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Fantasy formation: a child analyst's perspective.

Unconscious fantasy is the principal unit of psychoanalytic investigation. Though individual fantasies, either conscious or unconscious, may emphasize drive, defense, or superego interests, all fantasy life develops from a limited number of themes; these themes concern drive-related issues, experiences of helplessness, or combinations of both. Fantasy formation and fantasy content undergo developmental change. Sensorimotor, behavioral memories occur prior to fantasy and are influential in determining repetitive behavioral enactments. The complexities of infant behavior do not require the postulation of fantasy or representational memory. A complex, innate, instinctual organization of the newborn, similar in many respects to that of other newborn mammals, and distinct from the psychological organization of the older infant, is suggested as an explanation of these phenomena.

Adolescent↗

Involvement of serotonin in the enhancement of the rat spinal excitability by high pressures.

Using an electrical stimulation of the reticulospinal tract at the level of the medial longitudinal fasciculus, the effects, and the neurochemical mechanisms of these effects, of a progressive increase in helium-oxygen pressures, up to 50 bar, on the spinal cord excitability in the chronic rat are investigated. In control animals, high pressure exposure over 30 bar was found to increase markedly the electromyogram response evoked in nuchal muscles. This startlelike response was monosynaptically induced by stimulation of the reticulospinal tract. Conversly, no hyperbaric alteration in spinal excitability has been observed in animals pretreated with the classical 5-HT antagonist drug metergoline. These results emphasize the importance of spinal cord as a potential target for mediating hyperbaric effects on sensorimotor behaviors (i.e., motor disturbances of the HPNS). Moreover, our work suggests that serotonin could be implicated in hyperbaric spinal cord hyperexcitability.

Animals↗

Developmental lags in preterm infants from one to three years of age.

Assessments of play, sensorimotor, language, and general developmental skills were administered to 20 preterm and 20 full-term infants at comparable corrected and postnatal ages in 5 sessions during the second and third years of life. Clear effects of biological maturity on play and sensorimotor skills were demonstrated at 13 1/2 months, and less pervasive effects remained at 22 months. Furthermore, the preterm infants were significantly delayed in sensorimotor, personal-social, and gross motor abilities at 13 1/2 months and in language abilities at 22 months beyond that predicted by biological maturity alone. While these deficits were mostly overcome by 3 years, the preterm infants performed somewhat more poorly on visual information-processing tasks. This investigation demonstrated that the development of representational abilities as manifested in play and sensorimotor behaviors was clearly related to corrected age rather than postnatal age.

Child Development↗

Plasticity of neostriatal dopamine receptors after nigrostriatal injury: relationship to recovery of sensorimotor functions and behavioral supersensitivity.

Rats given unilateral injections of 6-OHDA along the course of the mesotelencephalic dopaminergic projection show impairments in contralateral sensorimotor functions from which they often recover. Such rats also display an enhanced sensitivity to DA receptor stimulants, e.g. apomorphine, as revealed by contralateral turning, and an increased binding of neuroleptic compounds (e.g. [3H]spiroperidol) to the denervated striatum. This research examines the relationship of these receptor changes to both behavioral supersensitivity and recovery of sensorimotor functions by quantifying the time course of each phenomenon after injury. The supersensitivity to apomorphine and the behavioral recovery developed with a similar time course after injury, being evident within 1.5-3 days and reaching nearly maximal levels by 2 weeks postoperatively. A significant increase in in vivo [3H]spiroperidol binding to the denervated striatum occurred by 4 days postoperatively, and the magnitude of this change increased linearly during the first postoperative month. In contrast, the in vitro binding of this ligand to membranes of the denervated striatum was not increased until 3 weeks after the lesion. The results suggest that a proliferation of DA receptors may contribute to the pharmacological supersensitivity and the recovery of function, and that these early receptor changes may be revealed with greater sensitivity using in vivo binding techniques.

Animals↗

Nonocclusive common carotid artery thrombosis in the rat results in reversible sensorimotor and cognitive behavioral deficits.

