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At least 631 records · Page 35Linked to original sources
PubMed1986

Apomorphine reverses direction of asymmetry in facial scanning after 10 days of unilateral vibrissae removal in rat: vibrissotomy-induced denervation supersensitivity?

Sensorimotor asymmetries of hemivibrissotomized rats were investigated in an open field. To examine possible behavioral plasticity after unilateral removal of the vibrissae, we compared two groups of rats which had experienced the sensory imbalance for different durations. One group was shaved on one side of the face daily for 10 days before behavioral testing (group 10-Days). The other group was first shaved 4 h prior to the behavioral testing and was sham-shaved for the preceding 10 days (group 4-H). On day 11, the undrugged behavior was examined, and then, one hour later, the behavior induced by apomorphine (0.75 mg/kg, s.c.) was analyzed. In the undrugged state both groups tended to scan the walls of the enclosure with the vibrissae side of the face. After injection of apomorphine, the 4-H group also scanned the walls preferentially with the vibrissae side. In contrast, the 10-Days group reversed the scanning asymmetry under the influence of this drug. That is, animals in this latter group now preferred to scan the walls with the shaved side of the face. These findings are suggestive of a plasticity in dopamine transmission subsequent to unilateral removal of vibrissae. The reversal in direction of asymmetry under apomorphine of the 10-Days group is reminiscent of the apomorphine-induced reversal in sensorimotor asymmetries found after unilateral 6-hydroxydopamine lesion of the substantia nigra, which has been attributed to dopamine receptor supersensitivity.

Animals↗
PubMed1988

Administration of GM1 ganglioside eliminates neuroleptic-induced sensorimotor deficits in MPTP-treated mice.

Injection of a low dose of haloperidol, that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and sensory neglect in MPTP-treated mice. GM1 ganglioside treatment eliminates all of these behavioral impairments and also partially restores striatal dopamine content. These observations suggest that the MPTP-treated mouse may be a valuable model for studying mechanisms underlying parkinsonism and that administration of GM1 ganglioside may be an effective therapy.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMedDate not supplied

[Effect of a constant and low frequency magnetic field on the behavioral and autonomic responses of the human operator].

The object of the study was conjugation of latencies of sensorimotor reactions and of following physiological characteristics: respiratory rate, heart rate, skin resistance and temperature, in man doing the work of operator, under the action of DC and AC (50 c/s) magnetic fields with maximal tension equalling 8-10 a/m on the head. "Disfunction" of behavioural reactions and of their vegetative sufficiency was observed in the magnetic field. The degree of deterioration of control and compensatory properties of the central nervous system is of inverse dependence on the quality of the operator's work and the level of the central nervous system functional possibilities.

Adult↗
PubMed2003

Effects of an adenosine A2A receptor blockade in the nucleus accumbens on locomotion, feeding, and prepulse inhibition in rats.

The nucleus accumbens (NAc) subserves behaviors governed by natural rewards, i.e., feeding or exploration, and has been implicated in control of prepulse inhibition (PPI), a measure of sensorimotor gating. The present study sought to determine whether a tonic stimulation of adenosine A(2A) receptors in the rat NAc is involved in control of spontaneous locomotor activity, feeding behavior, and PPI. To this end, bilateral microinfusions of a prodrug (MSX-3) (3 microg and 5 microg in 1 microl per side) of the selective A(2A) receptor antagonist MSX-2 or vehicle (1 microl per side) were administered into the NAc. Results show that blockade of intra-NAc adenosine A(2A) receptors by a high (5 microg), but not by a low (3 microg), dose of MSX-3 increased locomotor activity in an open field, reduced food intake, and delayed intake onset in food-deprived rats examined in a test cage with standard laboratory chow. Furthermore, PPI was significantly disrupted after intra-NAc infusion of 5 microg, but not 3 microg, MSX-3. These findings suggest that locomotor activity as well as intact PPI and feeding behavior rely on tonic activation of intra-NAc A(2A) receptors. The data add further support to the view that adenosine is a tonically active modulator of striatal function through actions on A(2A) receptors.

Animals↗
PubMed1985

Perinatal dietary supplementation with a commercial soy lecithin preparation: effects on behavior and brain biochemistry in the developing rat.

