Effects of early food deprivation on mouse behavior.
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To test the relative effectiveness of direct vs. indirect interaction with an enriched environment, some rats were housed in groups of 12 in large enriched condition (EC) cages while littermate "observer" (OC) rats were placed singly in small wire-mesh cages within EC. A third group was housed singly in an impoverished condition (IC) where stimulation was minimal. After 30 days, the animals were killed and the brains dissected. In both experiments the usual pattern of EC-IC differences in brain weights appeared, whereas OC showed no significant differences from IC. On measures of exploratory behavior taken during the last 2 days of the second experiment, IC fell significantly below EC, and OC was somewhat below IC. Thus EC differen from both IC and OC in brain and in behavior. Active contact with an enriched environment appears necessary for development of EC effects.
Two experiments using food-container avoidance as an index of neophobia are reported for two strains of laboratory and one strain of wild rats. In Experiment 1 rats were fed from a single familiar container until their consumption had stabilized. Upon replacing the familiar container with a novel container, the latency of all three strains to begin feeding increased. In Experiment 2 rats were offered a choice between a familiar and a novel container containing identical food. Though there was considerable individual variation among the three strains, the wild strain was more reluctant to eat from the novel container than a hooded laboratory strain, which, in turn, was nore reluctant than an albino laboratory strain. Nonetheless, all three strains showed an initial avoidance of the novel container. It was concluded that both wild and laboratory strains are neophobic and that strain differences are ones of degree, not of kind.
A series of experiments assessed the effects of ACTH and the ACTH analogue ACTH4-10 on drinking in conditioned taste aversion and neophobic situations. Both substances delayed the extinction of a conditioned taste aversion established by a single pairing of lithium chloride with milk (Experiment 1). However, in this situation, the ACTH parent peptide was more potent behaviorally. Administration of ACTH suppressed milk consumption in animals with no toxicosis experience (Experiment 2). This effect was apparently not due to the conditioning of a taste aversion (Experiment 3) with ACTH serving as a weak aversive unconditioned stimulus. Administration of exogenous ACTH (Experiment 4) or ACTH4-10 (Experiment 5) did not enhance neophobia; however, repeated injections of ACTH suppressed drinking. This ACTH suppression was related to the familiarity/novelty of the subtance being consumed. The neophobic response to milk eas no accompanied by pituitary-adrenal activation (Experiment 6). Both neophobic and conditioned taste aversion situation appear to be useful for assessing peptide effects on consummatory behavior.
The purpose of this study was to determine whether behavioral sparing would be demonstrated when septal lesions occurred prior to the age at which the tested behavior first appears in normal rats. Rats given septal lesions at 1 day or 7 days after birth performed at approximately chance on the Maier three-table task when tested at 90 days of age. Rats that had control electrode insertions at the same ages performed at a level similar to normal animals. Animals given septal lesions at either age explored significantly more than did control animals. Results are discussed in terms of the constancy over time of the septal contribution to performance on the three-table task and the involvement of the septum and hippocampus in the processing of spatial information.
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In rodents, the electroencephalogram (EEG) during paradoxical sleep and exploratory behavior is characterized by theta oscillations. Here we show that a deficiency in short-chain acyl-coenzyme A dehydrogenase (encoded by Acads) in mice causes a marked slowing in theta frequency during paradoxical sleep only. We found Acads expression in brain regions involved in theta generation, notably the hippocampus. Microarray analysis of gene expression in mice with mutations in Acads indicates overexpression of Glo1 (encoding glyoxylase 1), a gene involved in the detoxification of metabolic by-products. Administration of acetyl-L-carnitine (ALCAR) to mutant mice significantly recovers slow theta and Glo1 overexpression. Thus, an underappreciated metabolic pathway involving fatty acid beta-oxidation also regulates theta oscillations during sleep.
OBJECTIVES: Structural equation modeling of an abbreviated version of the conceptual model of the effects of micronutrient and energy supplementation on growth and development of undernourished children in West Java. The study focused on the baseline data from the Pangalengan longitudinal project. DESIGN: This trial included two cohorts of children classified as nutritionally-at-risk who were randomly assigned to three treatments (condensed milk + micronutrients (E); skimmed milk + micronutrients (M); skimmed milk (S)). Supplements were given for a period of up to 12 months. SETTING: The sites were six tea plantations in Pangalengan. SUBJECTS: A 12-month-old (n=53) and an 18-month-old (n=83) cohort were recruited from 24 day care centers. Twenty children that received the S supplement were part of the 12- and 18-month-old cohorts. Criteria for inclusion were: no chronic disease; length-for-age < -1 standard deviation (s.d.) and weight-for-length between -1 and -2 s.d. of the median of the reference of the World Health Organization. VARIABLES: Indicators of socioeconomic status were economic and educational resources; length-for-age and weight-for-length were used as indicators of nutritional status; motor development and motor activity were measured with custom-made procedures; and carrying by caretaker and manipulation of objects were used as indicators of caretaking and exploratory behavior. RESULTS: The model fitted the data of the older but not of the younger cohort (chi2 statistic and three other indices of goodness to fit). However, there were no differences between cohorts in the estimation of the models.
