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PubMed2000

Turning in rats following intraaccumbens shell injections of amphetamine or eticlopride.

In recent years there has been interest in possible differential behavioral functions of the core and shell subregions of the nucleus accumbens. The present study compared the effects of accumbens core and shell injections of (+)-amphetamine on turning behavior in rats; the turning effects of the selective D2 antagonist (-)-eticlopride injected into the shell were also tested. Rats (n = 28) were implanted unilaterally with guide cannulae and subsequently tested for turning in seven 20-min sessions. Amphetamine (10.0 and 20.0 microg but not 5.0 microg/ 0.5 microl) elicited contralateral turning following injection into the shell, while the same doses into the core had no effect. In animals given systemic amphetamine (2.0 mg/kg), eticlopride (10.0 but not 1.0 or 0.1 microg/0.5 microl) injected into the shell region of the accumbens produced ipsilateral turning. These results suggest that the accumbens shell, but not the core, is a critical site for turning behavior.

Amphetamine↗
PubMedDate not supplied

Subtypes of dopamine receptors involved in the mechanism of reinforcement.

Advancement in the study of receptors for neurotransmitters facilitated the analysis of neural mechanisms underlying reinforcement. Two subtypes of dopamine receptors, D1 and D2, play distinct roles in producing reinforcing effects. Experiments using SCH 23390 suggest that the reinforcing effects of food, water, saccharin, heroin and brain stimulation all critically depend on the activation of D1 dopamine receptors, particularly those in the nucleus accumbens and the ventral tegmental area. Raclopride, a D2 dopamine antagonist, also reduced bar-pressing responses for food, heroin, and brain stimulation. Thus, both D1 and D2 receptors seem to be involved in the reinforcement mechanisms. There were some differences between D1 and D2 dopamine antagonists in the manner of reducing operant responding. It appears that D1 receptors are related to the efficacy of reinforcements while D2 receptors are related to the type of reinforcers.

Animals↗
PubMed2000

Metal complexes of salicylhydroxamic acid (H2Sha), anthranilic hydroxamic acid and benzohydroxamic acid. Crystal and molecular structure of [Cu(phen)2(Cl)]Cl x H2Sha, a model for a peroxidase-inhibitor complex.

Stability constants of iron(III), copper(II), nickel(II) and zinc(II) complexes of salicylhydroxamic acid (H2Sha), anthranilic hydroxamic acid (HAha) and benzohydroxamic acid (HBha) have been determined at 25.0 degrees C, I=0.2 mol dm(-3) KCl in aqueous solution. The complex stability order, iron(III) >> copper(II) > nickel(II) approximately = zinc(II) was observed whilst complexes of H2Sha were found to be more stable than those of the other two ligands. In the preparation of ternary metal ion complexes of these ligands and 1,10-phenanthroline (phen) the crystalline complex [Cu(phen)2(Cl)]Cl x H2Sha was obtained and its crystal structure determined. This complex is a model for hydroxamate-peroxidase inhibitor interactions.

Copper↗
PubMed1988

Scopolamine interactions with D1 and D2 antagonists on radial-arm maze performance in rats.

Recent evidence indicates that acetylcholine and dopamine play complementary roles in cognitive as well as motor functions. In our previous study, the dopamine receptor blocker, haloperidol, was found to attenuate the radial-arm maze choice accuracy deficit caused by the muscarinic acetylcholine receptor blocker, scopolamine. Haloperidol has activity in blocking both D1 and D2 dopamine receptor subtypes. The current study was conducted to determine whether this dopamine-acetylcholine interaction specifically involved D1 or D2 dopamine receptors. The D1 antagonist, SCH 23390, and the D2 antagonist, raclopride, were administered with a dose of scopolamine which caused choice accuracy deficits in the radial-arm maze. The scopolamine-induced deficit was reversed by SCH 23390, the D1 antagonist, indicating that D1 blockade alone is sufficient to reverse the amnestic effects of muscarinic blockade. There was no indication in this study that the D2 blocker, raclopride, had a similar effect. However, this does not mean that such an effect may not be present at other doses of raclopride or with other D2 antagonists. The present finding that D1 blockade counteracts scopolamine-induced cognitive dysfunction not only furthers the understanding of dopamine-acetylcholine relationships in cognitive function, it also suggests a promising direction for the development of treatments for cognitive dysfunction due to cholinergic loss.

Animals↗
PubMed1998

Effects of specific dopamine D1 and D2 receptor antagonists and agonists and neuroleptic drugs on emotional defecation in a rat model of akathisia.