BACKGROUND AND PURPOSE: Microemboli released during transient ischemic attack, stroke, and cardiac surgery are thought to cause a variety of functional deficits in humans. The purpose of this study was to characterize the type and extent of neurobehavioral deficits present after photochemically induced common carotid artery thrombosis (CCAT), a thromboembolic model of stroke in the rat that results in a platelet emboli shower. METHODS: Thirty-two male Wistar rats were assigned to four groups. Groups 1 (n = 8) and 3 (n = 8) were long-term (6-week survival) and short-term (2-week survival) experimental groups subjected to right CCAT with the use of the photochemical technique. Groups 2 (n = 8) and 4 (n = 8) served as sham-operated controls for each experimental group. A battery of behavioral tests was applied daily beginning 24 hours after thrombosis; this consisted of elicited forelimb placing, postural reflex, beam balance, beam walking, and open field activity. Cognitive testing with a water maze task was performed on post-CCAT days 30 to 33 for groups 1 and 2 and on post-CCAT day 2 for groups 3 and 4. Ten-micrometer coronal brain sections were stained with hematoxylin and eosin, and infarct location and frequency were determined. RESULTS: Significant sensorimotor deficits were observed, which recovered within 2 weeks after CCAT. The data that follow are derived by combining the two experimental groups and comparing these with the two sham groups. The following tests showed significant effects after CCAT: contralateral elicited forelimb placing, ipsilateral elicited forelimb placing, beam balance, and beam walking score. Cognitive dysfunction was seen acutely (group 3 animals) at 2 days after CCAT; Morris water maze length and latency to target were significantly greater in the experimental group. No deficits were seen in postural reflex, open field activity, or delayed cognitive testing. Histopathological assessment revealed small infarcts in 11 of 16 thrombosed rats. However, a strong relationship between neurobehavioral deficits and infarct location was not consistently demonstrated. CONCLUSIONS: CCAT produces consistent sensorimotor and cognitive behavioral deficits that recover within 2 weeks of injury. Behavioral outcome was not necessarily associated with overt histopathological damage, suggesting that reversible injury mechanisms, both vascular and neuronal, may be partly responsible for the temporary loss of function. These data strengthen the role of CCAT as a clinically relevant model of thromboembolic stroke.

Animals↗

Enhanced behavioral recovery from sensorimotor cortex lesions after pyramidotomy in adult rats.

Unilateral transection of the bulbar pyramid, performed before the ablation of the ipsilateral sensorimotor cortex, has been shown to facilitate the recovery of operantly conditioned reflexes and compensatory processes in rats. Such enhanced behavioral recovery was absent when only the sensorimotor cortex was ablated. This phenomenon is explained by the switching of motor activity under the control of the cortico-rubrospinal system. Switching of the descending influences is accomplished through the following loop: cortico-rubral projection-red nucleus-inferior olive-cerebellum-thalamus-cerebral cortex. This suggests that a preliminary lesion of the peripheral part of the system, represented by a descending spinal projection, facilitates the recovery processes to develop during the subsequent destruction of its central part.

Animals↗

Alpha7 nicotinic receptor subunits are not necessary for hippocampal-dependent learning or sensorimotor gating: a behavioral characterization of Acra7-deficient mice.

The alpha7 nicotinic acetylcholine receptor (nAChR) subunit is abundantly expressed in the hippocampus and contributes to hippocampal cholinergic synaptic transmission suggesting that it may contribute to learning and memory. There is also evidence for an association between levels of alpha7 nAChR and in sensorimotor gating impairments. To examine the role of alpha7 nAChRs in learning and memory and sensorimotor gating, Acra7 homozygous mutant mice and their wild-type littermates were tested in a Pavlovian conditioned fear test, for spatial learning in the Morris water task, and in the prepulse inhibition paradigm. Exploratory activity, motor coordination, and startle habituation were also evaluated. Acra7 mutant mice displayed the same levels of contextual and auditory-cue condition fear as wild-type mice. Similarly, there were no differences in spatial learning performance between mutant and wild-type mice. Finally, Acra7 mutant and wild-type mice displayed similar levels of prepulse inhibition. Other behavioral responses in Acra7 mutant mice were also normal, except for an anxiety-related behavior in the open-field test. The results of this study show that the absence of alpha7 nAChRs has little impact on normal, base-line behavioral responses. Future studies will examine the contribution of alpha7 nAChR to the enhancement of learning and sensorimotor gating following nicotine treatments.

Animals↗

Role of the strychnine-insensitive glycine binding site in the nucleus accumbens and anterodorsal striatum in sensorimotor gating: a behavioral and microdialysis study.

