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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Soft computing 4 (2000), S. 214-223 
    ISSN: 1433-7479
    Keywords: Keywords Higher order neurons, Compensatory architecture, Sigma–pi–sigma architecture, Self-scaling scaled conjugate gradient algorithm, Lambda–gamma learning algorithm, Complex backpropagation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science
    Notes: Abstract  Here, we present two new neuron model architectures and one modified form of existing standard feedforward architecture (MSTD). Both the new models use self-scaling scaled conjugate gradient algorithm (SSCGA) and lambda–gamma (L–G) algorithm and entail the properties of basic as well as higher order neurons (i.e., multiplication and the aggregation functions). Of these two, compensatory neural network architecture (CNNA) requires relatively smaller number of inter-neuronal connections, cuts down on the computational budget by almost 50% and speeds up convergence, besides, gives better training and prediction accuracy. The second model sigma–pi–sigma (SPS) ensures faster convergence, better training and prediction accuracy. The third model (MSTD) performs much better than the standard feedforward architecture (STD). The effect of normalizing the outputs for training also studied here shows virtually no improvement, at low iteration level, say ∼500, with increasing range of scaling. Increasing the number of neurons beyond a point also shows to have little effect in the case of higher order neuron.The numerous simulation runs for the problem of satellite orbit determination and the complex XOR problems establishes the robustness of the proposed neuron models architectures.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Several hypothalamic neuropeptides and amino acids are known to inhibit or excite pituitary luteinizing hormone (LH) release, but the precise interplay between these 2 classes of signals in episodic LH discharge is not known. In this study, we have evaluated the interaction between neuropeptides shown previously to inhibit LH release in castrated rats and the excitatory amino acid agonist, N-methyl-D-aspartate (NMDA), on LH release in intact male rats. Rats received a permanent intracerebroventricular (i.c.v.) cannula and 9–12 days later an intrajugular cannula for frequent blood sampling. The next day, rats received i.c.v. either saline (SAL, 3 μl, controls) or a neuropeptide: the opioid β-endorphin (β-END; 2.9 nmol), the tachykinin neuropeptide K (NPK, 2.5 nmol) or the cytokine interleukin-1β (IL-1β, 5.9 pmol) in SAL. The LH response to 2 consecutive i.v. injections of NMDA (5 mg/kg) at 30 min intervals was evaluated. In control rats, each NMDA injection evoked a significant release of LH at 10 min. Quite unexpectedly, the three peptides, instead of exerting an inhibitory effect, enhanced the LH response to NMDA. The peak plasma LH levels after each NMDA injection and the cumulative LH responses were significantly higher in peptide-treated than in control rats. This peculiar ability of the peptides that inhibit LH release in castrated rats, to potentiate the NMDA-induced LH release in the presence of gonadal steroids was further validated in female rats treated with an opiate receptor agonist, morphine (MOR) which is also known to suppress LH release in ovariectomized rats. Rats were ovariectomized (ovx) and 14 days later received one estradiol-17β-containing Silastic® capsule s.c. (E2, 300 μg/ml oil). In addition, each rat received 1 pellet of placebo (PLA, control) or MOR (75 mg/pellet) s.c. followed 2 days later by 2 additional PLA or MOR pellets, and an intrajugular cannula. The LH response of these rats to 2 i.v. injections of NMDA (5 mg/kg) 30 min apart was evaluated. The results showed that each injection of NMDA elicited a pulse of LH with peak levels at 10 min in control rats. However, in MOR-treated rats the LH response to NMDA was amplified; peak and cumulative LH responses were significantly higher in these rats. To ascertain whether this augmentation of LH response induced by MOR was exerted at the hypothalamic level, the effects of NMDA on in vitro LHRH release from the median eminence-arcuate nucleus (ME-ARC) fragment of ovx rats similarly pretreated with E2 and PLA or MOR were compared. The results showed that LHRH efflux in response to 50 mM NMDA alone and in combination with 23 mM KCl was higher in MOR-treated than in control rats. Cumulatively, these results show that activation of hypothalamic opioid, tachykinin and cytokine receptors which ordinarily result in suppression of LH release in gonadal steroid deficient rats, concurrently enhances the excitatory LH response of NMDA under the influence of gonadal steroids. These unexpected findings reveal a novel modality of involvement of these peptides in the hypothalamic control of pituitary LH release. While these peptides may play a role in attenuating LH secretion in intact rats, our studies are in accord with the view that these peptides enhance the response of the hypothalamo-pituitary axis to incoming signals, including the excitatory amino acids, that excite the release of LH.