One of the major limitations in the use of genetically modified mice for studying cognitive functions is the lack of regional and temporal control of gene function. To overcome these limitations, a forebrain-specific promoter was combined with the tetracycline transactivator system to achieve both regional and temporal control of transgene expression. Expression of an activated calcium-independent form of calcium-calmodulin-dependent kinase II (CaMKII) resulted in a loss of hippocampal long-term potentiation in response to 10-hertz stimulation and a deficit in spatial memory, a form of explicit memory. Suppression of transgene expression reversed both the physiological and the memory deficit. When the transgene was expressed at high levels in the lateral amygdala and the striatum but not other forebrain structures, there was a deficit in fear conditioning, an implicit memory task, that also was reversible. Thus, the CaMKII signaling pathway is critical for both explicit and implicit memory storage, in a manner that is independent of its potential role in development.
Map-matching is the process of aligning a sequence of observed user positions with the road network on a digital map. It is a fundamental pre-processing step for many applications, such as moving object management, traffic flow analysis, and driving directions. In practice there exists huge amount of low-samplingrate (e.g., one point every 2-5 minutes) GPS trajectories. Unfortunately, most current map-matching approaches only deal with high-sampling-rate (typically one point every 10-30s) GPS data, and become less effective for low-sampling-rate points as the uncertainty in data increases. In this paper, we propose a novel global map-matching algorithm called ST-Matching for lowsampling-rate GPS trajectories. ST-Matching considers (1) the spatial geometric and topological structures of the road network and (2) the temporal/speed constraints of the trajectories. Based on spatio-temporal analysis, a candidate graph is constructed from which the best matching path sequence is identified. We compare ST-Matching with the incremental algorithm and Average-Fré chet-Distance (AFD) based global map-matching algorithm. The experiments are performed both on synthetic and real dataset. The results show that our ST-matching algorithm significantly outperform incremental algorithm in terms of matching accuracy for low-sampling trajectories. Meanwhile, when compared with AFD-based global algorithm, ST-Matching also improves accuracy as well as running time.
Agonists of the dopamine D1/D5 receptors that are positively coupled to adenylyl cyclase specifically induce a slowly developing long-lasting potentiation of the field excitatory postsynaptic potential in the CAl region ofthe hippocampus that lasts for >6 hr. This potentiation is blocked by the specific D1/D5 receptor antagonist SCH 23390 and is occluded by the potentiation induced by cAMP agonists. An agonist of the D2 receptor, which is negatively coupled to adenylyl cyclase through Gai, did not induce potentiation. Although this slow D1/D5 agonist-induced potentiation is partially independent of N-methyl-D-aspartate receptors, it seems to share some steps with and is occluded by the late phase of long-term potentiation (LTP) produced by three repeated trains of nerve stimuli applied to the Schaffer One modulatory system known to innervate the CAl region of the hippocampus is the mesolimbic dopaminergic pathway that ends on both the Dl and D5 dopaminergic receptors coupled to adenylyl cyclase (10, 11). Immunohistochemical localization of Dl and D5 receptors reveals a heavy staining along pyramidal cells and the stratum radiatum (12). Retrograde fluorescent tracers show that dopaminergic fibers that project from the ventral tegmental area innervate the CAl MATERIALS AND METHODSTransversely cut hippocampal slices (400 jim) were prepared from 5-to 6-week-old Sprague-Dawley rats and maintained in an interface chamber with continuous superfusion at 1.5-2 ml/min. The solution composition was 124 mM NaCl, 1.3 mM MgCl2, 4 mM KCl, 1.2 mM KH2PO4, 2.0-2.5 mM CaCl2, 25.6 mM NaHCO3, and 10 mM D-glucose, bubbled with 95% 02/5% CO2. The temperature of the bath was maintained at 28-29°C. After equilibration of the slices in the chamber for 2 hr, extracellular recordings were performed as described in a previous paper (7). Baseline responses were recorded for 30-60 min before drug application or LTP-inducing tetanization. Four biphasic constant current pulses (0.2 Hz; duration, 0.1-ms pulse) were used to generate test excitatory postsynaptic potentials (EPSPs) at 10-min intervals during the first hour after drug application or LTP induction and at 30-min intervals during the following hours. In LTP experiments an additional test was performed 1 min after tetanization to induce LTP. Three stimulus trains at 100 Hz, 1 s of 0.2-ms pulse duration were used, a tetanization protocol that produces long-lasting potentiation for up to 8 hr (6). The average waveform from four successive responses was saved and the EPSP slope (mV/ms) was measured.The following drugs were made and stored as concentrated stock solutions and dissolved in the superfusing medium to achieve the final concentrations used: D1/D5 agonist, SKF Abbreviations: LTP, long-term potentiation; E-LTP and L-LTP, early and late components of LTP; NMDA, N-methyl-D-aspartate; PKA, protein kinase A; EPSP, excitatory postsynaptic potential; APV, (±)-2-amino-5-phosphonopentanoic acid; PPHT, (±)-2-(N-phenylethyl-N-propyl)amino-5-hydroxytetralin hydrochloride; Sp-cAMPS, ad...
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