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PubMed1986

Recovery of functions after neonatal or adult hemispherectomy in cats. III. Complex functions: open field exploration, social interactions, maze and holeboard performances.

Complex behavioral patterns were studied in cats with removal of the entire left cerebral hemisphere either as neonates (n = 10) or adults (n = 11), and in intact control cats (n = 24). Adult-lesioned cats showed decreased open field activity in locomotion, rearing and sniffing. Lesioned kittens showed similar deficits at 100 days of age, but by 150 days of age they resembled normal littermates in all 3 measures. In the presence of another cat, adult-hemispherectomized cats violated species-typical body-buffer space, approaching and attacking other cats. By comparison, normal cats never attacked and seldom approached in the open field. Neonatal-lesioned adults showed only occasional approach and a tendency to sit or stiff-walk in the presence of other cats; attacks were rare. Adult-lesioned cats responded poorly to reversal training for preferred arm of a T-maze, whereas neonatal-lesioned adults were significantly more trainable. Similarly, adult-lesioned cats exhibited a search deficit in a baited holeboard, while neonatal-lesioned adults searched normally. Overall, these results demonstrate that in this animal model, enhanced recovery following early vs adult lesions can also be found in relatively complex, spontaneous behavioral responses not previously studied in this regard.

Aging↗
PubMed1996

Reference memory and allocentric spatial localization deficits after unilateral cortical brain injury in the rat.

Traumatic brain injury (TBI) produces learning and memory impairments in humans. This study investigated the effects of TBI on memory and spatial localization strategies in rats. Prior to TBI, separate groups of rats were trained in an 8-arm radial maze with either all 8 arms baited (Expt. 1) or only 4 of the 8 arms baited (Expt. 2). TBI was produced by a controlled pneumatic impactor striking the entire right sensorimotor cortex of the anesthetized rat. Rats used in Expt. 1 were selected because they did not use a stereotypic response strategy (going to adjacent arms) in performing the maze before injury. After TBI the rats were not different from control rats in the number of working memory (WM) errors made. They did, however, display a distinct propensity to go to adjacent arms, i.e., exhibit stereotypic behavior, with a right-handed (ipsiversive) bias (P < 0.005). After TBI, rats which were trained with only 4 of 8 arms baited committed more reference memory (RM) errors than control rats (P < 0.05). They did not differ from controls on WM errors. Injured rats took longer to re-attain criteria than controls (P < 0.0001). Injured rats also initially displayed a propensity to enter the adjacent arm sequentially before re-attaining criteria. Further analysis indicated that injured rats re-learned the maze with a right-hand bias (P < 0.0001). The results of both experiments suggest that after TBI, rats shifted from an allocentric to an egocentric strategy to re-learn the maze. It was suggested that damage to the parietal cortex may have been responsible for both RM errors and the shift away from an allocentric strategy to an egocentric strategy. Possibly, the ipsiversive (right-hand) bias may be the result of a behaviorally or injury-induced neurochemical asymmetry within the motor system.

Animals↗
PubMed1993

Phosphorylation of neuromodulin in rat striatum after acute and repeated, intermittent amphetamine.

Repeated, intermittent treatment of rats with amphetamine results in a sensitization of locomotor and stereotyped behaviors that is accompanied by an enhancement in stimulus-induced dopamine release. Increased phosphorylation of the neural specific calmodulin-binding protein, neuromodulin (GAP-43, B-50, F1) has been demonstrated in other forms of synaptic plasticity and plays a role in neurotransmitter release. To determine whether neuromodulin phosphorylation was altered during amphetamine sensitization, the in vivo phosphorylated state of neuromodulin was examined in rat striatum in a post hoc phosphorylation assay. Female, Holtzman rats received saline or 2.5 mg/kg amphetamine twice weekly for 5 weeks. One week after the last dose of amphetamine, rats were challenged with either 1 mg/kg or 2.5 mg/kg amphetamine or saline and the rats were sacrificed 30 min later. Purified synaptic plasma membranes were prepared in the presence of EGTA and okadaic acid to inhibit dephosphorylation, and were subsequently phosphorylated in the presence of purified protein kinase C and [gamma-32P]ATP. The protein kinase C-mediated post hoc phosphorylation of neuromodulin was significantly reduced in groups that received either acute or repeated amphetamine suggesting that neuromodulin in those groups contained more endogenous phosphate. The acute, challenge dose of amphetamine increased neuromodulin phosphorylation in the saline-treated controls but not in the repeated amphetamine-pretreated group. Anti-neuromodulin immunoblots showed no change in neuromodulin levels in any group. There was no significant change in protein kinase C activity in any treatment group. To further investigate the effect of acute amphetamine, the ability of amphetamine to alter neuromodulin phosphorylation in 32Pi-preincubated Percoll-purified rat striatal synaptosomes was examined. Amphetamine (10 microM) significantly increased phosphorylation of a 53 kDa band that migrated with authentic neuromodulin in the synaptosomes by 22% while 500 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) increased neuromodulin phosphorylation by 45%. These data suggest that one injection of amphetamine can increase neuromodulin phosphorylation in rat striatum and that this increase is maintained for at least 1 week following a repeated, sensitizing regimen of amphetamine. Since sensitization can be induced with one dose of amphetamine, it is possible that enhanced neuromodulin phosphorylation could contribute to neurochemical events leading to enhanced release of dopamine and/or behavioral sensitization.

