Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of exogenous neuraminidase on spontaneous and evoked synaptic activity was investigated following injection of the enzyme into frog spinal cord and into cord and into the carp optic tectum. 1. Injection of enzyme into spinal cord segments caused a significant increase of motoneuron activity in the corresponding spinal nerve, which lasted for 7--31 min. 2. The amplitude of postsynaptic evoked potentials in the optic tectum was increased after neuraminidase injection up to 200% of control level for 20--40 min, whereas the amplitude of summed action potentials of retino-tectal afferents remained unchanged. 3. Similar effects were observed in single cell responses of the optic tectum with some differences in the degree of increase in activity, as well as latency and final depression of the stimulus response. 4. The extent of neuraminic acid liberation following neuraminidase treatment was determined biochemically. In both tissues investigated the amount of free neuraminic acid was increased significantly (4--5.5 fold) after enzyme treatment. Whereas after enzyme injection into spinal cord and optic tectum the percentage release of total glycoprotein- and glycolipidbound neuraminic acid was 12% and 15%, respectively, liberation from enzyme incubated tissue homogenates was somewhat higher (20.5% and 24%).
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PMID:Effects of exogenous neuraminidase on unit activity in frog spinal cord and fish optic tectum. 21 38

The effects of mescaline and LSD on the flash-evoked cortical potential (FEP) were determined in unrestrained rats with chronically-implanted electrodes. Systemic administration of mescaline or LSD significantly attenuated the primary component of the FEP at three stimulus intensities with the greatest effect observed 60-90 minutes following drug administration. The magnitude and specificity of the effects of these agents on the primary response suggest that they produce deficits in conduction through the retino-geniculato-cortical system. The serotonin receptor antagonists, cyproheptadine and methysergide, antagonized the mescaline-induced depression of the FEP in accordance with neurochemical and behavioral evidence that mescaline acts as a partial agonist on serotonin receptors. Topical or intraocular administration of atropine antagonized the actions of systemically-administered mescaline. In addition, intraocular administration of mescaline or LSD attenuated the FEP indicative of an action of these hallucinogens on visual processing in the retina which is modulated by muscarinic receptor activity.
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PMID:Effects of intraocular mescaline and LSD on visual-evoked responses in the rat. 273 30

Field potentials evoked in the turtle general cortex by electric stimulation of the optic tectum were analyzed. Cathodal polarization and subtotal lesions of n. rotundus led to either facilitation or depression of later components of the cortical potential. On the contrary, cathodal polarization and lesions of n.geniculatus lateralis dorsalis similarly affected the initial component. After 21-23 months following eye enucleation or optic nerve section, the conduction of fast tectal volleys to the general cortex via n. geniculatus lateralis dorsalis was blocked, though the conduction of tectal impulses to the dorsal ventricular ridge via n.rotundus survived. It is concluded that in turtles one more visual channel, i.e., retino-tecto-geniculo-cortical, is functioning, in addition to well-known retino-tecto-rotundo-telencephalic and retino-geniculo-cortical channels.
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PMID:An underestimated visual pathway in reptiles. 404 69

Interactions between retino-collicular and retino-cortical pathways at the level of the lateral geniculate nucleus were studied in anesthetized and paralyzed rabbits. In a first series of experiments the cortico-geniculate influence was analyzed by cortical depression. The disruption of cortical functions led to a specific abolition of the geniculate responses to right-left movement of the stimulating spot. The response to the opposite direction was unaffected. In a second series of experiments the stimulus presentation was triggered by a spontaneous collicular spike. This resulted in a significant modification of the geniculate responses recorded simultaneously suggesting that the superior colliculus is capable of modifying the transmission that occurs through the geniculate. Data are discussed in view of the visuo-motor integration.
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PMID:[Interactions between retino-collicular and retino-cortical pathways at the level of the lateral geniculate nucleus]. 724 20

The pineal gland releases melatonin into the blood stream in response to sympathetic noradrenergic stimulation of pinealocytes. This process is inhibited by light via the retino-hypothalamic-pineal pathway. Hence melatonin is predominantly released in darkness. Because serotonin is a precursor of melatonin, the intake of dietary tryptophan may also influence melatonin levels. Although the exact physiological role of melatonin in humans is unclear, it appears to be implicated in reproductive physiology, especially in terms of the onset of menarche. Low levels of melatonin also occur in depression. In this review, studies of melatonin in patients with anorexia nervosa and bulimia nervosa are considered in relation to potential abnormalities of noradrenergic function and circadian rhythm. The influence of weight loss, binging and purging, and depression on melatonin is discussed. Other studies involving the assessment of melatonin in relation to menstrual function are required.
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PMID:Melatonin disturbances in anorexia nervosa and bulimia nervosa. 783 59