An increase in emotional defecation in rats in a well-habituated environment induced by neuroleptic drugs (NDef) has been proposed as a model for neuroleptic-induced akathisia. We examined the effects of dopamine receptor antagonists and agonists on this model. A selective dopamine D1 antagonist (SCH 23390) and a selective D2 antagonist (raclopride) induced increased defecation at higher doses, and demonstrated a synergistic effect at lower doses. Selective D1 (SKF 82958) and D2 (quinpirole) agonists did not have a significant effect on defecation, nor did they reverse the effect of haloperidol. In a further pilot study, we explored the effects of typical and atypical neuroleptics on this model. The haloperidol and risperidone treated rats produced more faecal boli than those treated with clozapine, thioridazine and chlorpromazine, with the former being non-significantly greater than the vehicle-treated group. The results of our studies suggest that NDef is most probably an effect of central dopamine antagonism that is not specific to D1 or D2 receptors, but that the two receptor subtypes have a synergistic effect. It is unlikely to be due to actions of neuroleptics on 5HT2 or alpha1 receptors as has sometimes been suggested. The results have implications for our understanding of the pathogenesis of akathisia.

Akathisia, Drug-Induced↗
PubMed1999

Involvement of catecholamines in recall of the conditioned NK cell response.

The primary goal of the study was to identify the types of catecholamines and the associated receptors which might be involved in the recall of the conditioned NK cell response. Specific catecholamine receptor antagonists were selected to block the conditioned NK cell response at the recall step. The regional contents of dopamine (DA), norepinephrine (NE), and epinephrine were determined in the brain of the conditioned animals by using the high performance liquid chromatography with electrochemical detection (HPLC/ED). Results showed that pre-disruption of the central alpha1-, alpha2-, beta1-, beta2-, D1-, or D2-receptors at the conditioned recall stage, interrupted the conditioned enhancement in NK cell activity. The NE contents at the cerebellum, and DA contents at the striatum and hippocampus, were significantly higher in the brain of the conditioned animals when compared to that of the control animals. These information indicated the possible roles of the central noradrenergic and dopaminergic systems in regulating the recall of the conditioned NK cell response.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2000

Facilitation of preparatory behavior in an artificial prey paradigm by D1-subfamily dopamine receptor activation.

Dopamine agonists facilitate, and antagonists inhibit, conditioned preparatory behaviors in rats. Similar effects are demonstrated on an unconditioned preparatory behavior: predatory search and contact of a moving artificial prey stimulus. Apomorphine (0.1, 0.2 mg/kg), a direct agonist, had no effect relative to a within-subject injection of saline vehicle but d-amphetamine (0.1 mg/kg), an indirect agonist, increased contact frequency without altering overall motor activation. To determine the relative importance of the D1 and D2 subfamilies of receptors in the amphetamine effect, separate groups of animals received amphetamine co-injected with either SCH23390 (0.01 and 0.005 mg/kg) or eticlopride (0.01 mg/kg), D1 and D2 antagonists, respectively. Whereas the eticlopride-amphetamine group showed no change in contact frequency from baseline, co-injections of either dose of SCH23390 and amphetamine led to near total suppression of contact, as did treatment with SCH23390 (0.005 mg/kg) alone. Treatment with 0.01 mg/kg eticlopride alone increased contact frequency while treatment with a higher dose (0.1 mg/kg) had no effect. Treatment with the D1-subfamily agonist SKF81297 (0.1 mg/kg) increased contact frequency. Collectively, these results support the hypothesis that dopamine mediates unconditioned preparatory behavior and suggest differing roles for the D1 and D2 receptor subfamilies.

Amphetamine↗
PubMed2000

D-amphetamine facilitation of morris water task performance is blocked by eticlopride and correlated with increased dopamine synthesis in the prefrontal cortex.

The effect of posttraining D-amphetamine on Morris water task (MWT) performance was analyzed in this study by training rats using a single training trial per day procedure. In addition to acquisition latency, learning was assessed by a probe trial given 24 h after the last training trial. Rats given immediate post-trial D-amphetamine demonstrated improved performance over saline rats on both acquisition and the probe trial. An analysis of the mechanisms underlying facilitation revealed that eticlopride (a D2 antagonist) blocked D-amphetamine's facilitatory effects on the probe trial and dopamine synthesis was increased in the medial prefrontal cortex in the D-amphetamine group relative to controls. These results show that chronic administration of posttraining D-amphetamine facilitated MWT performance, and this facilitation may be mediated by the dopaminergic system and dopamine synthesis in the prefrontal cortex.