Amphetamine↗
PubMed1995

Cocaine binges differentially alter striatal preprodynorphin and zif/268 mRNAs.

Several studies have demonstrated that cocaine increases preprodynorphin, c-fos, and zif/268 mRNAs in rat dorsal striatum. Multiple, closely spaced exposures to cocaine appear to elicit the greatest increases in dynorphin. However, the response of preproenkephalin, c-fos and zif/268 mRNAs to such a dosing regimen is unknown. Therefore, we used a 'binge' paradigm to evaluate changes in mRNA for preprodynorphin, preproenkephalin, c-fos and zif/268. Male Wistar rats received three hourly i.p. injections of saline or 10 or 20 mg/kg cocaine for 1, 5, or 10 days. Although cocaine-induced locomotor and stereotypical behaviors were significantly increased as compared to saline on days 1, 5 and 10, these behaviors were significantly less on day 10 than on days 1 and 5. One hour after the last injection on days 1, 5, or 10, the rats were anesthetized and decapitated for quantitative in situ hybridization histochemistry. C-fos mRNA was undetectable in all treatment groups whereas zif/268 mRNA in the dorsal striatum was increased in a dose-dependent manner (20 mg/kg > 10 mg/kg) but the intensity of hybridization signal decreased over time (1 day >> 5 days > 10 days) as compared to that in saline-treated controls. In contrast, 10 mg/kg cocaine binges caused an increase in preprodynorphin, but not preproenkephalin, mRNA in the dorsal, but not ventral, striatum in a time-dependent manner (day 10 >> day 5 > day 1) whereas 20 mg/kg cocaine binges caused an increase in striatal preprodynorphin that was greater on day 1 and day 5 than on day 10. These data indicate that (1) c-fos, zif/268 and preprodynorphin mRNAs are differentially regulated in dorsal striatum, (2) behavioral tolerance results from chronic binges with 10 and 20 mg/kg cocaine and (3) the preprodynorphin genomic response exhibits tolerance to chronic high dose, but not low dose, cocaine binges.

Analysis of Variance↗
PubMed1996

Behavioral effects of amylin injected intracerebroventricularly in the rat.

Amylin is a peptide of pancreatic origin that has been reported to possess high-affinity binding sites in the brain and to affect central dopaminergic and serotonergic neurotransmission. Administered ICV the peptide induced a dose-dependent decrease of locomotor activity without affecting grooming and sniffing. At a dose of 5 micrograms/ rat, it antagonized the hypermotility and stereotypies induced by s.c. injection of amphetamine (2 mg/kg) or of the dopamine receptor agonist, apomorphine (250 mg/kg). Amylin did not change significantly the effect of haloperidol (0.5 mg/kg, s.c.) on locomotor activity, grooming, and sniffing. Moreover, the peptide did not modify the locomotor behavior of animals injected with the 5-HT2 antagonist, ritanserin (2 mg/kg, s.c.). These results suggest that amylin may exert motor effects, probably by interfering with central dopaminergic neurotransmission.

Amphetamine↗
PubMed1993

Continuously infusing quinpirole decreases Ca2+/calmodulin-dependent phosphorylation in mouse striatum.

