Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spatial Behavior”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed1986

The right hemisphere: neuropsychological functions.

In the past two to three decades, clinicians and neuroscientists have been studying the functions of the right hemisphere. Neither hemisphere seems to be dominant in the absolute sense. Each appears to be specialized and is dominant for different functions. However, most functions require the cooperation of both hemispheres. When one is damaged, the other can often compensate for the damaged one. Lesions of the left hemisphere are associated with language (speech, reading, and writing) and praxic disorders, and lesions of the right hemisphere can result in visuospatial, attentional, and emotional disorders. The authors review some of the major behavior disorders associated with right hemisphere dysfunction and concentrate on three major types of disorders--visuospatial, attentional, and emotional. Although not all the behavioral defects associated with right hemisphere damage can be subgrouped under these three types, they are the ones most often associated with right hemisphere lesions.

Agnosia↗
PubMed2004

The role of NMDA receptor binding sites in ethanol place conditioning.

Little is known about the specific role of glutamate, in particular its actions at N-methyl-D-aspartate (NMDA) receptors, in ethanol reward. Pretreatment with channel blockers MK-801 and ketamine, NMDA NR2B receptor subunit antagonists ifenprodil and CP-101,606, and the glycine(B) partial agonist (+)-HA-966 did not alter acquisition of ethanol-induced conditioned place preference (CPP) in mice. However, pretreatment with the competitive antagonist CGP-37849 attenuated acquisition of ethanol-induced CPP. Follow-up experiments indicated that CGP-37849 also blocked acquisition of ethanol-induced and lithium chloride-induced conditioned place aversion but did not produce rewarding or aversive effects on its own. These results suggest that the NMDA receptor glutamate binding site is important for ethanol place conditioning. Moreover, these results suggest CGP-37849 modulates ethanol place conditioning by impairing the ability to learn these tasks.

Animals↗
PubMed1975

Nonverbal communication in the dentist-patient relationship.

This article presented a discussion of four aspects of the nonverbal communication process, suggesting implications for the dentist-patient relationship. The subjects reviewed and discussed included (1) environmental factors, (2) the perception and use of personal space (3) touching, and (4) various types of physical behavior. The outcome of any dentist-patient interaction can be significantly altered depending upon the dentist's awareness of, and responses to, the various nonverbal cues present in the dentist-patient interaction.

Dental Offices↗
PubMed2006

Differential effects of cyclooxygenase inhibitors on intracerebroventricular colchicine-induced dysfunction and oxidative stress in rats.

Alzheimer's disease is a progressive neurological and psychiatric disorder. Oxidative stress and neuroinflammation have been implicated in pathophysiology of Alzheimer's disease. Inflammatory cells, such as astrocytes and microglia, are activated in areas of the brain affected by amyloid plaques and inflammatory mediators including cytokines, chemokines, prostaglandins, oxygen free radicals and reactive nitrogen species may have a crucial role in Alzheimer's disease pathogenesis. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed to evaluate the effects of cyclooxygenase inhibitors against colchicine-induced cognitive dysfunction and oxidative stress in rats. Following intracerebroventricular (i.c.v.) administration of colchicine (15 microg/5 microl), rats exhibited poor retention of memory in Morris water maze and elevated plus maze task paradigms and oxidative stress in rats. Chronic treatment with naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) daily respectively for a period of 25 days beginning 4 days prior to colchicine injection significantly improved colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde and nitrite levels and depletion of reduced glutathione levels in the brains of rats. It also caused a decrease in acetylcholinesterase activity. Besides, improving cognitive dysfunction, chronic administration of cyclooxygenase inhibitors (naproxen and valdecoxib) significantly reduced elevated malondialdehyde, nitrite levels and restored reduced glutathione levels and acetylcholinesterase activity. The results of the present study indicated that naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) treatment has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress. The present findings further support the potential use of cyclooxygenase inhibitors in treatment of neurodegenerative diseases such as Alzheimer's disease.

Acetylcholinesterase↗
PubMed2006

The aging hippocampus: a multi-level analysis in the rat.