Animals↗
PubMed2002

Novel-object place conditioning: behavioral and dopaminergic processes in expression of novelty reward.

In a choice situation, rats given repeated access to novel objects in one of two distinct environments display an increase in preference for the novelty-paired environment. The experiments in this present report extend the generality of this effect to new procedures. Further, this shift in preference depends on object novelty; no systematic shift in preference was observed if the environment was paired with a familiar object. Experiments in the present report also provided evidence against non-associative accounts that rely on mechanisms that leave the paired environment more novel than the unpaired environment (e.g. object interaction interfering with environmental familiarization). Consistent with a conditioning account is the loss of place conditioning when access time with the novel objects was shortened from 10 min to 5 or 2.5 min. Interestingly, although a decrease in time with objects prevented place conditioning, these groups showed a novelty-conditioned increase in activity. Finally, treatment with the dopamine D(1) antagonist SCH-23390 (0.03 mg/kg) or the dopamine D(2)/D(3) antagonist eticlopride (0.1 mg/kg) before the post-conditioning preference test blocked expression of the novel-object place conditioning. Taken together, these experiments establish that the increased preference produced by object-environment pairings reflects a conditioned association between environmental cues and the appetitive effects of receiving access to novel stimuli.

Animals↗
PubMed2003

Altered action of dopamine and cholecystokinin on lateral hypothalamic neurons in rats raised under different feeding conditions.

Single-unit activity was recorded in the lateral hypothalamus (LH) of adult Wistar rats anaesthetized with urethane. The rats were differently nourished till weaning by raising in small (SL), control (CL) or large litters (LL). They gained significantly different body weight leading to overweight in SL (mean: 428.4 g on day 90) and underweight in LL rats (mean 399.5 g) compared to CLs (414.5 g). The mean basal firing rate of LH neurons differed, it was lowest in SL and highest in LL rats. The proportion of neurons changing their firing rate by more than 30% in response to iontophoretically administered dopamine (DA) was significantly greater in SL (76%) than LL rats (54%). Effects of DA were significantly more often blocked by a D1 receptor antagonist in LL than CLs. The responsiveness to cholecystokinin (CCK) alone and coadministered with DA was also greater in SL than LL. Furthermore, the proportion of neurons inhibited by DA alone and in the presence of CCK was significantly greater in SL than LL rats. In conclusion, litter size and difference in nourishment during early postnatal development of rats seem to determine LH basal firing rate. The increased neuronal responsiveness to exogenous DA and CCK in neonatally overfed SL rats may indicate a decreased activity of these endogenous signals which normally contribute to limitation of energy intake.

Action Potentials↗
PubMed1991

Evidence that dopamine in the nucleus accumbens is involved in the ability of rats to switch to cue-directed behaviours.

Recently we have reported that injections of d-amphetamine into the nucleus accumbens enhanced the number of switches to cue-directed behaviours without an effect on the number of switches to non-cue-directed behaviours in a swimming test. In the present study we investigated to what extent this effect is mediated via the dopaminergic system in the nucleus accumbens. For that purpose drugs selective for D1- and D2-receptors were studied in this swimming test. It was found that the selective D2-agonist LY 171 555 (50 ng/0.5 microliters) enhanced the number of different cue-directed behaviours. The selective D2-antagonist raclopride (50 ng/0.5 microliters) decreased it. Furthermore an ineffective dose of raclopride attenuated the effect of LY 171 555. Both the selective D1-antagonist SCH 23390 (400 ng/0.5 microliters) and the selective D1-agonist SKF 38393 (50-400 ng/0.5 microliters) decreased the number of different cue-directed behaviours. The effect induced by SCH 23390 could not be blocked by SKF 38393. Similarly the effect induced by SKF could not be attenuated by SCH 23390. These data point to a role for dopamine D2-receptors in the ability to switch to cue-directed behaviours. The present findings do not yet allow the conclusion that D1-receptors are involved.

Animals↗
PubMed1999

Dopamine antagonism in a novel-object recognition and a novel-object place conditioning preparation with rats.

Access to novel objects, similar to drugs of abuse, can enhance a place preference in rats. In the present experiments, the dopamine D1 receptor antagonist SCH-23390 blocked an increase in place preference conditioned by access to novel objects at doses that did not interfere with object interaction (0.01 and 0.03 mg/kg) or produce a place aversion in controls. However, eticlopride, a D2/D3 dopamine receptor antagonist, only blocked the conditioned increase in place preference at a dose (0.3 mg/kg) that impaired object interaction. In contrast, neither SCH-23390 nor eticlopride blocked preference for the novel object in an object recognition task at doses that did not interfere with object interaction. These experiments provide further evidence that the neural processes controlling learned associations between novel stimuli and the environment overlap with drugs of abuse.

