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Embedded systems normally have a tight energy budget. Since the on-chip cache typically consumes 25%-50% of the processor's area and energy consumption, scratch pad memory (SPM), which is a software-controlled on-chip memory, has been widely adopted in many embedded systems due to its smaller area and lower power consumption. However, as the speed of the CMOS transistors increases along with density, leakage power consumption is becoming a critical issue for memory components with a large number of transistors. In this paper, we propose a novel hybrid SPM which consists of static random-access memory (SRAM) and nonvolatile memory (NVM) to take advantage of the ultralow leakage power and high density of latter. A novel dynamic data management algorithm is also proposed to make use of the full potential of NVM. According to the experimental results, with the help of the proposed algorithm, the novel hybrid SPM architecture can reduce the memory access time by 18.17%, the dynamic energy by 24.29%, and the leakage power by 37.34% compared with a baseline pure SRAM SPM with the same area. [ABSTRACT FROM AUTHOR]

Objective: To study the effect of different oxygen therapies on the rats with carbon dioxide poisoning for screening out the best on-the-spot oxygen-therapy technology for treating acute carbon dioxide poisoning. Methods: The 60 healthy male Sprague Dawley rats were randomly divided into normal control group (A group), carbon dioxide poisoning group (B group), low-concentration oxygen inhalation treatment group (C group), high-concentration oxygen inhalation treatment group (D group) and hyperbaric oxygen-therapy group (E group). Various kinds of oxygen therapies were given after the contamination. The pH, partial pressure of oxygen (PO2) and partial pressure of carbon dioxide (PCO2) of arterial blood, serum troponin I (CTNI), creatine kinase (CK), glutamic-oxaloacetic transaminase (AST), γ-glutamyl transpeptidase (GGT), blood urea nitrogen (BUN), potassium (K), sodium (Na) and chlorine (Cl) for the rats of each group were inspected. The lung and the brain tissues were taken for observing the pathological changes.Results: There is no significant difference in pH, PO2 and PCO2 among all oxygen-therapy groups (p > 0.05). The levels of CTNI, CK and AST in E group are obviously lower than that in B, C and D groups (p < 0.05). The level of serum K in E group is obviously lower than that in B, C and D groups (p < 0.05). The levels of serum Na and Cl in E group are obviously higher than that in B, C and D groups (p < 0.05). The pathological change of lungs in E group is significantly better than that in C and D groups. Conclusions: We recommend that the medical units with related conditions can give the hyperbaric oxygen therapy to patients as soon as possible [ABSTRACT FROM AUTHOR]

We have shown that amphetamine produces a delayed and sustained increase in glutamate levels in the ventral tegmental area, a region containing dopamine cell bodies important in acute and chronic effects of amphetamine administration. The present study characterized the mechanism underlying amphetamine-induced glutamate efflux. It was abolished by the glutamate uptake inhibitor dihydrokainate, but unaffected by perfusion with a low Ca(2+)/high Mg(2+) solution, implicating glutamate transporters. Because reactive oxygen species inhibit glutamate uptake, we examined the effect of amphetamine on hydroxyl radical formation by perfusing with D-phenylalanine (5 mM) and monitoring p-tyrosine production. Although no increase in hydroxyl radical formation was detected, D-phenylalanine completely prevented the amphetamine-induced increase in glutamate efflux, as did systemic injection of another trapping agent, alpha-phenyl-N-tert-butyl nitrone (60 mg/kg). Thus, amphetamine-induced glutamate efflux may involve reactive oxygen species. In other studies, we found that repeated coadministration of alpha-phenyl-N-tert-butyl nitrone with amphetamine attenuated the development of behavioral sensitization. This supports prior results indicating that the increase in glutamate efflux produced by each amphetamine injection in a chronic regimen is important in triggering drug-induced adaptations in ventral tegmental area dopamine neurons, and that such adaptations may in part represent a response to metabolic and oxidative stress

We showed previously that amphetamine challenge produces a delayed increase in glutamate efflux in the ventral tegmental area of both naive and chronic amphetamine-treated rats. The present study examined the mechanisms underlying this response. The NMDA receptor antagonist MK-801 (0.1 mg/kg, i.p.) or the D1 dopamine receptor antagonist SCH 23390 (0.1 mg/kg, i.p.), given 30 min before acute amphetamine (5 mg/kg, i.p.), prevented amphetamine-induced glutamate efflux. Neither antagonist by itself altered glutamate efflux. Ibotenic acid lesions of the prefrontal cortex similarly prevented amphetamine-induced glutamate efflux, while producing a trend toward decreased basal glutamate levels (82.8% of sham group). Previous work has shown that the doses of NMDA and D1 receptor antagonists used in this study prevent the induction of behavioral sensitization when coadministered repeatedly with amphetamine, and that identical prefrontal cortex lesions performed before repeated amphetamine prevent the induction of ambulatory sensitization. Thus, treatments that prevent acute amphetamine from elevating glutamate efflux in the ventral tegmental area also prevent repeated amphetamine from eliciting behavioral sensitization. These findings suggest that repeated elevation of glutamate levels during a chronic amphetamine regimen may contribute to the cascade of neuroadaptations within the ventral tegmental area that enables the induction of sensitization.

