Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although alterations in development due to inorganic lead poisoning have been intensely investigated, little is known about the early toxicity of organic lead compounds. Assessment of developmental consequences due to triethyl lead (TEL) intoxication presently included (1) determination of the acute LD50 as 13 +/- 1 mg/kg, and (2) detailed examination of early neurobehavioral sequelae. The offspring of 12 Fischer-344 dams were administered on postpartum day 5 either a sham-injection, 15% ethanol, 3 mg/kg or 6 mg/kg TEL vis SC injection (20 microliters). Small, but significant, weight reductions of 6% and 13% for the 3- and 6- mg/kg TEL-dosed pups, respectively, were observed (days 14-30). Early sensory deficits of TEL pups as indicated by impaired olfactory discrimination on day 7 and decreased incidence of nipple attachment on day 9 were accompanied by the presence of fine whole body tremor (day 10). While these initial effects were transitory in nature, activity evaluations demonstrated persistent hypoactivity in high dose TEL males (days 15, 22, 24, 26, and 29). Passive avoidance acquisition was not affected by TEL treatment (day 18). However, 72 and 144 hr tests of passive avoidance retention (days 21 and 25) suggested alterations in affective behavior, i.e., hypoactivity in high dose TEL males and hyperactivity in low dose TEL females. A reduction in number, but not magnitude, of startle responses also occurred as a function of TEL exposure. The single postnatal day 5 injection of TEL thus produced transitory effects possibly reflecting direct TEL pharmacological activity, as well as apparent long-term effects suggesting potential permanent alterations in behavioral function.
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PMID:Neonatal triethyl lead neurotoxicity in rat pups: initial behavioral observations and quantification. 687 78

Some meadow voles (Microtus pennsylvanicus) exhibit prolonged tonic-clonic convulsions, possibly epileptiform seizures, when handled or exposed to a strange environment. These convulsions are often preceded by a period of slow head shaking and/or stiff-legged hopping, but never by the explosively wild running bouts that characterize convulsions in some mammals. Convulsions occasionally occur in meadow voles in response to mild disturbance, as when an individual in its home cage is carried from one room to another. In contrast, they can not be elicited by some of the auditory or olfactory insults used to induce epileptiform seizures in other mammals. Breeding experiments have established the genetic basis of the convulsions seen in meadow voles, and of particular interest here is the fact that some of the convulsing voles were caught in the wild. This raises the interesting possibility that wild voles in natural habitats might be susceptible to convulsions when startled.
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PMID:Tonic-clonic convulsions in meadow voles. 780 Jul 33

Decreased olfactory function commonly occurs in idiopathic Parkinson's disease (PD), regardless of stage, treatment, or duration of disease. In the present study, we sought to determine whether different subtypes of PD, categorized according to well-defined clinical criteria, evidence different degrees of olfactory dysfunction. Significantly different scores on the University of Pennsylvania Smell Identification Test (UPSIT) were present between patients with benign PD and malignant PD (respective means [SD] = 22.51 [8.50] and 17.38 [6.29]) and between tremor-predominant PD and postural instability-gait disorder (PIGD)-predominant PD (23.43 [8.18] versus 17.35 [6.00]). No statistically significant differences in UPSIT scores were observed between young-onset and older-onset PD patients. Women outperformed men in most subtypes examined.
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PMID:Olfactory function in Parkinson's disease subtypes. 830 71