Rats exposed perinatally to dietary commercial soy lecithin preparation (SLP) showed alterations in sensorimotor development and brain cell maturation. Latencies for righting responses (measured on postnatal Days 1-4) and negative qeotaxis (measured on postnatal Days 5-8) were shorter in the SLP treated animals. This pattern was accompanied by specific alterations in cerebellar development; biochemical markers for cellular maturation indicated a compression of the ontogenetic time course, as assessed by ornithine decarboxylase (ODC) activity, and levels of nucleic acids and proteins. In contrast, cellular development in the cerebral cortex indicated a generalized slowing of the time course of maturation and a deficit in the number of cells which persisted into adulthood. Behavioral abnormalities also did not disappear in adulthood, as morphine analgesia was markedly reduced in the SLP group. These results indicate that exposure of the fetus and neonate to dietary SLP during development leads to regionally specific alterations in brain cell maturation associated with disruption or behavioral patterns.

Animals↗
PubMedDate not supplied

Altered adult sexual behavior in the male rat following chronic prenatal hypoxia.

The last week of gestation is a critical period for the sexual differentiation of the brain in the rat. Exposure to prenatal stress during this period has been shown to demasculinize and/or feminize adult male sexual behavior. Many of the neurochemical and endocrine responses to hypoxia are similar to that observed under stressful conditions such as restraint stress. Therefore, we examined the postnatal consequences on reproductive and nonreproductive sexually dimorphic behaviors in male offspring of dams exposed to chronic hypoxia during the last week of gestation. In addition, we examined sensorimotor development in offspring of both sexes. Pregnant Sprague-Dawley dams were exposed to continuous hypoxia (10.5% O2 from gestational day 15 to 21). Offspring were weaned at 22 days of age and group housed. Behavioral tests were conducted with littermate representatives. In adulthood, male rats prenatally exposed to hypoxia had significantly delayed initiation latencies of masculine sexual behavior and decreased number of ejaculations, but did not display a significant increase in feminine sex behavior potentials. Developmentally, animals exposed to prenatal hypoxia did not differ significantly from controls with respect to day of eye or ear opening, or the in times of righting reflex, negative geotaxis or cliff avoidance. Wire hanging latencies in hypoxic exposed animals were significantly greater than controls around the time of eye opening, but did not differ at earlier or later ages. A significant effect of hypoxia was detected on stride length at 95 days of age, but other aspects of gait patterns were similar to controls. No group differences in gait patterns were observed at 17 or 45 days of age. In addition, no significant differences were observed in open field activity, circadian locomotor activity, saccharin preference, or Morris water maze test. This hypoxia regimen did not influence the occurrence of the prenatal or postnatal surge of plasma testosterone. Overall, these results provide some evidence that, in males, mild, chronic prenatal hypoxia may result in incomplete masculinization of adult reproductive behavior in the absence of overt changes in perinatal testosterone surges.

Animals↗
PubMed1987

Transcallosal evoked potentials in relation to behavior in the rat: effects of atropine, p-chlorophenylalanine, reserpine, scopolamine and trifluoperazine.

Single pulse electrical stimulation of the sensorimotor cortex in waking rats produced an evoked response in the contralateral sensorimotor cortex. The slow wave response consisted of: (1) an early component that was negative at the pial surface and in layer V, and was associated with multiunit discharge; and (2) a late component that was mainly negative at the surface, positive in layer V, and was associated with multiunit suppression. Previous research suggests that the early component represents summed excitatory postsynaptic potentials; the late component summed inhibitory postsynaptic potentials. Both components could be elicited by direct stimulation of the corpus callosum and both were abolished by midline callosal section. The amplitude and duration of the late component varied with concurrent motor activity in a striking manner. It was large during waking immobility and also during face-washing, licking the paws, chewing food and drinking water, but was much reduced or absent during head movements, walking and changes in posture. Only minor changes were associated with the transition from waking immobility to slow wave sleep. A series of pharmacological experiments indicated that the behavior-related variation in the late component of the transcallosal evoked response was dependent on both cholinergic and serotonergic transmission.

Animals↗
PubMed1997

Multiple differences in the play fighting of male and female rats. Implications for the causes and functions of play.