In the current experiment we conducted a multi-level analysis of age-related characteristics in the hippocampus of young adult (3 months), middle-aged (12 months), and old (24 months) Fisher 344xBrown Norway hybrid (FBNF1) rats. We examined the relationships between aging, hippocampus, and memory using a combination of behavioral, non-invasive magnetic resonance imaging and spectroscopy, and postmortem neuroanatomical measures in the same rats. Aging was associated with functional deficits on hippocampus-dependent memory tasks, accompanied by structural alterations observed both in vivo (magnetic resonance imaging-hippocampal volume) and postmortem (dentate gyrus neuronal density and neurogenesis). Neuronal metabolic integrity, assessed by levels of N-acetylaspartate with magnetic resonance spectroscopy, was however, preserved. Further, our results suggest that neurogenesis (doublecortin) seems to be related to both performance deficits on hippocampus-dependent tasks and hippocampal volume reduction. The observed pattern of age-related alterations closely resembles that previously reported in humans and suggests FBNF1 rats to be a useful model of normal human aging.

Aging↗
PubMed2003

A novel model for prenatal brain damage. II. Long-term deficits in hippocampal cell number and hippocampal-dependent behavior following neonatal GABAA receptor activation.

Premature infants are at especially high risk for asphyxia, seizures, and other conditions that cause hypoxia-ischemia. These events result in abnormal brain pathology and behavioral deficits that persist throughout adolescence and into adulthood. Current rodent models of human infant hypoxic-ischemic brain damage have focused on exogenous glutamate receptor agonist exposure in the postnatal day 7 rat. While this model is considered analogous to the newborn human, no adequate models for preterm infant brain damage have been developed. Recent work from our lab has proposed a potential model for preterm infant brain damage in which neonatal rats are treated with exogenous muscimol, the selective gamma-aminobutyric acid(A) (GABA(A)) receptor agonist, on postnatal days 0 and 1. In the companion paper to this one (Exp. Neurol., in press), we report fewer neurons in the hippocampal formation on postnatal day 7 (6 days after treatment), but the persistence of these anatomical deficits, and potential resultant behavioral dysfunctions, were not investigated. In the current experiment, we documented that muscimol exposure on postnatal days 0 and 1 leads to fewer neurons in the male and female rat hippocampus (CA1, CA2/3, and dentate gyrus) on postnatal day 21. Also, neonatal muscimol exposed males and females displayed deficits on hippocampal-dependent learning tasks such as a preweanling version of the Morris water maze task and the open field task. We conclude that exposure to exogenous GABA(A) receptor activation over the first 2 days of postnatal life, a model for preterm infant hypoxic injury, produces anatomical and behavioral deficits observed into adolescence.

Animals↗
PubMed2003

[The planning of action: can one separate attention from intention?].

Attention and motor preparation are two intimately linked processes. However, they can be dissociated in the laboratory in order to study their neuronal basis. Behavioral neurophysiology has thus shown that neurons that discharge in relation with attention or with motor preparation (or intention) exist in a variety of brain regions in the monkey, especially the prefrontal and premotor cortices. When examined more carefully, these two regions appear different in both the proportion of cells that respond during attention versus intention, and in the information coded in the so-called "preparatory activity". This activity reflects sensory selection in the prefrontal cortex (spatial attention/memory), motor selection in the premotor cortex. Furthermore, two regions in the dorsal aspect of premotor cortex can be distinguished on the basis of their relative involvement in attention: a rostral (anterior) region, functionally close to prefrontal cortex, and a caudal one, which appears functionally close to motor cortex. Using an experimental design derived from monkey experiments, a functional magnetic resonance imaging (fMRI) study recently indicated that the functional specialization within the premotor cortex is similar in monkey and man.

Animals↗
PubMed2004

No latitudinal differences in adrenocortical stress response in wintering black-capped chickadees (Poecile atricapilla).

Birds respond to deterioration in environmental conditions by elevating their corticosterone levels, which can enhance their survival. It is less clear if animals constantly living in energetically challenging environment show similar increases in adrenocortical function. Previous work has demonstrated that under controlled conditions black-capped chickadees (Poecile atricapilla) from northern latitudes cache more food and perform better on spatial memory tasks than their southern conspecifics. As elevated levels of corticosterone have been shown previously to correlate with spatial memory performance in chickadees, this study aimed to investigate whether black-capped chickadees from northern latitudes have elevated baseline levels of corticosterone and/or a stronger adrenocortical stress response than their southern conspecifics, irrespective of their immediate environment. We found no differences between Alaskan and Colorado chickadees maintained under identical conditions for 3 months in either baseline levels of corticosterone or maximum levels of corticosterone achieved during the stress response. Baseline corticosterone levels were negatively correlated with relative body mass across both groups of birds. Our results suggest that the population differences in food catching behavior and spatial memory were not related to differences in corticosterone levels. We conclude that many reported population differences in baseline levels and in strength of adrenocortical stress response may often reflect differences in local environmental conditions rather than population-specific physiological traits.