A novel cDNA clone, CR16, was isolated from a rat hippocampal cDNA library and characterized for responses to corticosteroids and regional expression. The 4-kb RNA was increased 3-fold by treatment of adrenalectomized (ADX) rats with corticosterone (CORT). Overlapping cDNA totaling 4,374 nt were used to define an open reading frame of 1,356 nt beginning 191 nt from the 5'-end and encoding a 45-kD protein containing 32% proline. CR16 has no obvious homologies to GenBank or protein databases. CR16 RNA was detected by in situ hybridization in neuron-rich layers of the hippocampal formation, layers II, III and VI of the cerebral cortex, thalamus, ventromedial nucleus of the hypothalamus, bed nucleus of the stria terminalis, lateral septal nucleus, nucleus accumbens, olfactory bulb, inferior colliculus, pons and inferior olive. The CR16 RNA has low prevalence in the hippocampus and cortex (< 10 pg/micrograms total RNA) and is elevated 3-fold in both structures in a dose-dependent manner by CORT in ADX rats. Treatment of ADX rats with aldosterone (ALDO), CORT, or RU28362 increased CR16 RNA to similar levels in the hippocampus while ALDO had minimal effects on the level of CR16 RNA relative to CORT or RU28362 in the cortex. Neither shaking stress (2 h) nor 2 h CORT significantly elevated CR16 RNA in the hippocampus, suggesting that its response to elevated CORT is not rapid. ADX lowered CR16 RNA levels by 50% relative to intact rats while low-level CORT replacement (> or = 4 ng/ml serum CORT) significantly elevated CR16 RNA 2-fold in ADX rats. These results are consistent with both the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) regulating the CR16 gene. This gene will be useful in dissecting the role of MR and GR in CNS neurons.
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PMID:Modulation of a novel RNA in brain neurons by glucocorticoid and mineralocorticoid receptors. 883 52

Angelman syndrome (AS) is a human genetic disorder characterized by mental retardation, seizures, inappropriate laughter, abnormal galt, tremor and ataxia. There is strong genetic evidence that the disorder is associated with a maternally expressed, imprinted gene mapping to chromosome 15q11-13. Affected patients demonstrate varied molecular abnormalities, including large maternal deletions, uniparental paternal disomy (UPD). Imprinting mutations and loss of function mutations of E6-associated-protein (E6-AP) ubiquitin-protein ligase (UBE3A). All of these abnormalities are associated with loss of maternal expression of UBE3A. Although mutations in UBE3A cause AS, indicating that maternal-specific expression of UBE3A is essential for a normal phenotype, evidence for maternal-specific expression of UBE3A has been lacking. Using mice with partial paternal UPD encompassing Ube3a to differentiate maternal and paternal expression, we found by in situ hybridization that expression of Ube3a in Purkinje cells, hippocampal neurons and mitral cells of the olfactory bulb in UPD mice was markedly reduced compared to non-UPD littermates. In contrast, expression of Ube3a in other regions of the brain was only moderately or not at all reduced in UPD mice. The major phenotypic features of AS correlate with the loss of maternal-specific expression of Ube3a in hippocampus and cerebellum as revealed in the mouse model.
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PMID:Imprinted expression of the murine Angelman syndrome gene, Ube3a, in hippocampal and Purkinje neurons. 928 1

It is possible to detect early signs of neurotoxic dysfunction associated with occupational and environmental exposure to manganese; neurophysiologic and neurobehavioral tests can be used in the absence of clinical manifestations. Although outcomes from individual studies vary, they collectively show a pattern of slowing motor functions, increased tremor, reduced response speed, enhanced olfactory sense, possible memory and intellectual deficits, and mood changes. This overall portrait is consistent with the action of manganese on the central nervous system. In reports to date, there is little consistency in dose-effect relationships between internal parameters of manganese exposure (blood manganese, urinary manganese, hair manganese) and external measures and neurologic outcomes. Several studies suggest the existence of dose-effect relationships, but additional clarification is needed.
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PMID:Early manifestations of manganese neurotoxicity in humans: an update. 931 35

Chicks exposed to light during late foetal life experience stimulation of the right eye only and, in consequence, develop asymmetries of the crossed visual projections from thalamus to forebrain and differences in performance of some visual tasks when using the right or left eye. The present study compared dark- and light-incubated chicks in a test of olfaction in which clove oil odour was presented together with a coloured bead. When the chicks were tested with a blue bead and using the right nostril (left nostril occluded by wax), head shaking and pecking were elevated, compared to pretest responses to an unscented, white bead. No significant elevation of head shaking occurred in chicks tested with the blue bead and using the left nostril, although pecking increased, which indicates that these chicks attended to the visual parameters of the bead but not the odour. It appears that, when the left nostril is used, attention to an attractive visual stimulus suppresses responses to olfactory input to the left hemisphere. When the clove oil odour was presented together with a less attractive, red bead, no significant lateralisation emerged. Light or dark experience prior to hatching had no effect on the lateralised performance of the blue-bead test.
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PMID:Light exposure of the embryo and development of behavioural lateralisation in chicks, I: olfactory responses. 986 44