Animals↗
PubMed1999

Examination of factors mediating the transition to behaviorally correlated nucleus accumbens cell firing during cocaine self-administration sessions in rats.

We have previously reported that at the initiation of cocaine self-administration sessions, neurons in the nucleus accumbens (NA) exhibit a spontaneous transition in firing rate from activity unrelated to the reinforced response, to one of four types of patterned discharges (Carelli RM, King VC, Hampson RE, Deadwyler SA. Firing patterns of nucleus accumbens neurons during cocaine self-administration in rats. Brain Res 1993;626:14-22; Carelli RM, Deadwyler SA. Dose-dependent transitions in nucleus accumbens cell firing and behavioral responding during cocaine self-administration sessions in rats. J Pharm Exp Ther 1996;277(1):385 393; Carelli RM, Deadwyler SA. Cellular mechanisms underlying reinforcement-related processing in the nucleus accumbens: electrophysiological studies in behaving animals. Pharmacol Biochem Behav 1997;57:(2)1-10). This transition in NA cell firing is cocaine dose-dependent and is accompanied by a shift from high response rates at the start of the session ('Load-up' behavior) to a lower steady rate of responding thereafter (termed 'Session' phase responding). Two experiments were conducted to examine further factors that may mediate this process. Experiment 1 examined the effects of pre-session, response-independent delivery of cocaine on behavioral/neural transitions. Results revealed an absence of Load-up responding and the immediate onset of NA patterned activity at the start of the session. Experiment 2 examined the involvement of dopamine D1 versus D2 receptors in mediating the corresponding behavioral/neural transitions. Animals were pretreated with either saline, the dopamine D1 receptor antagonist SCH23390 (2.5-20 microg/kg, s.c.), or the dopamine D2 receptor antagonist eticlopride (2.5-20 microg/kg, s.c.) 30 min prior to the cocaine (0.33 mg/inf) self-administration session. SCH23390 significantly increased the number of Load-up responses at 10 and 20 microg/kg and the number of responses following the Load-up phase (i.e. during the Session phase) at 5, 10, and 20 microg/kg. Eticlopride increased the number of Session responses (5, 10, and 20 microg/kg), but did not alter the number of Load-up responses at any dose tested. The transition in NA cell firing corresponded with the shift in behavioral responding and was delayed within the session following SCH23390 but not eticlopride pretreatment. These findings support the notion that cocaine self-administration sessions in rats consists of two distinct behavioral phases that are mediated by different neurophysiological mechanisms operating in the NA.

Analysis of Variance↗
PubMed2000

Prefrontal cortical manipulations alter the effects of intra-ventral striatal dopamine antagonists on fixed-interval performance in the rat.

The nature of the functional relationships between areas of prefrontal cortex and ventral striatum remain undefined. This study was designed to examine functional interactions between activity in two areas of prefrontal cortex, the prelimbic (PL) and agranular insular (AI) areas, and ventral striatal (VS) dopamine (DA) function. Interactions were assessed using a Fixed Interval (FI) schedule of reinforcement shown previously in our laboratory to be modulated by VS DA function. The study compared changes in FI performance following intra-VS DA antagonist injections alone (SCH23390 + eticlopride) to those observed when either saline or saline + lidocaine were injected into prefrontal cortex after the intra-VS DA antagonist injections. The intra-VS DA antagonists alone decreased FI response rates and increased postreinforcement pause times at both dose combinations (1/0.1 and 3/0.3 microg of SCH23390/eticlopride per side). Neither saline nor saline + lidocaine injected into the PL area of prefrontal cortex altered the effects of intra-VS DA antagonists on FI performance. Saline administration into the AI area of prefrontal cortex, however, eliminated the FI rate-decreasing effects of intra-VS DA antagonists. The agent or mechanism of this effect, whether it be saline, the act of inserting the cannulae into the cortical tissue, or the act of injecting fluid into this tissue, is not clear. This effect of AI saline was prevented by coadministration of lidocaine with saline into AI. These results, coupled with those from a previous experiment examining lesion effects in PL and AI on FI performance (Evans SB, Cory-Slechta DA. The effects of temporary lesions of the insular and medial prefrontal cortex on fixed-interval schedule-controlled behavior in the rat, Soc Neurosci Abstr 1996;22(1):159) suggest that PL might exert a tonic influence on VS DA function, since FI response rates gradually increase over a 2-week period following lesions of PL. In contrast, AI, although not normally modulating FI performance, can apparently influence VS DA function, possibly when alterations in activity are invoked in AI.