Adrenal Cortex↗
PubMed2004

The presynaptic active zone protein RIM1alpha is critical for normal learning and memory.

The active zone protein RIM1alpha is required both for maintaining normal probability of neurotransmitter release and for long-term presynaptic potentiation at brain synapses. We now demonstrate that RIM1alpha(-/-) mice exhibit normal coordination and anxiety-related behaviors but display severely impaired learning and memory. Mice with a synaptotagmin 1 mutation, which selectively lowers release probability, and mice with Rab3A deletion, which selectively abolishes presynaptic long-term potentiation, do not exhibit this abnormality. Our data suggest that a decrease in release probability or a loss of presynaptic LTP alone is not sufficient to cause major behavioral alterations, but the combination of presynaptic abnormalities in RIM1alpha(-/-) mice severely alters learning and memory.

Animals↗
PubMed2003

Neurokinin-1 receptor-expressing neurons in the amygdala modulate morphine reward and anxiety behaviors in the mouse.

Mice lacking the neurokinin-1 (NK1) receptor, the preferred receptor for the neuropeptide substance P (SP), do not show many of the behaviors associated with morphine reward. To identify the areas of the brain that might contribute to this effect, we assessed the behavioral effects of ablation of neurons expressing the NK1 receptor in specific regions of the mouse brain using the neurotoxin substance P-saporin. In a preliminary investigation, bilateral ablation of these neurons from the amygdala, but not the nucleus accumbens and dorsomedial caudate putamen, brought about reductions in morphine reward behavior. Subsequently, the effect of ablation of these neurons in the amygdala on anxiety behavior was assessed using the elevated plus maze (EPM), before conditioned place preference (CPP), and locomotor responses to morphine were measured. Loss of NK1 receptor-expressing neurons in the amygdala caused an increase in anxiety-like behavior on the EPM. It also brought about a reduction in morphine CPP scores and the stimulant effect of acute morphine administration relative to saline controls, without affecting CPP to cocaine. NK1 receptor-expressing neurons in the mouse amygdala therefore modulate morphine reward behaviors. These observations mirror those observed in NK1 receptor knock-out (NK1-/-) mice and suggest that the amygdala is an important area for the effects of SP and the NK1 receptor in the motivational properties of opiates, as well as the control of behaviors related to anxiety.

Amygdala↗
PubMed1996

Effects of ischemia-hypoxia induced by interruption of uterine blood flow on fetal rat liver and brain enzyme activities and offspring behavior.

The effects of acute perinatal ischemia-hypoxia on fetal liver and brain energy metabolism, fetal brain total free fatty acid concentration and subsequent offspring behavior were investigated in rats. Ischemia-hypoxia was induced at term either by ligation of the uterine blood vessels or submersion of the entire uterine horn in warmed saline. Fetuses of the adjacent horn served as within-dam controls for all assessments and fetuses of dams which had not undergone the surgical stress served as independent controls for enzyme assays. Ischemia-hypoxia was associated with reduced activity of fatty acid synthase in the liver and brain. Total free fatty acid concentration significantly increased in the fetal hypoxic brain. Pups not used for enzyme analyses were cross-fostered for behavioral assessments. Relative to the enzymatic alterations, there were few behavioral alterations associated with ischemia-hypoxia. At postnatal day 30, rats made hypoxic by ligation of the uterine blood vessels had decreased caudate nucleus and brain stem weights relative to within-dam controls. At postnatal day 85, rats made hypoxic by submersion of the uterine horn had decreased olfactory bulb weight. The results of this study indicate an initial acute response to a brief period of ischemia-hypoxia at term pregnancy in the fetal rat brain and liver.

Age Factors↗
PubMed1984

Pervasive hyperactivity and long-term learning impairments in rats with induced micrencephaly from prenatal exposure to methylazoxymethanol.

Pregnant Long-Evans rats were given a single i.p. injection of 30 mg/kg of methylazoxymethanol (MAM) acetate or saline on day 14 of gestation (vaginal plug = day 0). All litters were reduced to 8 at birth and were reared by their biological dams. Between 49-192 days of age all offspring were examined on open-field, figure-8 (at two different ages), and hole-board tests of activity, as well as passive avoidance and Biel water maze tests of learning (also at two different ages). The MAM offspring showed no increase in mortality, but weighed less than controls, a difference that remained relatively constant throughout the experiment. At 204-215 days of age the MAM offspring were confirmed to be micrencephalic, a known effect of this drug at this dose and exposure period. On all tests of activity the MAM offspring were markedly hyperactive. The female progeny also exhibited a pronounced impairment of normal activity habituation patterns. The MAM males, however, showed a marked impairment of passive avoidance performance, while the females did not. At 2 months of age the MAM offspring also showed a pronounced deficit in learning a water maze. This maze deficit had not abated when tested again at 6 months of age. The MAM induced brain and behavioral abnormalities provide a potentially useful animal model of congenital micrencephaly and associated mental retardation.

