Voltage-dependent N-type Ca 21 channels, along with the P/Q-type, have a crucial role in controlling the release of neurotransmitters or neuromodulators at presynaptic terminals. However, their role in hippocampus-dependent learning and memory has never been examined. Here, we investigated hippocampus-dependent learning and memory and synaptic plasticity at hippocampal CA3-CA1 synapses in mice deficient for the a 1B subunit of N-type Ca 21 channels. The mutant mice exhibited impaired learning and memory in the Morris water maze and the social transmission of food preference tasks. In particular, long-term memory was impaired in the mutant mice. Interestingly, among activity-dependent long-lasting synaptic changes, theta burst-or 200-Hzstimulation-induced long-term potentiation (LTP) was decreased in the mutant, compared with the wild-type mice. This type of LTP is known to require brain-derived neurotrophic factor (BDNF). It was found that both BDNF-induced potentiation of field excitatory postsynaptic potentials and facilitation of the frequency of miniature excitatory postsynaptic currents (mEPSCs) were reduced in the mutant. Taken together, these results demonstrate that N-type Ca 21 channels are required for hippocampus-dependent learning and memory, and certain forms of LTP.

These study findings suggest that anaemia can be used to identify patients with ACS who are at a high risk of death or adverse events, and it may become a promising risk stratification factor in ACS.

A longitudinal, prospective, controlled evaluation of magnetic resonance images (MRI) of long bones in sickle cell patients was undertaken simultaneously with assessment of clinical status and hematologic parameters, including dense erythrocytes. MRI of bone marrow in sickle cell patients during steady states appeared patchy and were markedly different from those in matched controls (P approximately 0). Patients with severe patchiness were older than those with mild or moderate patchiness (P less than .03). Sixty-nine MRI were performed during 28 painful episodes occurring in 14 subjects with sickle cell disease (SCD). Increased signals on intermediate and T2-weighted images were detected in 35.7% of painful episodes. These abnormalities were distinct and not observed to occur spontaneously during the steady- state examinations (P approximately 0). Bone marrow infarcts were confirmed by biopsy in two instances and autopsy in one instance. Dense red cells decreased by 40.81% of baseline during pain crises (P = .00005), more remarkably in those who had pain in the lower extremities (P = .0145). Patients with change in MRI during pain crises had a greater percentage change in the dense cells than those without the change in MRI (69.7% v 31.3%, P = .0120).

A longitudinal, prospective, controlled evaluation of magnetic resonance images (MRI) of long bones in sickle cell patients was undertaken simultaneously with assessment of clinical status and hematologic parameters, including dense erythrocytes. MRI of bone marrow in sickle cell patients during steady states appeared patchy and were markedly different from those in matched controls (P approximately 0). Patients with severe patchiness were older than those with mild or moderate patchiness (P less than .03). Sixty-nine MRI were performed during 28 painful episodes occurring in 14 subjects with sickle cell disease (SCD). Increased signals on intermediate and T2-weighted images were detected in 35.7% of painful episodes. These abnormalities were distinct and not observed to occur spontaneously during the steady- state examinations (P approximately 0). Bone marrow infarcts were confirmed by biopsy in two instances and autopsy in one instance. Dense red cells decreased by 40.81% of baseline during pain crises (P = .00005), more remarkably in those who had pain in the lower extremities (P = .0145). Patients with change in MRI during pain crises had a greater percentage change in the dense cells than those without the change in MRI (69.7% v 31.3%, P = .0120).