Play fighting is the most commonly occurring form of social play in juvenile mammals. Typically, males engage in more play fighting than females, and this difference has been shown to depend on the action of androgens perinatally. It is generally believed that the differences in play fighting between the sexes are quantitative and do not involve qualitative differences in the behavior performed. We show that this is an incorrect characterization of sex difference in play fighting. For example, in laboratory rats, there are at least five different mechanisms that contribute to the observed sex differences in play fighting. These mechanisms involve (I) the motivation to initiate play, (II) the sensory capacity to detect and respond to a play partner, (III) the organization of the motor patterns used to interact with a partner, (IV) age-related changes at puberty in initiating play and in responding to playful contact, and (V) dominance-related changes in adulthood in the pattern of playful interaction. Sex differences in the play fighting of rats are due to an interaction of all of these mechanisms, some of which are sex-typical not play-typical, and involve both quantitative and qualitative differences. This is clearly different from the prevailing view that play fighting is a unitary behavior which is masculinized perinatally. Indeed, even though all five mechanisms are androgenized perinatally, the sensorimotor differences also involve defeminization (i.e. reduction of female-typical qualities). This expanded view of the mechanisms contributing to the sex differences in play fighting has implications for both the analysis of the neural systems involved, and for the functional significance of this activity in childhood and adulthood.

Animals↗
PubMed1994

Recovery of sensorimotor function after distal middle cerebral artery photothrombotic occlusion in rats.

BACKGROUND AND PURPOSE: The purpose of the present study was to delineate the behavioral correlates of focal thrombotic occlusion of the distal middle cerebral artery in rats and to compare the pattern of deficits and subsequent recovery to that following proximal middle cerebral artery occlusion. METHODS: Ten Sprague-Dawley rats underwent photothrombotic occlusion of the distal middle cerebral artery with tandem occlusion of the common carotid arteries (dMCAO group); 10 animals served as operated controls. Beginning on postischemia day 2, animals were given a battery of five tests that assessed sensorimotor integration, attentional mechanisms, and muscle strength; testing continued twice weekly until day 30. Nine days of cognitive testing on the learning set of the water maze task were then given. Infarct volume and hemispheric atrophy were determined for each dMCAO animal. RESULTS: After ischemia, the dMCAO group exhibited significant behavioral deficits in posture reflex, ability to place a forelimb to various stimuli, limb adduction during rearing, and neglect of contralateral space. These deficits showed variable recovery rates. No deficits were observed in muscle strength or cognitive performance. The deficits and patterns of recovery were related to infarct location and to degree of hemisphere atrophy. CONCLUSIONS: The present study suggests that a battery of tests is necessary to fully characterize the pattern of behavioral deficits after focal cerebral ischemia. Location of infarct damage and associated degree of hemispheric atrophy were important variables in determining behavioral outcome. The present results are compared with those of the more traditional model of electrocoagulation of the proximal middle cerebral artery.

Animals↗
PubMed1978

Recurrent seizures induced by cortical iron injection: a model of posttraumatic epilepsy.

A single injection of 5 or 10 microliters of ferrous or ferric chloride into rat or cat sensorimotor cortex resulted in chronic recurrent focal paroxysmal electroencephalographic discharges as well as behavioral convulsions and electrical seizures. Iron-filled macrophages, ferruginated neurons, and astroglical cells surrounded the focus of seizure discharge. Recurrent focal epileptiform discharges caused by cortical injection of iron salts suggests that the development of human posttraumatic epilepsy may depend, in part, on neurochemical alterations induced by the principal metallic ions found in whole blood.

Animals↗
PubMed1985

The antidromic activation of tectal neurons by electrical stimuli applied to the caudal medulla oblongata in the toad, Bufo bufo L.

