PubMed Health⌕ Search

PubMed · 10935461

Pattern segmentation in a binary/analog world: unsupervised learning versus memory storing.

Abstract

We discuss the problem of segmentation in pattern recognition. We adopt the model and the general approach in the landmark paper by Wang, Buhmann and von der Malsburg (Neural Computation, (1990), 2, 94-106), and expand their model in a number of ways. We review their solution to the segmentation problem in associative memory, which consists in feature binding being expressed by synchrony relations between oscillators or populations of neurons. We extend the model by introducing a law of synaptic change, which allows the network to learn by structuring itself in response to stimuli with relevant features. We discuss the problem of interference between pattern completion and the learning of new memories. We also propose a form of multiplexing of input information taking advantage of the time-structure of the neurons' response. It is based on the assessment of analog as well as of binary properties of the stimuli and provides for an enhancement of the network's processing capacity. The relevance of the results for biological systems is pointed out.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C Lourenço, A Babloyantz, M Hougardy. 2000. Pattern segmentation in a binary/analog world: unsupervised learning versus memory storing.. https://doi.org/10.1016/s0893-6080(99)00087-8

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Stereoselectivities of enantiomers of huperzine A in protection against beta-amyloid(25-35)-induced injury in PC12 and NG108-15 cells and cholinesterase inhibition in mice.

Recently, the potent cholinesterase inhibitor (-)-huperzine A (HupA) was demonstrated to protect neuronal and glial cells against the cytotoxicity of beta-amyloid (Abeta). Since the unnatural (+)-HupA is a much less potent inhibitor, it was of interest to examine the stereoselectivity of cellular protection by the two isomers. In the present study, effects of (+)- and (-)-HupA on Abeta(25-35)-induced injury were compared in PC12 and NG108-15 neuroblastoma cell lines. Following a 24 h exposure to 1 microM Abeta(25-35), cell survival was markedly reduced, but preincubation with (+)-HupA or (-)-HupA (0.1-10 microM) enhanced survival significantly. The potency of (-)-HupA and (+)-HupA in protecting against Abeta toxicity was similar. This result contrasted with the stereoselectivity of cholinesterase inhibition in vitro and in vivo, in which (-)-HupA is about 50-fold more potent than (+)-HupA. It is concluded that the neuroprotective properties of HupA enantiomers have no relation to anti-cholinesterase activity.

Acetylcholine↗

Intravenously administered lidocaine in therapeutic doses increases the intraspinal release of acetylcholine in rats.

The local anesthetic lidocaine suppresses different pain conditions when administered systemically. Part of the antinociceptive effect appears to be mediated via receptor mechanisms. We have previously shown that muscarinic and nicotinic agonists that produce antinociception increase the intraspinal release of acetylcholine. In the present study it was hypothesized that systemically administered lidocaine is acting through the same mechanisms as cholinergic agonists and affects the intraspinal release of acetylcholine. Microdialysis probes were placed in anesthetized rats for sampling of acetylcholine. Ten and 30 mg/kg lidocaine injected intravenously significantly increased the intraspinal release of acetylcholine. The effect of lidocaine could be reduced by pretreatment with intraspinally administered atropine or mecamylamine. Our results suggest that the antinociceptive effect produced by systemically administered lidocaine is mediated through an action on muscarinic and nicotinic receptors.

Acetylcholine↗

Distribution of the high-affinity choline transporter in the human and macaque monkey spinal cord.

The distribution of the high-affinity choline transporter (CHT) was determined in the human and macaque monkey spinal cord using in situ hybridization histochemistry and immunohistochemistry. Signals for CHT mRNA were observed in somatic motor neurons, sympathetic preganglionic neurons, and neurons in the medial part of lamina VII. The mRNA for CHT was co-localized in single neurons with the mRNAs for vesicular acetylcholine transporter and cholineacetyltransferase. These same cholinergic neuronal groups were labeled by immunohistochemistry for human CHT. Of somatic motor neurons, smaller cell bodies of gamma-motor neurons were labeled very intensely, whereas larger cell bodies of alpha-motor neurons showed various degrees of labeling from weak to moderately intense. Human CHT is thus a novel cholinergic marker, which not only labels cholinergic neurons, but also reveals their heterogeneity.

Acetylcholine↗