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Query: UNIPROT:Q86TM3 (cage)
29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exploratory behavior and social interaction were investigated in rats that were reared in different social environments following neonatal injection with either water vehicle or the norepinephrine neurotoxin, DSP-4. At weaning, they were placed in a familiar or novel bedding type and were housed in either vehicle control-only, DSP-4-only, or mixed vehicle control and DSP-4 groups for 10 days. They were then observed in three different situations: the home cage, the cage of an unfamiliar rat, and an open field. Compared to rats housed in vehicle control-only or DSP-4-only groups, rats housed in mixed DSP-4 and vehicle control groups showed elevated exploration behavior in the home cage. Also, rats housed in mixed groups in the familiar bedding, but not the novel one, showed abnormally low levels of rearing in an open field test and reduced social interaction with unfamiliar rats. The implications of these results for a new animal model of anxiety are discussed.
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PMID:Housing influences exploration and social interaction of control and DSP-4-treated rats. 138 38

The escape reaction, as an indicator of behavioral thermoregulation, was studied in rats pretreated with the selective noradrenergic neurotoxin DSP-4. The animals were kept for 30 min in a heated floor (42, 44, 46, 48 and 50 degrees C) cage containing a wooden platform placed at a height of 12 cm, which enabled the rats to escape from the warm floor. The latency of escape and the time spent on the platform were recorded. The performance of DSP-4-treated rats was significantly inferior to that of the control rats at all tested temperatures. These findings indicate a general function of the central noradrenergic neurons in defense alarm reactions, including a significant role in heat defense behavior.
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PMID:Impaired escape reaction from noxious and nonnoxious heat in rats treated with the selective noradrenergic neurotoxin DSP-4. 178 9

Control juvenile rats adapted normally to a new home-cage bedding odor if they were caged with rats neonatally treated with 6-hydroxydopa, but not DSP-4. Neither social nor olfactory experience influenced preferences of NE-depleted rats. In some forebrain regions of controls caged with DSP-4 rats, monoamine concentrations were depressed and a metabolite elevated, suggesting the situation was stressful. DSP-4 treatment decreased the effect of footshock on hippocampal cholinergic activity, implying that NE depletion reduced sensitivity to stress. Thus, norepinephrine may modulate the biobehavioral effects of the postweaning olfactory and social environment.
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PMID:Norepinephrine depletion reduces the effects of social and olfactory experience. 212 78

The possibility that variables affecting rats' home-cage odor preferences also influence hoarding behavior was examined. Neonatal male rats were injected SC with the noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), or with vehicle. At weaning, rats were assigned to control-only, DSP-4-only, or mixed groups of DSP-4 and control rats. For the next 10 days, half the rats in each social condition were housed in cedar shavings, and remaining rats were housed in pine. Exposure to cedar significantly increased preference for the odor in control-only groups, but not in DSP-4-only or mixed treatment groups. Control-only groups also hoarded significantly more pellets per animal than rats in the other two social conditions. The results suggest that both olfactory adaptation and hoarding can be impaired by either neonatal NE depletion or an abnormal social environment.
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PMID:Impaired hoarding and olfactory learning in DSP-4-treated rats and control cagemates. 221 96

Control cagemates of rats treated with the norepinephrine (NE) neurotoxin DSP-4, showed normal olfactory learning as infants, but abnormal aversion to home-cage odors as juveniles. Neither age nor social housing conditions influenced the odor preferences of DSP-4-treated rats: they showed tolerance or attraction to familiar odors at both developmental stages. Controls, but not DSP-4-treated juveniles, housed in mixed treatment groups, showed elevated concentrations of a serotonin metabolite and reduced NE concentrations in the hippocampus, suggesting that this social situation was particularly stressful for the controls. DSP-4-treated juveniles, but not infants, produced odors that were discriminable from controls'. Thus, conflicting olfactory signals in the home-cages of mixed juvenile groups may have led to the development of stress in controls. NE depletion appeared to lessen social stress effects in their DSP-4-treated cagemates. These findings support other data suggesting that NE modulates the biobehavioral effects of the social environment.
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PMID:DSP-4 treatment influences olfactory preferences of developing rats. 868 Aug 71