This study examined the role of the strychnine-insensitive glycine binding site of the NMDA receptor in prepulse inhibition (PPI) of the acoustic startle response (ASR) in rats. PPI is an operational measure of gating processes which normally lead to a diminished ASR when a startling stimulus is preceded by a weak prepulse. PPI is impaired in schizophrenics and, therefore, experimentally induced PPI deficits in rats can be regarded as a model for gating deficits in schizophrenia. Local administration of 7-chlorokynurenate (7-CLKYN), an antagonist of the strychnine-insensitive glycine site of the NMDA receptor, into the nucleus accumbens reduced PPI. This sensorimotor gating deficit was antagonized by systemic pretreatment of the rats with the glycine site agonist D-cycloserine, indicating that the effect of 7-CLKYN was due to a blockade of the NMDA receptor associated glycine binding site. A similar deficit in PPI was observed after intra-accumbal administration of the competitive NMDA receptor antagonist AP-5. PPI was normal after injecting these drugs into the anterodorsal striatum. The hypothesis that the PPI deficit is accompanied by a change in dopamine release was tested by a neurochemical analysis of the effects of local injection of 7-CLKYN. Microdialysis data showed no increase of accumbal and striatal dopamine release after blockade of the glycine site with 7-CLKYN. Our data demonstrate that the glycine/NMDA receptor in the nucleus accumbens plays a important role in sensorimotor information processing that depends not on a hyperactive dopamine system.

Animals↗

Relationship between dendritic pruning and behavioral recovery following sensorimotor cortex lesions.

A unilateral injury to the forelimb area of the sensorimotor cortex results in an increase in dendritic arborization in the contralateral homotopic cortex which is followed by a pruning back of these dendritic arbors. The increase in arborization is due to an increase in the use of the unimpaired forelimb for postural-motor support; whereas, the dendritic pruning is related, in time, to the return to more symmetrical limb use, but is not prevented by the maintenance of asymmetrical limb use. Dendritic pruning can be prevented by administering an NMDA receptor antagonist (such as MK801 or ethanol) during the pruning phase. This manipulation also coincides with the chronic reinstatement of behavioral deficits. The purpose of this study was to see whether removing the antagonism of the NMDA receptor results in the eventual return of dendritic pruning and behavioral recovery. Therefore, MK801 was administered to lesioned animals starting at post-lesion day 18. One group received MK801 injections until day 60 (Lesion + MK60) and another lesioned group received MK801 until day 30 after which the injections were changed to saline until day 60 (Lesion + MK30). Lesion + MK60 animals showed a prevention of dendritic pruning as well as a chronic reinstatement of forelimb deficits. Lesion + MK30 animals also showed a prevention of dendritic pruning, however, they showed behavioral recovery. These findings suggest that pruning of dendritic arbors may not be directly related to behavioral recovery.

Animals↗

Coping characteristics of disabled and nondisabled young children.

The coping characteristics of a large sample of disabled and nondisabled children under three years old are assessed across three categories of behavioral patterns: sensorimotor organization, reactive behavior, and self-initiated behavior. The influence of family income, gender, age, and ethnicity are examined and the implications for early intervention discussed.

Adaptation, Psychological↗

Melatonin receptor (MT1) knockout mice display depression-like behaviors and deficits in sensorimotor gating.

Although critical for transducing seasonal information, melatonin has also been implicated in several physiological systems, as well as the regulation of behavioral and cognitive processes. Therefore, we investigated the neurobehavioral effects of mice missing the type 1 melatonin receptor (MT1). Male and female MT1 knockout (MT1-/-) and wild-type (WT) mice were tested in the acoustic startle/prepulse inhibition (PPI), open field and Porsolt forced swim tests. Male and female MT1-/- mice displayed dramatically impaired prepulse inhibition in the acoustic startle response. Female WT mice were more active in the open field than WT males. However, male and female MT1-/- mice did not differ in total locomotor activity. WT animals spent significantly more time in the center of the arena (a behavioral outcome associated with reduced anxiety-like behavior) than MT1-/- mice. Also, the sex difference between male and female WT mice in the amount of time spent in the center versus periphery was not observed among MT1-/- mice. Both male and female MT1-/- mice significantly increased the time spent immobile in the forced swim test, an indication of depressed-like behavior. The lifetime lack of MT1 signaling contributes to behavioral abnormalities including impairments in sensorimotor gating and increases in depressive-like behaviors. Taken together, MT1 receptor signaling may be important for normal brain and behavioral function.

