity (during ingestion of food) and glycogen is the product of the digestive gland during food assimilation. Our observations of metabolic dynamics during the feeding period allowed us to examine the feeding process. The metabolic activity of the digestive gland was highest 6 h after feeding. This could mean that assimilation, having started 2 h after food intake, peaked 6 h after feeding. Eight hours after feeding, the oxygen consumption rate of the digestive gland decreased and fell to values similar to those recorded for animals subjected to 72 h of fasting.