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Behavioral deficits

Berman NE, Marcario JK, Yong C et al (1999) Microglial activation and neurological symptoms in the SIV model of NeuroAIDS association of MHC-II and MMP-9 expression with behavioral deficits and evoked potential changes. Neurobiol Dis 6 486 98 Biber K, Zuurman MW, Dijkstra IM et al (2002) Chemokines in the brain neuroimmunology and beyond. Curr Opin Pharmacol 2 63-68... [Pg.166]

Veltkamp R, Warner DS, Domoki F, Brinkhous AD, Toole JF, Busija DW. Hyperbaric oxygen decreases infarct size and behavioral deficit after transient focal cerebral ischemia in rats. Brain Res 2000 853 68-73. [Pg.120]

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... [Pg.332]

Meredith M. (1991b). Vomeronasal damage, not nasopalatine duct damage, produces mating behavior deficits in male hamsters. Chem Senses 16, 155-167. [Pg.230]

Meredith M. and Howard G. (1992). Intra-cerebroventricular LHRH relieves behavioral deficits due to vomeronasalectomy. Brain Res Bull 29, 75-79. [Pg.230]

Studies in animals have provided abundant support for the plausibility of the neurodevelopmental effects of lead that have been associated with lead exposure in children, and researchers have begun to identify potential mechanisms (i.e., Cory-Slechta 1995a). However, mechanistic connections between behavioral deficits, or changes observed in animals, and those that have been associated with lead exposure in children have not been completely elucidated. Understanding of such connections would be valuable for developing better and more relevant animal models of lead toxicity. [Pg.356]

Tiffany-Castiglioni E Texas A M University, College Station, TX Molecular-and cellular uptake and tolerance to Pb and associated behavioral deficits (rat) National Institute of Environmental Health Sciences... [Pg.369]

Rice DC. 1984. Behavioral deficit (delayed matching to sample) in monkeys exposed from birth to low levels of lead. Toxicol Appl Pharmacol 75 337-345. [Pg.567]

Fetal alcohol syndrome (FAS) is a pattern of birth defects caused by maternal consumption of ethanol during pregnancy. It is recognized by growth deficiency, a characteristic set of craniofacial features and neurodevelopmental abnormalities leading to cognitive and behavioral deficits [85]. FAS is considered to be the most common non-hereditary cause of mental retardation. [Pg.435]

Subtle behavioral deficits in A(3 plaque-depositing transgenic mice... [Pg.322]

Joseph J, Arendash G, Gordon M, Diamond D, Shukitt-Hale B and Morgan D. 2003. Blueberry supplementation enhances signaling and prevents behavioral deficits in an Alzheimer disease model. Nutr Neurosci 6 153-163. [Pg.43]

Joseph JA, Shukitt-Hale B, Denisova NA, Bielinski D, Martin A, McEwen JJ and Bickford PC. 1999. Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation. J Neurosci 19(18) 8114-8121. [Pg.172]

Significantly, immunotherapy in transgenic mice is successful in partially clearing Ap, in attenuating learning and behavioral deficits in at least two cohorts of mutant APP mice, and in reducing tau abnormalities in the triple transgenic mice [83-85]. [Pg.787]

Male weanlings exposed to age 50 days to drinking water with 25 mg Pb/L, as lead acetate At day 86 behavioral deficits blood concentrations of 150-200 pg Pb/L brain lead levels (pg/kg) 70 in treated group vs. 28 in controls 26... [Pg.313]

In mice, exposure to DDT during gestation and in the neonatal stage has also caused developmental neurotoxicity, in the form of behavioral deficits in the learning process, that persisted into adulthood. Human studies have suggested that alterations in functions that are hormonally controlled such as duration of lactation, maintenance of pregnancy, and fertility may occur from DDT exposure. ... [Pg.203]

Unpredictability also is a central feature in the concept of learned helplessness. This concept, using uncontrollable shock, was introduced by Overmier and Seligman (1967) and is based on the observation that animals exposed to an invariable stressor such as electric foot shock, which, due to the experimental set-up, is uncontrollable in nature, developed behavioral deficits. As first shown by Weiss (1968), rats exposed to uncontrollable shock showed significant weight loss due to decreased food and water intake. Moreover, these animals spent more time immobile in the forced swim test, and they revealed altered sleep patterns as well as a weakened response to previously rewarding brain stimulation, i.e., anhedonia (Henn et al. 1985 Weiss 1991). Importantly, these changes are not seen in animals that receive the same shocks but can exert control over their duration. [Pg.58]

Stressful stimuli of many types produce marked increases in brain noradrenergic function. Stress produces regional selective increases in NE turnover in the locus coeruleus (LC), limbic regions (hypothalamus, hippocampus, and amygdala), and cerebral cortex. These changes can be elicited with immobilization stress, foot-shock stress, tail-pinch stress, and conditioned fear. Exposure to stressors from which the animal cannot escape results in behavioral deficits termed learned helplessness. The learned helplessness state is associated with depletion of NE, probably reflecting the point where synthesis cannot keep up with demand. These studies have been reviewed elsewhere in detail (Bremner et al. 1996a,b). [Pg.212]

There is strong evidence that function of the brain noradrenergic system is involved in mediating fear conditioning (Rasmussen et al. 1986 Charney and Deutch 1996). Neutral stimuli paired with shock (CS) produce increases in brain NE metabolism and behavioral deficits similar to those elicited by the shock alone (Cassens et al. 1981) as well as increased firing rate of cells in the LC (Rasmussen et al. 1986). An intact noradrenergic system appears... [Pg.214]

Kometsky C, Mirsky AF, Kessler EK, and Dorff JE. The effects of dextro-amphet-amine on behavioral deficits produced by sleep loss in humans. I Pharmacol Exp Ther 1959 127 46-50. [Pg.443]


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See also in sourсe #XX -- [ Pg.36 , Pg.96 , Pg.139 ]




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