Group III metabotropic glutamate receptors (especially mGlu4, mGlu7, mGlu8) are thought to be involved in modulating visual processing in the adult superior colliculus, a major termination site of retinal input in the rodent brain. We have investigated this role by making field EPSP recordings in response to optic tract stimulation in superior colliculus slices taken from rats aged from P14 to P180. Application of the Group III agonist L-AP4 at a concentration (10 microM) effective to activate mGlu4 and mGlu8 receptors, but not mGlu7 receptors, resulted in reductions of the field EPSP in all ages, although the effect was greatest in slices taken from P14 rats. Increasing the L-AP4 concentration to 100 microM so as to also activate mGlu7 receptors resulted in further field EPSP reductions. Similar reductions were seen in the combined presence of the GABA antagonists picrotoxin and CGP55845A, indicating a lack of involvement of GABAergic mechanisms in the action of L-AP4. Pairing of optic tract stimuli (20 ms separation) resulted in paired-pulse depression at all ages. L-AP4 was found to reduce paired-pulse depression at both 10 microM and 100 microM in slices from all ages of rat. The results of this study suggest that mGlu4/mGlu8 and mGlu7 receptors modulate retino-tectal transmission via a presynaptic mechanism, and that these effects are greatest in young animals. This is the first demonstration of a functional change in Group III receptor effect with aging, and this would be consistent with developmental regulation of these receptors.
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PMID:Modulation of retino-collicular transmission by Group III metabotropic glutamate receptors at different ages during development. 1602 83

To gain a deeper understanding of the transmission of visual signals from retina through the lateral geniculate nucleus (LGN), we have used a simple leaky integrate and-fire model to simulate a relay cell in the LGN. The simplicity of the model was motivated by two questions: (1) Can an LGN model that is driven by a retinal spike train recorded as synaptic ('S') potentials, but does not include a diverse array of ion channels, nor feedback inputs from the cortex, brainstem, and thalamic reticular nucleus, accurately simulate the LGN discharge on a spike-for-spike basis? (2) Are any special synaptic mechanisms, beyond simple summation of currents, necessary to model experimental recordings? We recorded cat relay cell responses to spatially homogeneous small or large spots, with luminance that was rapidly modulated in a pseudo-random fashion. Model parameters for each cell were optimized with a Simplex algorithm using a short segment of the recording. The model was then tested on a much longer, distinct data set consisting of responses to numerous repetitions of the noisy stimulus. For LGN cells that spiked in response to a sufficiently large fraction of retinal inputs, we found that this simplified model accurately predicted the firing times of LGN discharges. This suggests that modulations of the efficacy of the retino-geniculate synapse by pre-synaptic facilitation or depression are not necessary in order to account for the LGN responses generated by our stimuli, and that post-synaptic summation is sufficient.
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PMID:A simple model of retina-LGN transmission. 1776 31

The effects of N-methyl carbamate pesticides on the photic after discharge (PhAD) of flash evoked potentials (FEPs) and the relationship between inhibition of brain cholinesterase (ChE) activity and the PhAD were evaluated. FEPs were recorded in Long Evans rats treated with physostigmine (s.c.) 0, 0.05, 0.1, 0.2 or 0.3mg/kg (free base), in an ascorbic acid/saline vehicle, carbaryl (p.o.) 0, 1, 3, 10, 30, 50 or 75 mg/kg, or propoxur (p.o.) 0, 0.3, 3, 10, 20, 30, or 40 mg/kg in a corn oil vehicle. Physostigmine served as positive control based on literature data. Early (e.g. peak N(36)) and late FEP components (peak N(166) and PhAD) are related to the initial retino-geniculate afferent volley and higher cortical processing of visual information, respectively. Compared to controls, the PhAD duration decreased following treatment with 0.1 and 0.3mg/kg physostigmine, 7 5 mg/kg carbaryl or 30 mg/kg propoxur. Lesser changes were noted in FEP amplitudes or peak latencies. Treatment with 0.2 or 0.3 mg/kg physostigmine increased peak N(36) latency. Peak N(166) latency increased only following exposure to 40 mg/kg propoxur. None of the compounds altered peak N(36) or N(166) amplitudes. Hypothermia was observed at doses greater than 0.05 mg/kg physostigmine, at 30 or 50 mg/kg carbaryl, and after treatment with 10, 20 or 40 mg/kg propoxur. Inhibition of brain ChE activity occurred at dosages greater than 0.05 mg/kg physostigmine, 1mg/kg carbaryl, and 0.3 mg/kg propoxur. Linear regression analysis indicated that the decrease in PhAD duration correlated with decrease in brain ChE activity. The results indicate that at 30 min after treatment, inhibition of brain ChE activity did not affect cortical processing of the input from the retino-geniculate volley (evidenced by unaltered peak N(36) amplitude). However, the data suggest that disruption of cortical processing of visual signals related to FEP late components, as indicated by depression of the PhAD, was related to inhibition of brain ChE activity.
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PMID:Depression of the photic after discharge of flash evoked potentials by physostigmine, carbaryl and propoxur, and the relationship to inhibition of brain cholinesterase. 1795 Aug 90

Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases that play an instrumental role in signal transduction from the cell surface to the nucleus. These enzymes are major intracellular mediators of developmental events and recently have been shown to control also synaptic plasticity processes [Sweatt, J.D., 2004. Mitogen-activated protein kinases in synaptic plasticity and memory. Curr. Opin. Neurobiol. 14, 311-317; Thomas, G.M., Huganir, R.L., 2004. MAPK cascade signalling and synaptic plasticity. Nat. Rev. Neurosci. 5, 173-183]. Mammalian members of this family are extracellular signal-regulated kinases 1/2 (ERK 1/2), c-Jun amino-terminal kinases or stress-activated protein kinases (JNK/SAPKs) and p38 kinases (p38(MAPK)). At the level of the visual system, it has been demonstrated that the ERK pathway regulates developmental plastic processes at both retino-thalamic and thalamo-cortical level and that p38(MAPK) controls a peculiar form of long-term depression in the visual cortex [Di Cristo, G., Berardi, N., Cancedda, L., Pizzorusso, T., Putignano, E., Ratto, G.M., Maffei, L., 2001. Requirement of ERK activation for visual cortical plasticity. Science 292, 2337-2340; Naska, S., Cenni, M.C., Menna, E., Maffei, L., 2004. ERK signaling is required for eye-specific retino-geniculate segregation. Development 131, 3559-3570; Xiong, W., Kojic, L.Z., Zhang, L., Prasad, S.S., Douglas, R., Wang, Y., Cynader, M.S., 2006. Anisomycin activates p38 MAP kinase to induce LTD in mouse primary visual cortex. Brain Res. 1085, 68-76]. Here, as a first approach to gain more insight on the role of two MAPKs - ERK1/2 and p38(MAPK) - in visual system maturation, we characterized by western blot the regulation of their phosphorylation/activation in rat retina, superior colliculus and visual cortex, during postnatal development from birth to adult age. Our main results show that: (i) in the retina p38(MAPK) activation peaks at P4, and then, from P15 to P45, both ERK1/2 and p38(MAPK) phosphorylation increases; (ii) in the superior colliculus phosphorylation of both MAPKs increases between P4 and P15; (iii) in the visual cortex ERK1/2 phosphorylation increases from P15 to P45, while phosphorylation of p38(MAPK) increases starting from P4. The present data demonstrate a distinct regulation of the activation of ERK1/2 and p38(MAPK) in the three visual areas analyzed which occurs in temporal correlation with critical events for visual system maturation. These results suggest an important role for ERK1/2 and p38(MAPK) in the postnatal development of the rat visual system.
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PMID:The activation of ERK1/2 and p38 mitogen-activated protein kinases is dynamically regulated in the developing rat visual system. 1828 Jun 91

For more than 50 years, Parkinson's disease (PD) has been conceptualized as a product of nigro-striatal dopamine (NSD) system degeneration. In spite of a growing body of evidence depicting the mammalian brain as an interrelated complexity of circuitous systems, dopamine (DA) deficiency of the NSD is still regarded as the main problem, with DA replacement being the purpose of therapeutic intervention. For at least 191 years circadian involvement in various aspects of PD, including depression and insomnia, has been recognized as an integral part of the symptom matrix of PD and yet attempts to elucidate the involvement of this system is uncharted territory. The present review attempts a major reorganization of mammalian brain into a coordinated complex involving the NSD and the retinal hypothalamic tract (RHT) as the primary systems involved in the retino-diencephalic/mesencephalic-pineal (RDMP) axis. Secondary systems including the lateral hypothalamus (LH), the area postraema (AP) and the subthalamic nucleus (STN) also form an integral part of this system as they have been shown to be either intimately related to the primary systems of the RDMP axis or have been shown to be significantly involved in the expression and treatment of PD. A large volume of evidence suggests that the RDMP axis is activated during the course of PD and during therapeutic intervention. Four types of neurotoxicity associated with melatonin are identified and the susceptibility of various parts of the RDMP axis to undergo neuropathological change, the tendency for melatonin to induce PD-like behavioural toxicity, and the relationship of this to PD symptomotology are described. This includes adverse effects of melatonin on motor function, hypotension, the adjuvant use of benzodiazepines, depression, insomnia, body weight regulation and various biochemical effects of melatonin administration: all problems currently facing the proposal to introduce melatonin as an adjuvant. It is suggested further that traditional DA replacement may well work by exerting its effect upon the circadian system, rather than simply replacing deficient DA. Activation of the circadian function by antagonizing melatonin with bright light not only has therapeutic value in treating the primary symptoms of PD but it shares a common mechanism with L-dopa in reducing the occurrence of seborrheic dermatitis. Concepts at the centre of understanding pineal function in PD, including pineal calcification, melatonin deficiency, symptomatic versus protective features of melatonin and antioxidative effects, are explained in a counterintuitive context. Intriguing propositions including the role of the retina in the aetiology of PD and that the nigra functions as a retina in this disorder are presented with the intention to provide a new understanding of the underlying compromised function in PD and to provide new treatment strategies. For the first time, abundant evidence is presented describing PD as an endocrine disorder of melatonin hyperplasia. The role of circadian interventive therapies and internal desynchrony in the aetiology and progression of PD provides a new direction for understanding the underlying physiology of a disease which is currently in a state of impasse and provides new hope for those who suffer from its debilitating effects.
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PMID:Parkinson's disease as a neuroendocrine disorder of circadian function: dopamine-melatonin imbalance and the visual system in the genesis and progression of the degenerative process. 1914 86


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