Animals↗
PubMed1998

Transformation of monomorphic Trypanosoma brucei bloodstream form trypomastigotes into procyclic forms at 37 degrees C by removing glucose from the culture medium.

African trypanosomes have been shown previously to undergo efficient transformation from bloodstream forms to procyclic (insect dwelling) forms in vitro by adding citrate and/or cis-aconitate to the culture medium and lowering incubation temperature to 27 degrees C. In this paper, it is shown that strain 427 monomorphic bloodstream forms of Trypanosoma brucei grown in axenic culture at 37 degrees C can be transformed to procyclic forms by simply replacing the glucose carbon source in the culture medium with glycerol. The removal of glucose from the medium results in the loss of the variant surface glycoprotein, the acquisition of cell surface procyclic acidic repetitive protein, the synthesis of procyclic-specific glycosylphosphatidylinositol precursors and the acquisition of substantial resistance to salicyl hydroxamic acid and glycerol within 72 h. A procyclic-specific cytoskeletal protein, known to be a marker of the late stage of transformation, is fully expressed by 96 h but full trans-sialidase activity appears only after 18-30 days. The transformation process described here is slower and less efficient than that previously described for monomorphic trypanosomes, using citrate and/or cis-aconitate and temperature shift as triggers. However, the separation of the transformation process from these stimuli is significant and the effects of glucose deprivation described here may reflect some of the events that occur in vivo in the tsetse fly midgut, where glucose levels are known to be very low.

Animals↗
PubMed2000

Comparison of HOCl traps with myeloperoxidase inhibitors in prevention of low density lipoprotein oxidation.

In this study, the production of the highly toxic oxidant hypochlorous acid (HOCl) by the phagocytic enzyme myeloperoxidase (MPO) was quantitated and the concomitant alterations of low density lipoprotein (LDL) were analyzed in view of the potential role of LDL in atherosclerosis. Using the monochlorodimedone assay, it was found that HOCl is produced in micromolar concentrations. The kinetics of the decrease of tryptophan fluorescence appeared to be a sensitive method to monitor LDL alterations under near in vivo conditions. Therefore, this method was used to subsequently compare the effectiveness of MPO inhibitors that block production of HOCl with compounds that act as HOCl traps. The efficiency of MPO inhibitors to prevent LDL damage increased in the series benzohydroxamic acid < salicylhydroxamic acid < 3-amino-1,2,4-triazole < sodium azide < potassium cyanide < p-hydroxy-benzoic acid hydrazide, while for the HOCl traps the protective efficiency increased in the series glycine < taurine < methionine. We conclude that HOCl traps may have high potential therapeutic impact in vivo due to their low toxicity, although high concentrations of them would have to reach sites of inflammation. In contrast, only low concentrations of a specific MPO inhibitor would be required to irreversibly inhibit the enzyme.

Arteriosclerosis↗
PubMed1998

The effect of acute kainic acid treatment on dopamine D2 receptors in rat brain.

Acute exposure to kainic acid (KA) induces neurochemical changes in dopaminergic systems in the brain and the aim of the present study was to investigate the acute toxicity of KA upon dopamine D2 receptors. Adult rats were injected intraperitoneally with either saline or 16 mg/kg KA. Brains were removed after 4 h. Membrane homogenates were prepared from seven brain regions and in addition, frozen coronal sections were sectioned for comparative quantitative autoradiographic analysis. Dopamine D2 receptors were characterised by saturation studies using [125I]iodosulpiride, [3H]raclopride and [3H]spiperone. KA produced a 2-fold decrease in receptor affinity for [125I]iodosulpiride and a 2-fold increase in receptor density in all regions studied except striatum. Quantitative autoradiography with [125I]iodosulpiride showed similar increases in D2 labelling following KA except in caudate putamen, nucleus accumbens and olfactory tubercle. In contrast, there was no change in [3H]spiperone binding in whole brain minus striatum nor in striatum alone after KA treatment. KA produced a significant increase in Bmax for [3H]raclopride in whole brain minus striatum and in striatum alone with minimal changes in affinity. These findings demonstrate acute changes in rat brain dopamine D2 receptors labelled with [125I]iodosulpiride and [3H]raclopride but not [3H]spiperone after KA treatment predominantly in extra striatal regions.

Animals↗