Continuously administering the D2 dopamine agonist quinpirole to mice for 6 days produces an initial stereotypy that is reduced by 2 h and is absent from 3 h to the 6 day duration of the infusion. In an attempt to determine the biochemical correlates for this down-regulation of stereotypic behavior, the effects of continuously administering quinpirole on a number of biochemical parameters were measured in mouse corpus striatum. After 6 days of infusion with quinpirole, the striata were analyzed for D1 and D2 dopamine receptors, for the activities of several protein phosphorylation reactions which are thought to be involved in receptor activity and for the levels of calmodulin-binding proteins. Quinpirole decreased the D2 receptors in striatum and produced a small but statistically non-significant increase in D1 receptors, resulting in a significant increase in the ratio of D1 to D2 dopamine receptors. An examination of the effects of quinpirole on protein phosphorylation systems showed that the agonist failed to alter the activity of cyclic AMP-dependent protein kinase or protein kinase C but significantly decreased the Ca2+/calmodulin-dependent phosphorylation of striatal membranes. However, this decrease in Ca2+/calmodulin-dependent phosphorylation was not associated with changes in the levels of calmodulin-binding proteins. The results suggest that behavioral down-regulation following the continuous administration of a D2 dopamine agonist is associated with at least two biochemical events: a down-regulation of D2 dopamine receptors and a decrease of Ca2+/calmodulin-dependent phosphorylation of striatal membranes.

Animals↗
PubMed1980

Induction of wet-dog shakes by intracerebral 'acid' TRH in rats.

Less than Glu-His-Pro-OH or 'acid' TRH, until now considered to be an inactive metabolite of TRH, induces in rats when administered intracerebroventricularly (i.c.v.), stereotyped behavior and, from 12.5 micrograms, wet-dog shakes (WDS). WDS induced by 200 micrograms less than Glu-His-Pro-OH are antagonized by apomorphine, haloperidol and cyproheptadine while phentolamine and naloxone are without effect. For this action 'acid' TRH appears as effective as TRH itself and might have the same mechanism.

Animals↗
PubMed1995

Effect of NE-100, a novel sigma receptor ligand, on phencyclidine- induced delayed cognitive dysfunction in rats.

Phencyclidine (PCP), in a dose of 15 mg/kg, produced delayed cognitive dysfunction (at 24 h) in rats subjected to water maze tasks. At 24 h after PCP administration, ataxia, hyperlocomotion and stereotyped behavior were not induced. NE-100, N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-enthylamine monohydrochloride, a selective and potent sigma receptor ligand, was administered orally 10 min after PCP administration or 15 min before the first trial (24 h after PCP administration). In both cases, NE-100 dose-dependently attenuated the delayed cognitive dysfunction induced by PCP. As these findings show that ingestion of PCP led to delayed cognitive dysfunction similar to the cognitive signs of psychosis seen in humans, NE-100 is being further studied for possible treatment of subjects with schizophrenia.

Animals↗
PubMed1982

Alterations in the stages of continuous amphetamine intoxication produced by lesions of locus coeruleus and substantia nigra.

1. Slow-release silicone pellets containing d-amphetamine base were implanted subcutaneously in rats 20 days following radio-frequency lesions of the locus coeruleus (LC), substantia nigra (SN), or control operations. 2. LC-lesioned rats exhibited enhanced motor stereotypies soon after implantation, while SN-lesioned animals showed increased locomotion but decreased stereotypy and anorexia. 3. The later behavioral stages of continuous amphetamine intoxication were attenuated in both lesioned groups as controls then entered the most intense stereotypy, showed the greatest withdrawal to the burrows, and maximally exhibited the increase in socially disruptive behaviors which appear following four days of constant amphetamine intoxication. 4. The integrity of both dopaminergic and noradrenergic systems was necessary for the full expression of the late stages of this animal model of amphetamine psychosis.

Amphetamine↗
PubMed1995

The sigma-selective ligand NE-100 attenuates the effect of phencyclidine in a rat diving model.

1. Phencyclidine (PCP) reduces the latency of rats diving into a water-filled pool from a hidden platform, without stereotyped behavior. 2. The sigma-selective ligand, NE-100 (N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-ethyl-amine monohydrochloride), attenuates the effects of PCP in this procedure. 3. The serotonin2 (5-HT2) antagonist, ritanserin, and the sigma receptor ligands, 1-(cyclopropylmethyl)-4-[2'(4"-fluorophenyl)-2'-oxoethyl]- piperidine HBr (Dup734), 4-[2'-(4"-cyanophenyl)-2'-oxoethyl]-1- (cyclopropylmethyl)piperidine (XJ448), alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazine butanol (BMY14802) and rimcazole similarly attenuate the effects of PCP. 4. The dopamine D2/sigma ligands, haloperidol and cis-N-(1-benzyl-2-methyl-pyrrolidin-3-yl)-2-methoxy-5-chloro-4- methylaminobenzamide (YM-09151-2) completely reverse the effects of PCP, whereas the same dose ranges of these drugs produce sedation. 5. The dopamine D2-selective antagonist, sulpiride, has no apparent effect on the PCP latency to the rat dive. 6. Thus, PCP-induced diving behavior was improved by sigma ligands and the 5-HT2 antagonist. This model of negative symptoms in an experimental animal will facilitate experiments on drug treatments for schizophrenia.