In order to specify the tectal projection to the bulbar/spinal regions, the antidromic responses of the physiologically identified tectal neurons as well as the gross antidromic field responses in the optic tectum to electrical stimuli applied to the caudal medulla were examined in the paralyzed common toad, Bufo bufo. The antidromic field potential was recorded in the optic tectum in response to electrical stimuli applied to the ventral paramedian portion of the contralateral caudal medulla (where the crossed tecto-spinal pathway of Rubinson (1968) and Lázár (1969) runs), but generally not when they were applied to various parts of the ipsilateral caudal medulla. The antidromic field potential was largest at the superficial part of Layer 6 or at the border between Layers 6 and 7 of the optic tectum, indicating that neurons in these layers project to the contralateral caudal medulla. Mapping experiments of the antidromic field potential over the optic tectum showed that the antidromic field potential was recorded mainly in the lateral part of it, indicating that this part of the optic tectum is the main source of projection neurons to the contralateral caudal medulla. Various classes of tectal neurons as well as retinal ganglion neurons were identified from the characteristics of the response properties to moving visual stimuli and the properties of the receptive fields. Of these, the Class T1, T2, T3, T4, T5(1), T5(2), T5(3), and T5(4) tectal neurons were activated antidromically by stimuli applied to the contralateral caudal medulla. Only a limited proportion of the Class T5(1) neurons was activated antidromically by stimuli applied to the ipsilateral caudal medulla. On the other hand, the Class T7 and T8 neurons, as well as the Class R2, R3, and R4 retinal neurons, were not activated antidromically by stimuli applied to the caudal medulla of either side. These results suggest a possibility that these tectal neurons which project to the medullary regions form the substrate of the sensorimotor interfacing and contribute to the initiation or coordination of the visually guided behavior, such as prey-catching.

Animals↗
PubMed2001

Kainic acid-induced dorsal and ventral hippocampal seizures in rats.

Despite reports of differing regional seizure susceptibility in the hippocampus, hippocampal initiation of limbic seizures has not been precisely localized. We compared seizures induced by kainic acid microinjection into the left dorsal and ventral hippocampus of rats. Discharges following ventral injections rapidly propagated to the left amygdala and sensorimotor cortex unlike seizures following dorsal injections. The ventral group showed various ictal behaviors including motor manifestations, while dorsally injected rats showed only immobilization.

Amygdala↗
PubMed2000

Multiple memory systems, development and conditioning.

A century of behavioral and neurobiological research suggests that Pavlovian conditioning involves three component memory systems: sensorimotor, affective and cognitive. In classical eyeblink conditioning, there is evidence that these three memory systems involve, respectively, the cerebellum, amygdala and hippocampus. This article reviews developmental research on eyeblink conditioning in rodents that is beginning to characterize ontogenetic dissociations and interactions among these memory systems. This research shows that the functional development of the affective system (conditioned fear response) precedes that of the sensorimotor system (conditioned eyeblink reflex). Modulation of these two systems by cognitive processes also seems to emerge at different points in ontogeny. Implications for cognitive development and research on multiple memory systems are discussed.

Animals↗
PubMed1999

Effects of regional striatal lesions on motor, motivational, and executive aspects of progressive-ratio performance in rats.

The striatum is implicated in response selection and performance, the dorsal striatum in sensorimotor control and habit learning, and the ventral striatum in motivation and rewarded behaviors. Ventral striatal lesions produce performance changes on food-reinforced, progressive-ratio (PR) schedules, but the effects of dorsal striatal lesions on this task are not known. In this study, neither medial nor lateral dorsal striatal lesions produced deficits on the main motivational indices of PR performance. In contrast, significant impairments were observed in motoric or "executive" aspects of performance. Motivationally related manipulations of the task (food deprivation and reward magnitude) produced some subtle lesion-specific changes in behavior on these motoric or executive aspects of performance. Findings are discussed in relation to the roles of the dorsal and ventral striatum in reward-related behaviors.

Animals↗
PubMed2005

Delayed treatment with monoclonal antibody IN-1 1 week after stroke results in recovery of function and corticorubral plasticity in adult rats.