We tested the hypothesis that day-old chicks, Gallus gallus domesticus, can learn to avoid an aversive stimulus if they observe the responses of another chick. In experiment 1, one of a pair of chicks (the actor) was allowed to peck at a bead coated in the bitter-tasting substance methylanthranilate (MeA), while we prevented the other chick (the observer) from pecking the bitter-tasting bead by separating the chicks with a piece of wire mesh. Both chicks avoided pecking at a similar but dry bead 0.5, 3 and 24 h after the observer chick saw the actor chick peck at an MeA-coated bead. By contrast, when the actor chick had pecked at a water-coated bead, both chicks continued to peck at a dry bead at 0.5, 3 and 24 h after training. Experiment 2 investigated whether observer chicks showed avoidance if they were prevented (by the insertion of an opaque barrier) from observing their companion pecking at the MeA-coated bead during either training or testing. Observer chicks that could not see their companion during training but could observe the actor chicks at test showed no subsequent avoidance whereas chicks that observed the actor chick at training, but not during testing, showed high levels of avoidance. Although the sensory cues (visual, auditory or olfactory) or types of behaviour (i.e. levels of pecking or head shaking) that the observer chick used to maintain avoidance remain unclear, the results show that chicks can learn about an aversive object by observing the responses of a conspecific. (c) 1998 The Association for the Study of Animal Behaviour.
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PMID:Observation learning in day-old chicks using a one-trial passive avoidance learning paradigm. 993 30

A simple procedure for testing newly hatched chicks' responses to olfactory stimuli is described. Chicks that were hand held under a heatlamp became inactive and closed their eyes (as if asleep) within 2 min. Sleeping chicks displayed overt behavioral responses to an odorized q-tip (head shaking, beak clapping) that were not observed in awake chicks. Sleeping latencies were shorter for 1-day-old chicks that had been food deprived prior to testing than for chicks that had ad lib access to food and water. When airborne odors were presented by squeezing a soft plastic odor bottle near the beak, sleeping chicks' reactions to mint were of a greater magnitude than their responses to lavender or orange scents. Nonetheless, all three odors elicited more pronounced behavioral responses than did the water control stimulus. This method allows rapid testing of individual chicks for odor detection and discrimination.
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PMID:A simple method for testing odor detection and discrimination in chicks. 1049 67

Several neurological conditions have been reported to be associated with peripheral or central deficits of olfactory system. In recent years particular emphasis has been placed on the early and severe olfactory impairment in Parkinson's disease (PD), in which limited neuropathological studies have revealed a marked dopaminergic deficit in the olfactory tubercles. Moreover, indirect evidence suggests that dysfunction of the dopaminergic pathways from mesencephalon to the piriform cortex may play a role in olfactory impairment in PD. A large number of clinical studies have reported that olfactory loss in idiopathic PD is bilateral, present in hemiparkinsonism, unrelated to the stage or clinical subtype of the disease, and independent of antiparkinsonian medication. In addition, major olfactory alterations have been reported in familial PD and dementia with Lewy bodies but not in progressive supranuclear palsy and essential tremor. These findings might stimulate further research targeted to determine the biological substrate of dissimilar olfactory performances in these movement disorders. The present review summarizes standardized procedures for the assessment of olfactory acuity (detection threshold), identification (multiple choice odor naming), discrimination (differentiation between similar/dissimilar odorants), and memory (recognition of a substance previously smelled). Specific suggestions concerning the psychometric and neuropsychological evaluation of PD patients are provided.
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PMID:Olfaction in Parkinson's disease: methods of assessment and clinical relevance. 1075 Nov 9


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