Chronic mild unpredictable stress, which reduces rewarded behaviour in rats, is becoming increasingly popular as an animal model of depression. The effect of chronic mild stress (applied to animals housed five per cage for 15 days) on forced swimming and open field behaviour, and on beta-adrenoceptor binding was studied in naive rats and after the denervation of the locus coeruleus projections by DSP-4 (50 mg kg(-1)) treatment. In the forced swimming test, chronic mild stress reduced the immobility time on the second day of testing in both vehicle- and DSP-4-treated rats, indicating rather an antidepressant-like effect. This antidepressant-like effect of chronic mild stress in the forced swimming test was not present in individually housed rats which suggests that this paradigm is sensitive to housing conditions. Stress had no clear effect on the open field locomotion in naive animals (but caused a reduction in defecations), but completely blocked the DSP-4-induced decrease in the exploratory activity. As measured by 3H-dihydroalprenolol binding, DSP-4 treatment increased the beta-adrenoceptor affinity in the frontal cortex and the number of binding sites in the hippocampus and in the cerebral cortex (total-frontal cortex). Stress had no effect on the beta-adrenoceptor binding in the frontal cortex and cerebral cortex, but prevented the increase in affinity caused by DSP-4 treatment in the frontal cortex. In the hippocampus, chronic mild stress and DSP-4 treatment increased the number of beta-adrenoceptor binding sites. Neither chronic mild stress nor DSP-4 treatment had any effect on CCK(B) receptor binding in the cerebral cortex and striatum. These results show that chronic mild stress applied to group-housed rats can prevent the development of certain behavioural and biochemical changes caused by the denervation of the locus coeruleus projection areas.
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PMID:Chronic mild unpredictable stress after noradrenergic denervation: attenuation of behavioural and biochemical effects of DSP-4 treatment. 1064 90

Noradrenaline has been shown to control dopamine turnover and release in rat brain. Noradrenergic lesion with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) decreases dopamine release in the striatum and enhances catalepsy in experimental models of Parkinson's disease. However, in due course, sprouting of remaining noradrenergic axons, to compensate for the decreased noradrenaline is said to occur in specific brain regions. Though this is to some extent understood, the longstanding effects of noradrenergic lesion on dopaminergic neurons of the basal ganglia and in Parkinsonian behavior is not known. Here the question is addressed, whether locus coeruleus lesion with DSP-4 in rats alters dopamine concentration of the basal ganglia and influences Parkinsonian behavior in a long term (6 months). Parkinsonian behavior was assessed by catalepsy and activity cage after challenging with subthreshold dose of haloperidol (0.2 mg/kg), on 7, 30, 90, 120 and 180 days after DSP-4 lesion. The concentrations of noradrenaline and dopamine and its metabolites were estimated by HPLC. 6 months after DSP-4 lesion, increased concentration of noradrenaline was found in prefrontal cortex and hippocampus. Other regions remain unaffected. The concentration of dopamine remained unchanged. However, dopamine turnover appeared to be increased in prefrontal cortex and reduced in striatum and nucleus accumbens. Catalepsy and hypoactivity were observed in DSP-4 lesioned animals after haloperidol challenge on 7th, 30th and 60th day. Though dopamine turnover was reduced after 6 months in the striatum, haloperidol-induced catalepsy was not observed after 60 days. These results indicate a gradual functional recovery, perhaps hyperinnervation of noradrenergic neurons after DSP-4 treatment and the reversal of its effects on dopaminergic neurons and on Parkinsonian symptoms.
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PMID:Functional recovery of locus coeruleus noradrenergic neurons after DSP-4 lesion: effects on dopamine levels and neuroleptic induced-parkinsonian symptoms in rats. 1471 12

Environmental stress produces adverse affects on memory in humans and rodents. Increased noradrenergic neurotransmission is a major component of the response to stress and noradrenaline (NA) plays an important role in modulating processes involved in learning and memory. The present study investigated the effect of NA depletion on stress-induced changes on memory performance in the mouse. Central NA depletion was induced using the selective neurotoxin N-(2-chloroethyl)-N-ethyl-2 bromobenzylamine (DSP-4) and verified by high performance liquid chromatography (HPLC). A novel cage stress procedure involving exposure to a new clean cage for 1 h per day, 4 days per week for 4 weeks, was used to produce stress-induced memory deficits measured using the object recognition task. 50 mg/kg DSP-4 produced large and sustained reductions in NA levels in the frontal cortex and hippocampus measured 24 h, 1 week and 5 weeks after treatment. Four weeks of exposure to novel cage stress induced a memory deficit in the object recognition task which was prevented by DSP-4 pre-treatment (50 mg/kg 1 week before the commencement of stress).These findings indicate that chronic environmental stress adversely affects recognition memory and that this effect is, in part, mediated by the noradrenergic stress response. The implication of these findings is that drugs targeting the noradrenergic system to reduce over-activity may be beneficial in the treatment of stress-related mental disorders such as post-traumatic stress disorder or anxiety in which memory is affected.
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PMID:Central noradrenergic depletion by DSP-4 prevents stress-induced memory impairments in the object recognition task. 1972 Jan 15