Amphetamine or selective D1 and D2 dopamine receptor agonists and antagonists were administered to the ventral tegmental area (VTA) through a microdialysis probe to determine their effects on glutamate and aspartate efflux in rats pretreated for 5 days with vehicle or 5 mg/kg (+)-amphetamine sulfate. In vehicle rats, glutamate efflux declined during 2 h of perfusion with the D1 receptor agonist SKF-82958 (10 and 100 microM). After SKF-82958 perfusion ended, glutamate efflux rebounded to basal levels and continued to increase gradually over the next 2 h. A similar biphasic pattern was observed with intra-VTA amphetamine (10 and 100 microM) and with another D1 agonist (100 microM SKF-38393). The biphasic effects of SKF-82958 were prevented by coperfusion with a D1 antagonist (SCH-23390; 30 microM). Glutamate efflux was unaffected by a D2 agonist (100 microM quinpirole) and by D1 or D2 antagonists administered alone (SCH 23390 and eticlopride; 30 microM). In amphetamine-pretreated rats tested 2 days after the last injection, both the decrease during SKF-82958 perfusion and the delayed increase in glutamate efflux were attenuated. In rats tested 12-14 days after the last amphetamine injection, only the decrease during SKF-82958 perfusion was attenuated. None of these drug treatments produced consistent effects on aspartate efflux. We showed previously that systemic amphetamine (5 mg/kg, i.p.) has no immediate effect on VTA glutamate efflux but produces a delayed increase in glutamate efflux that reaches statistical significance 2-3 h after injection. Because behavioral sensitization can be elicited either by repeated systemic or repeated intra-VTA administration, neurochemical effects common to both routes (such as the delayed increase in glutamate efflux) are most likely to contribute to its induction.

We examined the effect of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX), an antagonist of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptor, on the development and expression of behavioral sensitization to amphetamine and cocaine in rats. A single injection of NBQX (12.5 mg/kg) administered 30 min prior to cocaine during the induction phase (days 1-5) prevented the development of cocaine sensitization, assessed by responsiveness to cocaine challenge on day 8. This NBQX regimen did not affect development of amphetamine sensitization. Two pretreatment injections of NBQX, one 20 min before and one 70 min after amphetamine on each day of the induction phase (days 1-6), did not affect sensitization of stereotypy but prevented sensitization of post-stereotypy ambulatory hyperactivity (both assessed by responsiveness to amphetamine challenge on day 8). The effect of NBQX on ambulatory sensitization was dose-dependent (attenuation with 12.5 mg/kg, complete prevention with 25 mg/kg). In contrast to its effects on development, NBQX (25 mg/kg) did not prevent expression of sensitization to cocaine or amphetamine. NBQX itself exerted no significant effects on locomotor activity in either drug-naive rats or rats that had received either NBQX or amphetamine repeatedly. These findings support a requirement for AMPA receptor stimulation in the development of locomotor sensitization to cocaine and amphetamine, but suggest a different mechanism for sensitization of amphetamine stereotypy.

Recent evidence suggests that behavioral sensitization to amphetamine is associated with alterations in excitatory amino acid (EAA) transmission in perikarya (ventral tegmental area) and terminal regions (nucleus accumbens [NAc]) of the mesoaccumbens dopamine system. The present study determined whether repeated amphetamine administration alters expression of mRNAs for AMPA receptor subunits. We studied the NAc, because it is the site of expression of amphetamine sensitization, and the prefrontal cortex (PFC), because it is the origin of EAA projections that regulate the mesoaccumbens dopamine system. Rats were treated for 5 days with 5 mg/kg/day amphetamine sulfate or vehicle (controls) and perfused 3 or 14 days after the last injection. We used a novel in situ hybridization method that allows quantification of mRNA levels [Lu et al. (1996) J. Neurosci. Methods, 65:69-76]. Repeated amphetamine administration decreased levels of GluR1 and GluR2 but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal. In contrast, levels of GluR1 mRNA in the PFC were increased at 3 but not 14 days of withdrawal, while GluR2 and 3 mRNAs were unchanged. Levels of GluR4 mRNA were very low in both NAc and PFC. Functional properties of heteromeric AMPA receptors are determined by subunit composition. Thus, the observed changes in mRNAs for AMPA receptor subunits may result in altered AMPA transmission in NAc and PFC. This, in turn, may influence the responsiveness of the mesoaccumbens DA system to psychomotor stimulants and potentially contribute to behavioral sensitization.

Recent work indicates an important role for excitatory amino acids in behavioral sensitization to amphetamine. We therefore examined, using in vivo microdialysis in awake rats, the effects of amphetamine on efflux of glutamate, aspartate, and serine in the ventral tegmental area and nucleus accumbens, brain regions important for the initiation and expression of amphetamine sensitization, respectively. Water-pretreated and amphetamine-pretreated rats were compared to determine if sensitization altered such effects. In both brain regions, Ca2+-dependent efflux of glutamate accounted for approximately 20% of basal glutamate efflux. A challenge injection of water or 2.5 mg/kg of amphetamine did not significantly alter glutamate, aspartate, or serine efflux in the ventral tegmental area or nucleus accumbens of water- or amphetamine-pretreated rats. However, 5 mg/kg of amphetamine produced a gradual increase in glutamate efflux in both regions that did not reverse, was observed in both water- and amphetamine-pretreated rats, and was prevented by haloperidol. Although increased glutamate efflux occurred with too great a delay to mediate acute behavioral responses to amphetamine, it is possible that repeated augmentation of glutamate efflux during repeated amphetamine administration results in compensatory changes in levels of excitatory amino acid receptors in the ventral tegmental area and nucleus accumbens that contribute to development of expression of amphetamine sensitization.