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Norio Matsuki

Publications and source records attributed to Norio Matsuki.

41 records · Page 3Linked to original sources

BDNF attenuates hippocampal LTD via activation of phospholipase C: implications for a vertical shift in the frequency-response curve of synaptic plasticity.

Recent evidence shows that neurotrophins are not only involved in neuronal survival and differentiation during development but also in modulating synaptic strength in the mature brain. To understand how neurotrophins alter this synaptic modification, we have investigated the effect of brain-derived neurotrophic factor (BDNF) on long-term depression (LTD) at Schaffer collateral-CA1 synapses in rat hippocampal slices. The slices treated with BDNF for 5 min showed significantly less LTD in response to a 1-Hz tetanus compared with controls but displayed normal LTD when the afferents were tetanized at 10 Hz. Because BDNF enhanced long-term potentiation (LTP) induced by a 30-Hz tetanus, the synaptic modification threshold (theta(m)) as defined in the 'BCM' theory of Bienenstock Cooper & Monroe [Bienenstock et al. (1982), J. Neurosci., 2, 32-48] was not shifted. BNDF is likely to alter the capability of the plastic changes in synaptic efficacy, i.e. to produce an upward shift in the BCM curve. The suppressive effect of BDNF on LTD was prevented by either the tyrosine kinase (Trk) receptor inhibitor K252a or the phospholipase C inhibitor U73122. Thus, TrkB activation may attenuate LTD through phospholipase C signalling pathway.

Animals↗

Hippocampal long-term depression as an index of spatial working memory.

Long-term potentiation (LTP), a form of synaptic plasticity in the hippocampus, is a cellular model for the neural basis of learning and memory, but few studies have investigated the contribution of long-term depression (LTD), a counterpart of LTP. To address the possible relationship between hippocampal LTD and spatial performance, the spatial cognitive ability of a rat was assessed in a spontaneous alternation test and, thereafter, LTD in response to low-frequency burst stimulation (LFBS) was monitored in the dentate gyrus of the same rat under anaesthesia. To enhance a divergence in the ability for spatial performance, some of the animals received fimbria-fornix (FF) transection 14 days before the experiments. LTD was reliably induced by application of LFBS to the medial perforant path of intact rats, while no apparent LTD was elicited in rats with FF lesions. The behavioural parameters of spatial memory showed a significant correlation with the magnitude of LTD. We found no evidence that the cognitive ability correlated with other electrophysiological parameters, e.g. basal synaptic responses, stimulus intensity to produce half-maximal responses, paired-pulse facilitation or paired-pulse depression. These results suggest that the magnitude of LTD in the dentate gyrus serves as a reliable index of spatial cognitive ability, providing insights into the functional significance of hippocampal LTD.

Animals↗

Effects of 17beta-estradiol and xenoestrogens on the neuronal survival in an organotypic hippocampal culture.

Xenoestrogens are man-made compounds that mimic the actions of estrogens through interactions with estrogen receptors (ERs). Although xenoestrogens have received a great deal of attention as possible causes of brain disfunctions, little information concerning the effects of xenoestrogens on the central nervous system is available. In this study, we investigated the effects of 17beta-estradiol (E(2)) and four xenoestrogens (17alpha-ethynylestradiol, diethylstilbestrol, p-nonylphenol and bisphenol A (BPA)) on the neuronal survival using organotypic hippocampal slice cultures. When the cultured hippocampal slices were exposed to glutamate (1 mM, 15 min), the CA1-selective neuronal damage was induced. Pretreatment with E(2) and the xenoestrogens (24 h) selectively exacerbated the CA3 neuronal damage caused by glutamate. In spite of the marked difference of binding affinities to ERs, all compounds revealed maximal effects at 1 nM. ER antagonists, tamoxifen and ICI 182,780, did not affect responses to E(2) and the xenoestrogens, indicating that these effects are mediated through mechanisms other than ERs. In spite of the fact that BPA has little interaction with ERs at 1 nM, E(2) and BPA equally increased the expression of N-methyl-D-aspartate receptor in CA3 and upregulated the spine density of the apical portion of CA3 dendrites at 1 nM. These compounds also enhanced the sprouting of mossy fibers to CA3 neurons. These results suggest that exposure to E(2) and xenoestrogens during the developmental stage results in a marked influence on synaptogenesis and neuronal vulnerability through mechanisms other than ERs.

Animals↗

Hyperpolarization-activated current I(h) in nucleus of solitary tract neurons: regional difference in serotonergic modulation.

The nucleus of solitary tract (NTS) contains diverse neural circuits responsible for basic vital functions. We examined the effect of serotonin (5-HT) on hyperpolarization-activated current (I(h)) in neurons acutely isolated from caudal, medial and rostral parts of the NTS. Caudal and medial NTS neurons showed a large amplitude of I(h) compared with rostral neurons. In these neurons, perfusion with 5-HT potentiated Ih amplitude in a concentration-dependent manner. The effect of 5-HT was blocked by NAN-190, a 5-HT1A receptor antagonist. Thus, 5-HT1A receptors may regulate I(h) channel activity in caudal and medial NTS neurons.

Analysis of Variance↗

Vasopressin induces emesis in Suncus murinus.

This paper reports that vasopressin is emetogenic in the house musk shrew Suncus murinus. Either intravenous or intracerebroventricular administration of vasopressin caused vomiting within a few minutes. The ED50 of intravenous vasopressin was as high as 4.67 microg/kg, whereas intracerebroventricularly injected vasopressin was effective at a low dose of 20 ng/brain. The emetogenic target of vasopressin may therefore be present in the central nervous system. We propose the Suncus as a useful animal for investigation of vasopressin-mediated emesis, including motion sickness.

Animals↗