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Effects of cholinergic modulation on responses of neocortical neurons to fluctuating input 总被引:1,自引:0,他引:1
Neocortical neurons in vivo are spontaneously active and intracellular
recordings have revealed strongly fluctuating membrane potentials arising
from the irregular arrival of excitatory and inhibitory synaptic
potentials. In addition to these rapid fluctuations, more slowly varying
influences from diffuse activation of neuromodulatory systems alter the
excitability of cortical neurons by modulating a variety of potassium
conductances. In particular, acetylcholine, which effects learning and
memory, reduces the slow alterhyperpolarization, which contributes to spike
frequency adaptation. We used whole-cell patch-clamp recordings of
pyramidal neurons in neocortical slices and computational simulations to
show, first, that when fluctuating inputs were added to a constant current
pulse, spike frequency adaptation was reduced as the amplitude of the
fluctuations was increased. High- frequency, high-amplitude fluctuating
inputs that resembled in vivo conditions exhibited only weak spike
frequency adaptation. Second, bath application of carbachol, a cholinergic
agonist, significantly increased the firing rate in response to a
fluctuating input but minimally displaced the spike times by < 3 ms,
comparable to the spike jitter observed when a visual stimulus is repeated
under in vivo conditions. These results suggest that cholinergic modulation
may preserve information encoded in precise spike timing, but not in
interspike intervals, and that cholinergic mechanisms other than those
involving adaptation may contribute significantly to cholinergic modulation
of learning and memory.
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110.
Abstract Protein-chemical and molecular studies were conducted on all osteogenesis imperfecta (OI) type III/IV patients referred to our hospital during the last 15 y. Of a total of 16 OI type III/IV patients studied, 15 patients were heterozygous for a mutation in one of the two genes coding for collagen I, COL1A1 or COL1A2. Cultured fibroblasts from these 15 patients produced both normal and abnormal collagen I molecules, pointing to a dominant-negative effect of the mutation. Nine mutations had not been described previously. Parental mosaicism was demonstrated in three families. In the 16th child the causative mutation was not found. In conclusion, OI type III/IV in most patients of Western European ancestry is caused by dominant mutations in the genes for collagen I, and recurrence of OI is caused in most cases by parental gonadal mosaicism. 相似文献