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ciliary neurotrophic factor (CNTF), a cytokine of the interleukin-6 superfamily, has been shown to induce hypophagia and weight loss. Neuropeptide Y (NPY) and orexin are potent orexigenic signals in the hypothalamus. Anorexia, normally seen in response to infection, injury and inflammation, may result from diminished hypothalamic orexigenic signalling caused by persistently elevated cytokines, including CNTF. To test this hypothesis, we first examined the effects of chronic intracerebroventricular (i.c.v.) infusion of CNTF for 6–7 days on food intake and body weight as well as hypothalamic NPY and orexin gene expression in male rats. Subsequently, the effectiveness of NPY replacement to counteract the effects of CNTF by coinfusion of NPY and CNTF was evaluated. Chronic i.c.v. infusion of CNTF (2.5 µg/day) reduced body weight (14.3% vs control) at the end of 7 days. Food intake remained suppressed for 5 days postinfusion and subsequently gradually returned to the control range by day 7. Serum leptin concentrations in these rats were in the same range seen in control rats. Chronic i.c.v. infusion of higher doses of CNTF (5.0 µg/day) produced sustained anorexia and body weight loss (29% vs controls) through the entire duration of the experiment. This severe anorexia was accompanied by markedly suppressed serum leptin concentrations. Furthermore, CNTF infusion alone significantly reduced hypothalamic NPY gene expression (P 〈 0.05) without affecting orexin gene expression. As expected, in fusion of NPY alone (18 µg/day) augmented food intake (191.6% over the initial control, P 〈 0.05) and produced a 25.1% weight gain in conjunction with a 10-fold increase in serum leptin concentrations at the end of the 7-day period. Interestingly, coinfusion of this regimen of NPY with the highly effective anorectic and body reducing effects of CNTF (5.0 µg/day) not only prevented the CNTF-induced anorexia and weight loss, but also normalized serum leptin concentrations and hypothalamic NPY gene expression. These results demonstrate that chronic central infusion to produce a persistent elevation of the cytokine at pathophysiological levels (a situation that may normally manifest during infection, injury and inflammation) produced severe anorexia and weight loss in conjunction with reduction in both serum leptin concentrations and hypothalamic NPY gene expression. Reinstatement of hypothalamic NPY signalling by coinfusion of NPY counteracted these CNTF-induced responses.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Microinjection of colchicine (COL), a neurotoxin that blocks axoplasmic flow in the neurons, bilaterally into the ventromedial nucleus (VMN) evokes transient hyperphagia and body weight gain. These shifts in energy balance occurred in conjunction with development of increased sensitivity to neuropeptide Y (NPY), the endogenous orexigenic signal. In order to trace the aetiology of NPY supersensitivity, we have evaluated (1) NPY Y1 and Y5 receptor (R) gene expression in the hypothalamus and (2) the possibility of alterations in the inhibitory action of leptin, a hormone produced by lipocytes. Adult male rats were rendered hyperphagic with bilateral microinjections of COL (4 μg/side) into the VMN. We observed that hypothalamic NPY Y1 mRNA levels, as measured by RNAase protection assay, were significantly increased on day 2 and returned to the control level on day 4 in COL-injected rats. The effects on NPY Y5R mRNA were not as clear cut. Interestingly, serum leptin levels increased in association with the hyperphagia and body weight gain, thereby raising the likelihood of development of resistance to the suppressive effect of endogenous leptin on food intake. Indeed, intracerebroventricular injection of 7 μg human recombinant leptin, a dose that attenuated daily food intake in normal and fasted rats, was completely ineffective in attenuating hyperphagia in COL-treated rats. These results show that transient hyperphagia induced by interruption of signalling in the VMN may be caused by increased sensitivity to NPY, which may be caused, in part, by increased expression of NPY Y1R in hypothalamic sites involved in regulation of ingestive behaviour. Additionally, the observation of increased leptin release and concurrent development of leptin resistance suggest that a normally functioning VMN may be necessary for the central inhibitory effects of leptin on food intake.
    Type of Medium: Electronic Resource
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