OBJECTIVES: This paper presents the results of a structural equation model testing whether the longitudinal data of the Pangalengan subjects fit the theoretical model regarding the intellectual delay of undernourished children. DESIGN: Two cohorts of children were randomly assigned to three treatments: E = 1171 kJ + 12 mg iron; M = 12 mg iron + 209 kJ; S = 104 kJ. Supplementation was given for 6 months. SETTING: The sites were six tea plantations in Indonesia. SUBJECTS: A 12-month-old (n = 53) and an 18-month-old (n = 83) cohort were recruited from day-care-centers. Inclusion criteria were: no chronic disease; length-for-age = < 1 standard deviation (s.d.) and weight-for-length between -1 and -2 s.d. of the median of the reference of the World Health Organization. METHODS: Twenty-four-hour dietary intakes were assessed using the weighted individual inventory technique. Body weight and length were obtained using standard procedures; motor development was assessed with the Bayley Scale and with a custom made scale for motor development leading to bipedal locomotion. Four-hour observations were made of the child's interactions with the environment. Carrying a child in the arms and exploratory behavior were used as indicators of caregiving and exploration. All measurements were obtained every 2 months. RESULTS: The original model did not fit the data. The model was then modified with the inclusion of two new pathways: from activity and from motor development to mental development. Following these adjustments the model fit the data for each cohort and for both cohorts combined.
People are very likely to start psychoactive drug use during adolescence, an earlier onset being associated with a higher risk of developing addiction later in life. In experiment I, Pre- (postnatal day (pnd) 23-35), Mid- (pnd 36-48), or Post- (pnd 49-61) adolescent mice underwent a restricted-drinking period (2 h/day for 12 days), one bottle containing water and the other containing nicotine (10 mg/l) or water. After this period, Mid-adolescents showed prominent exploration and reduced anxiety in the plus-maze. This ontogenetic profile was dampened by nicotine consumption. After 2 months, these mice were tested in a novel environment (30 min/day for 3 days). Locomotor-habituation profiles were specifically disrupted by nicotine consumption during Mid-adolescence, suggesting this age as a critical period. In experiment II, Mid-adolescent (pnd 35-44) and adult (pnd > 70) mice were pretreated with nicotine (0, 0.03, 0.10, 0.30 mg/kg/day for 10 days). Acute nicotine administration had opposite effects on anxiety in adolescents and adults. At 2 months after pretreatment, we measured levels of AMPA GluR2/3 subunits, thought to be involved in the control of addictive behaviors. Nicotine exposure during Mid-adolescence dose-dependently downregulated these subunits in the striatum and hippocampus, but comparable exposure during adulthood had either opposite or no effects. NMDA NR2A/B subunits were affected by nicotine, but without age-related differences. The present data identified a nicotine-vulnerable age window, characterized by long-term disruption of locomotor habituation and downregulation of AMPA receptors. These findings support neurobiological vulnerability to drugs in adolescent humans.
1. Changes in arterial pressure associated with a repertoire of natural behaviour patterns in the rat were examined. 2. A hierarchy of such changes was found. Eating and drinking were associated with higher pressures than grooming and exploration, which in turn were associated with higher pressures than resting. 3. Desynchronized sleep was associated with higher pressures than slow-wave sleep. 4. Lesions of the catecholamine neurons of the A2 region of the medulla did not disrupt the normal hierarchy but resulted in an exaggerated pressor response.
To test the theory that sleep is a regional, use-dependent process, rats were subjected to unilateral sensory stimulation during waking. This was achieved by cutting the whiskers on one side, in order to reduce the sensory input to the contralateral cortex. The animals were kept awake for 6 h in an enriched environment to activate the cortex contralateral to the intact side. Whiskers are known to be represented in the barrel field of the contralateral somatosensory cortex and their stimulation during exploratory behavior results in a specific activation of the projection area. In the 6 h recovery period following sleep deprivation, spectral power of the nonrapid eye-movement (NREM) sleep EEG in the 0.75-6.0 Hz range exhibited an interhemispheric shift towards the cortex that was contralateral to the intact whiskers. The results support the theory that sleep has a regional, use-dependent facet.
The effects of diazepam, I-propranolol and isamoltane (CGP 361 A) (I-isopropylamino-3[2-(I-pyrrolyl)-phenoxy]-2-propranol), a drug with beta-receptor blocking and anxiolytic-like properties, on behavioral responses in rats encountering either a novel object or a drinking bottle in an unfamiliar open-field ("neophobic" behavior) were evaluated. Diazepam (1-5 mg/kg p.o.) and isamoltane (0.5-1.0 mg/kg p.o.) showed a similar pattern of effects in both test paradigms used. They counteracted the fear-induced suppression of behavioral responses in the presence of novelty: they shortened the approach latencies, increased the exploration-oriented activities and reduced grooming. Propranolol, however, in comparison with isamoltane (1.0 and 2.5 mg/kg i.p.) at equivalent doses, failed to significantly change any of the parameters measured in either of the two test situations. The results therefore indicate that neophobic behavioral responses discriminate between central anxiolytic and peripheral beta-blocking actions of drugs and further validate neophobic behavior as an animal model of anxiety.
When some infant mammals are placed outside their nest, a sequence of exploratory behavior occurs, displaying a regular buildup and spread of activity. This "warm-up" involves repetition of movement along specific dimensions and an orderly transition from one dimension to the next, with cephalocaudal recruitment of body and limb segments. A similar principle of organization applies to neurological recovery from lateral hypothalamic akinesia.
Evolvability is an organism's capacity to generate heritable phenotypic variation. Metazoan evolution is marked by great morphological and physiological diversification, although the core genetic, cell biological, and developmental processes are largely conserved. Metazoan diversification has entailed the evolution of various regulatory processes controlling the time, place, and conditions of use of the conserved core processes. These regulatory processes, and certain of the core processes, have special properties relevant to evolutionary change. The properties of versatile protein elements, weak linkage, compartmentation, redundancy, and exploratory behavior reduce the interdependence of components and confer robustness and flexibility on processes during embryonic development and in adult physiology. They also confer evolvability on the organism by reducing constraints on change and allowing the accumulation of nonlethal variation. Evolvability may have been generally selected in the course of selection for robust, flexible processes suitable for complex development and physiology and specifically selected in lineages undergoing repeated radiations.