Although long-term potentiation (LTP) is long-lasting, it is not permanent and decays within weeks after its induction. Little is known about the processes underlying this decay. Here we assessed the contribution of synaptic activity to LTP decay by determining the effect of the competitive NMDA receptor antagonist CPP on the decay of perforant path-dentate LTP. CPP blocked decay over a one-week period when administered daily following the induction of LTP, and blocked decay of the late, protein-synthesis-dependent phase of LTP when administered two days after LTP induction. CPP administered for a five-day period following spatial memory training enhanced subsequent memory retention. These data suggest that LTP is normally a persistent process that is actively reversed by NMDA receptor activation, and that both the early and late phases of LTP are dynamic processes regulated by NMDA receptors. These data also support the view that LTP is involved in maintaining spatial memory.
Previous investigations have shown that ethanol is neuroprotective following experimental traumatic brain injury (TBI). This study sought to determine if the neuroprotective effects of ethanol in a controlled cortical impact (CCI) injury model are related to its effects on cerebral glucose metabolism and blood flow. Adult rats were given ethanol (1.0 g/kg) or saline by intraperitoneal injection followed 40 min later by injury. Regional cerebral blood flow (CBF) and cerebral metabolic rates of glucose (CMRglc) were determined immediately, and at 3, 6, 12, 24, and 72 h postinjury using quantitative autoradiography. Immediately after injury, CMRglc in the contusion core and penumbra was reduced in the ethanol group compared to the saline group: (core CMRglc: 52.2 +/- 16.0 versus 94.2 +/- 14.1 micromol/100 g/min, respectively,p < 0.001; penumbral CMRglc: 58.2 +/- 12.8 versus 82.8 +/-19.7 micromol/100 g/min, respectively; p < 0.05) However, at 24 and 72 h postinjury, penumbral CMRglc in the ethanol group was increased compared to the saline group (p < 0.05 and p < 0.001, respectively). Regarding CBF, contusion core values in the ethanol group were elevated compared to the saline group immediately postinjury, (70.4 +/- 17.1 versus 31.5 +/- 27.8 mL/100 g/min, respectively (p < .05), and at 6, 12, and 24 h postinjury (p < 0.05). Penumbral CBF was also higher at 6 and 72 h in the ethanol group compared to the saline group (p < 0.05). These results indicate that low-dose ethanol is associated with a marked attenuation of immediate postinjury hyperglycolysis and with more normal glucose metabolism in the injury penumbra over the ensuing 3 days. Simultaneously, the reduction in CBF typically seen within the contusion core and penumbra after CCI is less severe when ethanol is present. The net effect of these changes is a decreased degree of uncoupling between glucose metabolism and CBF that otherwise occurs in the absence of ethanol. These changes may likely explain the neuroprotective effect of ethanol.
A 49-year-old woman with a history of asthma and a pneumatocele secondary to a past pneumonia (Fig. 1, prior baseline chest X-ray) presented with fever, cough, and shortness of breath. This was her third admission for similar symptoms. In the past, these symptoms had resolved with antibiotics and percutaneous drainage of the infected pneumatocele. Her admission chest X-ray revealed a fluid-filled pneumatocele (Fig. 2). Given the recurrent nature of her disease, a right middle lobectomy was performed. Her recovery after surgery was uneventful, and she continues to do well 4 months later.Pneumatoceles are air-filled cysts that occur because of trauma or inflammation in the lung parenchyma. The most common cause is pneumonia and they occur most frequently in children. Complications of pneumatocele include pneumothorax and, as in this patient, secondary infection. In most instances the pneumatocele resolves after treating the underlying pneumonia, but surgical intervention is sometimes required to have a definitive cure.
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