Neuronal death due to ischemic stroke results in permanent deficits in sensory, language, and motor functions. The growth-restrictive environment of the adult central nervous system (CNS) is an obstacle to functional recovery after stroke and other CNS injuries. In this regard, Nogo-A is a potent neurite growth-inhibitory protein known to restrict neuronal plasticity in adults. Previously, we have found that treatment with monoclonal antibody (mAb) IN-1 to neutralize Nogo-A immediately after stroke enhanced motor cortico-efferent plasticity and recovery of skilled forelimb function in rats. However, immediate treatment for stroke is often not clinically feasible. Thus, the present study was undertaken to determine whether cortico-efferent plasticity and functional recovery would occur if treatment with mAb IN-1 was delayed 1 week after stroke. Adult rats were trained on a forelimb-reaching task, and the middle cerebral artery was occluded to induce focal cerebral ischemia to the forelimb sensorimotor cortex. After 1 week, animals received mAb IN-1 treatment, control antibody, or no treatment, and were tested for 9 more weeks. To assess cortico-efferent plasticity, the sensorimotor cortex opposite the stroke lesion was injected with an anterograde neuroanatomical tracer. Behavioral analysis demonstrated a recovery of skilled forelimb function, and anatomical studies revealed neuroplasticity at the level of the red nucleus in animals treated with mAb IN-1, thus demonstrating the efficacy of this treatment even if administered 1 week after stroke.

Animals↗
PubMed1976

EEG and clinical studies of the development of alumina cream epileptic focus in split-brain cats.

Alumina cream epileptic focus was established in the right sensorimotor cortex in 20 split-brain cats (partial or complete). EEG and behavioral observations were made in a period ranging from 24 to 836 days. Four types of EEG changes after alumina cream injection were differentiated. These types could be related to the direct effects of brain damage and to development of epilepsy. Spikes and sharp waves and paroxysmal discharges (focal and multifocal) were observed in about 60% of the cats. Clinical seizures developed in about the same percentage of the animals. These values are below those reported for cats with intact interhemispheric commissures. Diphenylhydantoin (DPH) was given orally in a daily dose of up to 15 mg/kg body weight in 9 animals with developed epileptic EEG activity. Five of them had epileptic seizures. DPH was introduced not earlier than 1.5 months after intracortical alumina cream injection. The plasma level of DPH varied between 7-20 mug/ml. This dose produced chronic symptoms of intoxication. Neither EEG changes nor clinical seizures were entirely controlled by this drug. Additional doses of Relanium (diazepam), and phenobarbital were necessary to stop generalized seizures or status epilepticus.

Aluminum↗
PubMed2004

Multiple episodes of mild traumatic brain injury result in impaired cognitive performance in mice.

OBJECTIVES: Results from recent studies on animal models of concussion suggest that multiple, rather than single, episodes of mild traumatic brain injury result in impaired cognitive performance in mice. The objective of the present study was to administer multiple impacts to the heads of mice while directly measuring the force of the impacts to determine how these parameters are related to transient loss of consciousness, cognitive deficits, and potential neuropathologic effects. METHODS: even-week-old male C57BL/6 mice were randomly assigned to experimental conditions involving three impacts (weight-drop method) to the head to induce mild traumatic brain injury or to sham control procedures. Some impacted (n = 10) and sham control (n = 10) mice were evaluated behaviorally and tested for spatial learning using the Morris water maze (MWM), whereas other impacted (n = 10) and sham control (n = 5) mice were used for histopathologic analysis. RESULTS: The mean ( +/- SD) force of impact was 19 ( +/- 3.5) N. Impacted mice took longer to regain consciousness compared with sham control mice (p < 0.0005). Behavioral test results showed that the groups did not differ on activity or sensorimotor tests or during cued trials in the MWM. Impacted mice exhibited impaired spatial learning performance during place trials in the MWM (p < 0.05). Silver staining revealed a contra-coup type of injury involving ventral brain structures in contact with or in close proximity to the skull. CONCLUSIONS: This multiple-impact model, delivered within a specifiable force range, results in transient, reversible loss of consciousness, a contra-coup brain injury, and cognitive impairment.

Animals↗
PubMed1978

Chronic focal epileptiform discharges induced by injection of iron into rat and cat cortex.

A single injection of 5 or 10 microliters of ferrous or ferric chloride into rat or cat sensorimotor cortex resulted in chronic recurrent focal paroxysmal electroencephalographic discharges as well as behavioral convulsions and electrical seizures. Recurrent focal epileptiform discharge caused by cortical injection of iron salts suggests that the development of human posttraumatic epilepsy may depend, in part, on the neurochemical alterations induced by the principal metallic ions found in whole blood.

Animals↗