Animals↗
PubMed2004

Characteristics of behavioral abnormalities in alpha1d-adrenoceptors deficient mice.

To investigate the functional role of alpha1d-adrenergic receptor (alpha1d-AR) in the CNS, we have generated mutant mice lacking the alpha1d-AR using a gene targeting approach and examined in detail the effects of alpha1d-AR knockout mice on motor function, sensory function, and learning and memory. alpha1d-AR knockout mice showed better motor coordination at the highest rotating speed of the rotarod performance and stronger muscle tone using the traction meter, but their locomotor activity and swimming ability in the water maze were not affected. In the water maze requiring reference memory, alpha1d-AR knockout mice showed normal spatial learning. In the Y-maze task requiring working memory or attention, alpha1d-AR knockout mice displayed an impaired spontaneous alternation performance. The alpha1d-AR knockout mice tended to display lower levels of acoustic startle responses than the wild-type group at lower pulse intensities, although the acoustic prepulse inhibition was not impaired in the alpha1d-AR knockout mice. Furthermore, the NMDA receptor antagonist, MK-801-induced deficits of acoustic prepulse inhibition were not observed in the alpha1d-AR knockout mice. These results clearly demonstrate that the alpha1d-AR receptor plays an important role in the process of auditory sensory function, attention or working memory rather than reference memory, and the sensorimotor gating deficits induced by the NMDA receptor antagonist.

Acoustic Stimulation↗
PubMed2004

Maternal hypoxia during pregnancy induces fetal neurodevelopmental brain damage: partial protection by magnesium sulfate.

Fetal low brain oxygenation may be an outcome of maternal complications during pregnancy and is associated with increased risk of cerebral palsy and periventricular leukomalacia in newborns. One treatment used for prevention of fetal brain damage is maternal treatment with MgSO(4). Although this treatment is indicated to reduce the risk of cerebral palsy in newborns, its use remains controversial. We have shown previously that pretreatment with MgSO(4) in a mouse model of maternal hypoxia prevented a delay in the development of motor reflexes induced by hypoxia. We demonstrate here that pretreatment with MgSO(4) reduces hypoxia-induced motor disabilities in adult offspring. This effect is associated with histologic protection of the Purkinje cells in the cerebellum and stabilization of brain-derived neurotrophic factor (BDNF) levels in the cerebellum. MgSO(4) did not prevent the reduction in cerebral cortex cell density and cell size induced by maternal hypoxia, however, nor did it interfere with the modulation of BDNF and nerve growth factor (NGF) expression in the cerebral cortex. MgSO(4) pretreatment also prevented the impairment of short-term memory (30 min, P < 0.05) but not long-term memory (7 days). Nevertheless, maternal pretreatment with MgSO(4) reduced CA1 cell layer width and induced alterations in both NGF and BDNF in the hippocampus. These results support the prophylactic effect of MgSO(4) against motor disabilities; however, they may also indicate possible harmful effects on the cerebral cortex and hippocampus.

Age Factors↗
PubMedDate not supplied

[Behavior characterization of a model of Huntington's disease in rats, induced by quinolinic acid].

INTRODUCTION: Huntington's disease (HD) is a progressive neurodegenerative disorder, characterized by severe degeneration of basal ganglia neurons. Behavioral symptoms of HD include abnormal, uncontrollable and constant choreiform movements, impaired cognitive function and emotional disturbance. OBJECTIVE: In order to explore the changes of cognitive and motor functions induced by quinolinate lesion we realized this experiment. MATERIALS AND METHODS: We studied the behavior of rats with unilateral quinolinate induced lesions of the medial striatum. Intact 3 months old male rats (n = 23) were trained in the Morris Water Maze during three consecutive days, eight trials/day (acquisition), and before surgery they were randomly assigned either to intact or lesion groups. Fifteen days after the lesion the rats were tested using retention test (one day/four trials, with the escape platform in the same position as in acquisition test), on the next three days the rats were tested in the transfer test (three days/eight trials-day, with the platform in the new position). The Paw reaching test and the asymmetrical rotational behavior test in respond to amphetamine were also tested in these rats. RESULTS: Lesioned animals exhibited deficient retrieval of stored memories of visuospatial skills and impaired transfer of learning. In relation with motor activity the lesioned rats showed a profound impairment in the skill of the left forelimb for reaching food compared with its right forelimb as well as with the forelimb abilities of intact rats. The lesioned animals showed significant rotational behavior induced by amphetamine agonist, ipsilateral to the lesioned striatum. CONCLUSIONS: These results are consistent with the notion that the striatal degeneration could sufficiently account for the cognitive abnormalities associated with HD, and with the key role played by basal ganglia in enabling voluntary and postural adjustment of the movements.

