Survival of motor neurons and expression of beta-amyloid protein in the aged rat spinal cord.

The present study investigated expression of beta-amyloid protein (AP) and Amyloid precursor protein (APP) in spinal motor neurons of young adult (3 month old) and aged (26-30 month old) rats. The total number of spinal motor neurons in the seventh cervical (C7) spinal segment was also examined in both young adult and aged rats. There was an approximately 21% (p<0.001) decrease in the number of motor neurons of the C7 spinal segment in aged rats compared with young ones. Immunoreactivity (IR) of AP and APP was not observed in spinal motor neurons of young adult rats. In contrast, approximately 50% of the spinal motor neurons of the aged rats were APP positive. Furthermore, extensive immunoreactivity was found in the processes of spinal motor neurons of aged rats. These results have shown that AP and APP is coincident with the loss of motor neurons in the spinal cord of aged rats, and might be associated with the degenerative processes of ageing motor neurons.

Deprivation of endogenous brain-derived neurotrophic factor results in impairment of spatial learning and memory in adult rats.

Brain-derived neurotrophic factor (BDNF) is abundantly expressed in the hippocampus and cerebral cortex and is involved in synaptic plasticity and long-term potentiation (LTP). The present study was under taken to investigate whether endogenous BDNF was required for spatial learning and memory in a rat model. Antibodies to BDNF (anti-BDNF, n=7) or control immunoglobulin G (control, n=6) were delivered into the rat brain continuously for 7 days with an osmotic pump. The rats were then subjected to a battery of behavioral tests. The results show that the average escape latencies in the BDNF antibody treated group were dramatically longer than those of the control (F=13.3, p<0.001). The rats treated with control IgG swam for a significantly longer distance in the P quadrant (where the escape plane had been placed) compared with the other three quadrants (p<0.05). In contrast, anti-BDNF-treated rats swam an equivalent distance in all four quadrants. The average percentage of swimming distance in the P quadrant by anti-BDNF-treated rats was much less than that by control IgG treated rats (p<0.001). These results suggest that endogenous BDNF is required for spatial learning and memory in adult rats.

GABAergic and asymmetrical synapses on somata of GABAergic neurons in CA1 and CA3 regions of rat hippocampus. A quantitative electron microscopic analysis.

BACKGROUND AND PURPOSE: CA1 pyramidal neurons in hippocampus die while CA3 neurons survive after transient ischemia. The imbalance of excitation and inhibition may contribute to this selective vulnerability. The purpose of this study was to examine the morphological basis of the above hypothesis. METHODS: Male Wistar rats were perfused with 4% parafor-maldehyde and 0.2% glutaraldehyde in 0.15 mol/L phosphate buffer. Coronal sections (50 microns) cut on a microtome were processed for gamma-aminobutyric acid (GABA) immunocytochemistry. Sections for electron microscopy were postfixed in 0.5% osmium tetroxide and embedded in high-viscosity epoxy resin. Ultrathin sections were cut and observed with an electron microscope. RESULTS: GABA-positive neurons in the stratum pyramidale received more GABAergic synapses than asymmetrical synapses. The percentage of somatic membrane of GABA-positive neurons covered by asymmetrical synapses in the CA1 region (3.17 +/- 1.13%) was higher than that in the CA3 region (2.15 +/- 0.18%, P < .05). The ratio of asymmetrical to GABAergic synapses per 10 microns somatic membrane in the CA1 region (0.71 +/- 0.22) was higher than that in the CA3 region (0.53 +/- 0.14, P < .05). The ratio of the percentage of somatic membrane covered by asymmetrical/ GABAergic synapses in the CA1 region (0.33 +/- 0.14) was also significantly higher than that in the CA3 region (0.20 +/- 0.07, P < .05). CONCLUSIONS: The GABAergic neurons in the CA1 region receive stronger excitatory inputs than those in the CA3 region, which provides a morphological basis for differences in excitability that may contribute to selective vulnerability after transient ischemia.

Study of the external counterpulsation (ECP) therapy for senile dementia of the Alzheimer's type (SDAT).

Ten patients with SDAT received the ECP therapy. The examination of Hasegawa's Dementia Scale (HDS), single photor emission computed tomography (SPECT) brain imaging, and some biochemical parameters in blood and CSF were selected to evaluate the effect of ECP for SDAT. After ECP treatment, the average HDS score of the patients increased, the value of P was close to 0.05; and the cortical cerebellar ratios of SPECT brain scan, the superoxide dismutase (SOD) activity and the concentrations of somatostatin-like immunoreactivity (SLI), dynorphin AL-13 (Dyn Al-13) in blood and/or CSF were significantly elevated. The results indicated that ECP could not only improve cerebral blood flow, but also make a notable impact on biological active substances in blood and CSF. It is suggested that ECP is beneficial to SDAT patients.