Animals↗
PubMed1995

Repeated amphetamine administration induces a prolonged augmentation of phosphorylated cyclase response element-binding protein and Fos-related antigen immunoreactivity in rat striatum.

Semi-quantitative immunocytochemistry was used to investigate the levels of cyclase response element-binding protein, phosphorylated cyclase response element-binding protein, Fos and Fos-related antigen immunoreactivity in the striatum of rats after acute or repeated amphetamine administration. Rats were perfused 20 min (phosphorylated cyclase response element-binding protein) or 2 h (cyclase response element-binding protein, phosphorylated cyclase response element-binding protein, Fos, Fos-related antigen) after a single injection (5 mg/kg, i.p.) or five daily injections of amphetamine. The latency to onset of stereotypical behaviors was significantly reduced in rats exposed to repeated amphetamine as compared to acute amphetamine, indicating development of behavioral sensitization. Cyclase response element-binding protein immunoreactivity was not altered in the dorsal or ventral striatum following acute or repeated amphetamine. Phosphorylated cyclase response element-binding protein immunoreactivity was significantly induced 20 min, but not 2 h, following acute amphetamine, whereas a significant induction of phosphorylated cyclase response element-binding protein immunoreactivity was found 20 min and 2 h after repeated amphetamine in the dorsal striatum only. Fos immunoreactivity was significantly induced in the dorsal striatum following acute and repeated amphetamine. Fos immunoreactivity in the core of the nucleus accumbens was significantly increased following repeated amphetamine only. Acute amphetamine induced, and repeated amphetamine further augmented, Fos-related antigen immunoreactivity in the dorsal striatum, while not affecting Fos-related antigen immunoreactivity in the nucleus accumbens. These data demonstrate that repeated amphetamine administration results in a prolonged induction of phosphorylated cyclase response element-binding protein and Fos-related antigen immunoreactivity in the dorsal striatum, indicating that alterations in striatal gene expression associated with the development of behavioral sensitization may be mediated, in part, by these transcription factors.

Amphetamine↗
PubMed1983

Psychiatric aspects of abnormal movement disorders.

It has been postulated that some movement disorders are secondary to unresolved, unconscious mental conflict; however, psychotherapeutic intervention has been unsuccessful and psychoanalytic formulations have not been shown to be valid. In addition, there is the interesting observation that some medications, stereotactic surgery and biofeedback have been successful in treating movement disorders. Moreover, as in the cases of amphetamine-induced stereotyped behavior, Parkinsonism, the acute dyskinesias, and Tardive Dyskinesia, there is evidence that some involuntary disorders of movement are biochemically mediated. Organicity, in varying degrees and involving different anatomical and physiological areas, has been observed in Tourette's Syndrome, Parkinson's disease and Huntington's disease. These diseases are usually associated with adjustment problems because of the effect that they have on the patient and the patient's family. Some of these psychosocial problems are discussed.

Antipsychotic Agents↗
PubMed1984

Effects of intranigral injections of dopamine agonists and antagonists, glycine, muscimol and N-methyl-D,L-aspartate on locomotor activity.

Previously it has been shown that bilateral intranigral injections of dopamine into rats pretreated with a monoamine oxidase inhibitor induced prolonged stimulation of locomotor activity, while bilateral intranigral injections of haloperidol reduced the locomotor stimulation evoked by systemic amphetamine. In the present studies, the role of the substantia nigra in locomotor activity was further investigated using a variety of dopaminergic and other agonists and neuroleptics. Ergometrine, epinine, (+/-)-2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronapthalene hydrobromide (ADTN), 1,2,3,4-tetrahydro-6,7,-dihydroxyisoquinoline hydrochloride (THIQ), muscimol and glycine elicited locomotor activity when injected into the substantia nigra pars reticulata bilaterally. Additionally the non-dopaminergic agonists also elicited a degree of stereotyped behavior. Locomotor activity induced by intranigral ergometrine was blocked by systemic haloperidol but was not affected by intranigral haloperidol. Locomotor activity elicited by systemic amphetamine was blocked by bilateral intranigral alpha-flupenthixol, but that elicited by bilateral intra-accumbens ergometrine was not affected by alpha-flupenthixol or haloperidol injected into the substantia nigra pars reticulata bilaterally. The results provide further evidence that alterations of neurotransmission in the substantia nigra exert effects on locomotor activity.