Animals↗
PubMed2004

Environmentally-controlled, density-dependent secondary dispersal in a local estuarine crab population.

The mechanisms driving the pelagic secondary dispersal of aquatic organisms following initial settlement to benthic habitats are poorly characterized. We examined the physical environmental (wind, diel cycle, tidal phase) and biological (ontogenetic, density-dependent) factors that contribute to the secondary dispersal of a benthic marine invertebrate, the blue crab (Callinectes sapidus) in Pamlico Sound, NC, USA. Field studies conducted in relatively large (0.05 km2) seagrass beds determined that secondary dispersal is primarily undertaken by the earliest juvenile blue crab instar stages (J1 crabs). These crabs emigrated pelagically from seagrass settlement habitats using nighttime flood tides during average wind conditions (speed approximately 5 m s-1). Moreover, the secondary dispersal of J1 crabs was density-dependent and regulated by intra-cohort (J1) crab density in seagrass. Our results suggest that dispersal occurs rapidly following settlement, and promotes blue crab metapopulation persistence by redistributing juveniles from high-density settlement habitats to areas characterized by low postlarval supply. Collectively, these data indicate that blue crab secondary dispersal is an active process under behavioral control and can alter initial distribution patterns established during settlement. This study highlights the necessity of considering secondary dispersal in ecological studies to improve our understanding of population dynamics of benthic organisms.

Analysis of Variance↗
PubMed2007

Biochemical, molecular and behavioral phenotypes of Rab3A mutations in the mouse.

Ras-associated binding (Rab) protein 3A is a neuronal guanosine triphosphate (GTP)-binding protein that binds synaptic vesicles and regulates synaptic transmission. A mouse mutant, earlybird (Ebd), with a point mutation in the GTP-binding domain of Rab3A (D77G), exhibits anomalies in circadian behavior and homeostatic response to sleep loss. Here, we show that the D77G substitution in the Ebd allele causes reduced GTP and GDP binding, whereas GTPase activity remains intact, leading to reduced protein levels of both Rab3A and rabphilin3A. Expression profiling of the cortex and hippocampus of Ebd and Rab3a-deficient mice revealed subtle differences between wild-type and mutant mice. Although mice were backcrossed for three generations to a C57BL/6J background, the most robust changes at the transcriptional level between Rab3a(-/-) and Rab3a(+/+) mice were represented by genes from the 129/Sv-derived chromosomal region surrounding the Rab3a gene. These results showed that differences in genetic background have a stronger effect on gene expression than the mutations in the Rab3a gene. In behavioral tests, the Ebd/Ebd mice showed a more pronounced mutant phenotype than the null mice; Ebd/Ebd have reduced anxiety-like behavior in the elevated zero-maze test, reduced response to stress in the forced swim test and a deficit in cued fear conditioning (FC), whereas Rab3a(-/-) showed only a deficit in cued FC. Our data implicate Rab3A in learning and memory as well as in the regulation of emotion. A combination of forward and reverse genetics has provided multiple alleles of the Rab3a gene; our studies illustrate the power and complexities of the parallel analysis of these alleles at the biochemical, molecular and behavioral levels.

Adaptor Proteins, Signal Transducing↗
PubMed1984

Spatial summation in dark-adapted human infants.

Behavioral measures of spatial summation in 4- and 11-week old human infants were obtained using the forced-choice preferential looking technique. Infants exhibit complete spatial summation over large areas (4 weeks: 8.9 degrees; 11 weeks: 5.5 degrees), much larger than those of adults tested in the same apparatus (2.6 degrees). Thus, infants' summation areas are larger than adults' by factors of 12 at 4 weeks and 4 at 11 weeks. It is argued that at most, one-half of this difference between the infant and adult data may be due to optical factors (e.g. defocus and small eye size). The remainder probably reflects differences in the neural organization of the immature and mature visual systems.

Adult↗