Animals↗

Computational approaches to sensorimotor transformations.

Behaviors such as sensing an object and then moving your eyes or your hand toward it require that sensory information be used to help generate a motor command, a process known as a sensorimotor transformation. Here we review models of sensorimotor transformations that use a flexible intermediate representation that relies on basis functions. The use of basis functions as an intermediate is borrowed from the theory of nonlinear function approximation. We show that this approach provides a unifying insight into the neural basis of three crucial aspects of sensorimotor transformations, namely, computation, learning and short-term memory. This mathematical formalism is consistent with the responses of cortical neurons and provides a fresh perspective on the issue of frames of reference in spatial representations.

Animals↗

Sensorimotor period and adaptive behavior development of severely and profoundly mentally retarded children.

The relationship of the Uzgiris and Hunt Scales of Sensorimotor Development with six of the AAMD Adaptive Behavior Scale (ABS) domains and the Receptive-Expressive Emergent Language (REEL) Scale was investigated. One significant canonical root was found. Three independent variables (vocal imitation, object permanence, and gestural imitation) and six dependent variables (ABS domains Language, Socialization, Independent Functioning, and Self-Direction and REEL-Receptive and REEL-Expressive) loaded highly on the canonical root. Regression was used to analyze these variables further. The results were interpreted as generally consistent with prior theory and research, although there were some difficult interpretations and contradictions of previous research.

Child↗

A comparison of GluR-A-deficient and wild-type mice on a test battery assessing sensorimotor, affective, and cognitive behaviors.

Previous studies have demonstrated a spatial working memory deficit in glutamate receptor (GluR)-A (GluR1) AMPA receptor subunit knockout mice. The present study evaluated male and female wild-type and GluR-A-/- mice on a test battery that assessed sensorimotor, affective, and cognitive behaviors. Results revealed a behavioral phenotype more extensive than previously described. GluR-A-/- mice were hyperactive, displayed a subtle lack of motor coordination, and were generally more anxious than wild-type controls. In addition, they showed a deficit in spontaneous alternation, consistent with previous reports of a role for GluR-A-dependent plasticity in hippocampus-dependent, spatial working memory. Although changes in motor coordination or anxiety cannot explain the dissociations already reported within the spatial memory domain, it is clear that they could significantly affect interpretation of results obtained in other kinds of behavioral tasks.

Affect↗

Trigeminal sensorimotor mechanisms and ingestive behavior.

Selective section of trigeminal orosensory nerves was carried out to assess the contributions of trigeminal orosensation to the control of food and water intake in the rat. Trigeminal orosensory deafferentation reduces a responsiveness to food and water, disrupts jaw-opening and tongue protrusion reflexes mediating eating and drinking, impairs dietary self-selection and reduces the level of long-term body weight regulation. The magnitude of the feeding behavior deficits is a joint function of the extent of the denervation and the sensory properties of the diet, and recovery takes place along a palatability gradient. Analysis of feeding and drinking patterns and of learned instrumental behaviors indicates that deafferentation reduces the probability of initiating a feeding or drinking bout and profoundly disrupts performance of operant responses reinforced with food or water. We conclude that the trigeminal system contributes to both the sensorimotor and motivational control of ingestive behavior. Its motivational contributions differ in both kind and magnitude from those of the gustatory system.

Afferent Pathways↗

Two effective behavioral tasks for evaluating sensorimotor dysfunction following traumatic brain injury in mice.

Variants of two sensorimotor tasks, the gridwalk and spontaneous forelimb use (SFL) tasks, were assessed for their ability to reveal behavioral dysfunction following traumatic brain injury (TBI) in mice. These tests have previously been used almost exclusively in evaluating models of spinal injury, ischemia and other forebrain lesions in rats. Male C57BL/6 mice were anesthetized and given unilateral parasagittal controlled cortical impact injury or sham (n = 9) procedures, targeting right anterior (n = 9), middle (n = 9), or posterior (n = 10) locations relative to bregma. Significant forelimb and hindlimb deficits contralateral to the injured hemisphere were observed for at least 1 month and 3 weeks, respectively, on the gridwalk task depending upon insult location. The SFL task revealed a significant asymmetry in forelimb use for at least 5 months following injury. These results demonstrate the effectiveness of the SFL and gridwalk tests in evaluating sensorimotor deficits in mouse injury models involving unilateral forebrain damage.

Animals↗