Adult male mice were maintained on a 12 hr light/dark cycle. Studies were conducted during the light phase of the cycle. The antinociceptive effect was assessed using the tail-flick test. The latency to the first sign of a rapid tail-flick was taken as the behavioral endpoint. Each mouse was tested for baseline latency by immersing one-third of its tail in 52°C water and recording the time

to response. All drugs dissolved in 5 μl of distilled water were administered via lumbar puncture. Delt I or Delt I with NTI, SNC80, or L-ENK was administered i.t. 30 min before the morphine treatment (1.5 μg, i.t.). NTI (1 μg, i.t.) was administered together with morphine (1 μg, i.t.). TAT-fused proteins (1, 5, or 10 mg/kg) were applied (i.p.) 2.5 hr, 1.5 hr, or 30 min before the morphine treatment (2 mg/kg, s.c.). A maximum score was assigned (100%) to animals not responding within 10 s to avoid tissue find more damage. Antinociception was calculated by the following formula: % maximum possible effect (M.P.E) = 100 × (test latency − baseline latency)/(10 − baseline latency). Data are presented as mean ± SEM. Statistical analysis was performed using PRISM (GraphPad Software) with a two-tailed, paired or unpaired Student’s t test. For behavioral tests, single-dose data were analyzed using one-way ANOVA, followed by a two-tailed, Apoptosis Compound Library datasheet unpaired Student’s t test for between group comparisons. Differences were considered significant at p <

0.05. We thank Dr. L. Ma for providing the DOR (M) plasmid and Dr. R. Elde for the DOR antibodies. This work was supported by National Natural Science Foundation of China

(30630029 and 30621062) and National Basic Research Program of China (2009CB522005, 2010CB912000, 2011CBA00400, 2007CB914501). “
“Changes in synaptic weights and neuronal excitability are considered to be the neural substrates Metalloexopeptidase for the storage of memory engrams (Johnston and Narayanan, 2008 and Malenka and Bear, 2004). Studies using extracellular field recordings and field stimulations at the Schaffer collateral-CA1 synapse have led to the synaptic tagging and capture (STC) model. This model states that synapses at which any form of long-term potentiation (LTP) (i.e., the longer lasting, protein synthesis-dependent late-phase of long-term potentiation [L-LTP], and the shorter lasting, protein synthesis-independent E-LTP) is induced become tagged in a protein synthesis-independent manner. The induction of L-LTP leads to protein synthesis, and all tagged synapses can use the resulting plasticity-related protein products (PrPs) to express L-LTP (Frey and Morris, 1997 and Frey and Morris, 1998). This facilitation is time limited and occurs regardless of whether the E-LTP-inducing stimulation precedes the L-LTP-inducing stimulation or vice versa (Frey and Morris, 1997). However, much remains unknown about the temporal and spatial restriction of the facilitation and various parameters that affect its strength.