Amphetamine↗
PubMed1993

Interaction between alcohol deprivation and morphine withdrawal in mice.

Hybrid mice having had 12 weeks free access to flavored alcohol were deprived of it for 3 days. The increase in alcohol intake rate during first 1.5 h of renewal access as compared with its intake rate during the remaining 22.5 h (alcohol-deprivation effect, ADE) was used to select individuals having (HD) or lacking (LD) the ADE. The mice received morphine or placebo pellet implantation for 4 days followed by removal of alcohol and pellets. Cross-maze, acoustic startle response, and tail flick tests were conducted 1 day after morphine withdrawal and after 2 days of alcohol deprivation. Next day, during a second ADE test, placebo-treated HDs again showed ADE and LDs showed no ADE; the HDs during morphine withdrawal also still showed an ADE similar to those in placebo HDs, but LDs after morphine removal differed in showing an ADE. Significantly more hyperalgesia in HD than LD mice was observed during morphine withdrawal. Placebo HDs differed from placebo LDs in showing stereotyped behavior and kindling-like rise in acoustic startle response. Morphine withdrawal caused body weight loss, and converted the startle response curve in both LD and HD mice to a bell-shape curve. In HD mice the alcohol deprivation behavioral pattern was substituted by the corresponding morphine withdrawal pattern. The existence of distinct neural circuits responsible for the development of alcohol and morphine dependence is proposed.

Alcoholism↗
PubMed1996

A structure-activity relationship for the neurotoxicity of triazole fungicides.

Previous work has demonstrated that acute exposures to the triazole fungicide triadimefon affects central nervous system (CNS) catecholamines and induces a transient syndrome in rats that consists of hyperactivity and stereotyped behaviors. The present research was designed to determine whether this type of CNS toxicity is characteristic of other triazoles. Dose-effect functions were determined for 14 different triazoles or structurally related pesticides in adult male Long-Evans rats. All chemicals were administered per os in corn oil. Hyperactivity was measured for 2 h in figure-eight mazes. Results indicated that only triadimefon and triadimenol were able to induce hyperactivity; none of the other chemicals produced this effect. These data suggest a very rigid structure-activity relationship (SAR) for the hyperactivity syndrome and indicate that CNS effects may be minimized in the future design of triazoles without impacting fungicidal efficacy.

Animals↗
PubMed1991

Effects of Croton zehntneri aqueous extracts on some cholinergic- and dopaminergic-related behaviours of laboratory rodents.

The effects of aqueous Croton zehntneri leaf and branch extracts, orally administered, on some dopaminergic- and cholinergic-related behaviours were studied in rats and mice. The leaf extract did not modify apomorphine-induced stereotypic behavior, haloperidol-induced catalepsy and active avoidance/escape responses. The branch extract reduced stereotypy but did not interfere with catalepsy and active avoidance behavior. Both extracts were capable of increasing the tremor induced by oxotremorine.

Animals↗
PubMedDate not supplied

Empirically derived consequences: a data-based method for prescribing treatments for destructive behavior.

Behavioral treatments are often prescribed on the basis of a functional assessment. However, in a significant number of cases, functional assessment results are equivocal or suggest that internal stimuli are maintaining the behavior. In this investigation, we evaluated an alternative data-based assessment that may be useful in such cases. This assessment was used to identify reinforcers and punishers based on the reinforcement assessment procedure described by Pace, Ivancic, Edwards, Iwata, and Page (1985). We then assessed whether empirically derived reinforcers and punishers could be combined to treat the destructive behaviors of two clients. For both clients, the rates of destructive behavior decreased markedly. The results suggest that empirically derived consequences may be useful in decreasing destructive behavior when a functional assessment is inconclusive or is consistent with the hypothesis that the behavior is stereo-typic and maintained by internal stimuli.

Aggression↗
PubMedDate not supplied

Positive side effects in the treatment of SIB using the Self-Injurious Behavior Inhibiting System (SIBIS): implications for operant and biochemical explanations of SIB.

The rate of self-injurious head hitting was reduced using contingent electric shock delivered via the Self-Injurious Behavior Inhibiting System (SIBIS). Positive side effects indicating an improved affective state and increased interaction with the environment were documented. Treatment gains were maintained at a 1-year follow-up assessment. The consistent reports of positive affective side effects from successful treatment studies using SIBIS and contingent electric shock are noted. Implications for current operant-based theories of SIB based on the communication function of SIB and endogenous opiate mechanisms are discussed.

Aversive Therapy↗