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Biomedical subjects

J M van Ree

Publications and source records attributed to J M van Ree.

At least 91 records · Page 5Linked to original sources
PubMed1990

Chronic pretreatment with naltrexone facilitates acquisition of intravenous cocaine self-administration in rats.

Opioid systems may be involved in the reinforcing effects of drugs of abuse. It has been shown that the opioid antagonist naltrexone attenuates acquisition of intravenous cocaine self-administration behaviour in rats. Using a similar experimental set-up the effect of chronic blockade of opioid systems prior to cocaine exposure was examined. Rats were tested for acquisition of self-administration of one of 3 graded unit doses of cocaine (0.08, 0.16 and 0.32 mg.kg-1 per infusion) or saline. Chronic pretreatment with naltrexone (10 mg.kg-1 per day for 12 days) enhanced acquisition of intravenous cocaine self-administration but only in rats tested with the medium cocaine unit dose. It is concluded that chronic blockade of opioid systems facilitates acquisition of cocaine self-administration, probably by enhancing the reinforcing effect of cocaine.

Animals↗
PubMed1990

Alpha-methyldopa induces a naltrexone-insensitive antinociception and hypomotility in rats.

1. This study served to investigate whether endogenous opioid peptides play a role in the putative antinociceptive and the sedative actions of alpha-methyldopa. 2. In conscious normotensive rats, alpha-methyldopa induced hypotension, starting around 1 h and reaching a maximum 3-4 h after administration. Pretreatment with naltrexone resulted in an inhibition of alpha-methyldopa-induced hypotension. 3. alpha-Methyldopa dose-dependently increased hot plate latency which became evident after a 4 h lag period and reaching a maximum effect at 6 h. The antinociceptive effect of alpha-methyldopa was not affected by naltrexone. 4. In a small open field, alpha-methyldopa dose-dependently suppressed locomotion and sniffing behaviour. These effects of alpha-methyldopa were apparent 1 h after administration and were naltrexone-insensitive. 5. No changes in the level of beta-endorphin-like immunoreactivity in plasma and cerebrospinal fluid were observed after administration of alpha-methyldopa. 6. The results indicate that endogenous opioid peptides are involved in the hypotensive action of alpha-methyldopa but not in alpha-methyldopa-induced hypomotility and antinociception.

Analgesics↗
PubMed1990

A single injection of a biodegradable microsphere formulation of the ACTH-(4-9) analogue ORG 2766 accelerates functional recovery after brain damage.

The functional recovery from impaired motor activity induced by 6-hydroxydopamine lesions in rat nucleus accumbens was accelerated by subcutaneous treatment with the ACTH-(4-9) analogue Met/O2/-Glu-His-Phe-D-Lys-Phe (ORG 2766). Treatment was effective after daily injections of ORG 2766 dissolved in saline during the first 6 days following the lesion (ED50: 28.5 ng kg-1 day-1) or after a single injection of the peptide in a biodegradable microsphere formulation administered after the lesion (ED50: 8.9 ng kg-1 day-1). This study shows that a single injection of a microsphere preparation can replace multiple injections with ORG 2766 in order to facilitate functional recovery after brain damage.

Adrenocorticotropic Hormone↗
PubMed1989

Neuropeptides: animal behaviour and human psychopathology.

Animal studies have demonstrated that neuropeptides modulate nervous system functions. It has been postulated that disturbances in neuropeptide systems may be aetiological factors in psychiatric and neurological disorders. Neuropeptides related to ACTH/MSH, including ORG 2766, increase motivation and attention and facilitate recovery processes after nerve damage. These peptides may be effective during the early stage of dementia. Vasopressin and related peptides improve memory processes in animals and humans. In addition, these peptides influence social behaviour, mood and addictive behaviour. The non-opioid gamma-type endorphins have neuroleptic-like activities in animals and antipsychotic effects in a category of schizophrenic patients. Peptides related to CCK have also been found to be effective in these patients. Some neuropeptides, e.g. TRH and PLG, have been reported to exert antidepressant effects. Further research may eventually produce neuropeptides with therapeutic action in psychiatric and neurological diseases.

Aging↗
PubMed1989

Infusion of gamma 2-MSH produce a conditioned taste aversion in morphine-dependent rats.

A two flavour, unbiased, taste preference conditioning procedure was used to test for possible motivating effects of gamma 2-MSH. Three training trials failed to produce any significant effect with doses ranging from 2.4 to 40 micrograms/ICV infusion in drug-naive, non-operated or placebo-implanted rats. However, in rats made dependent by SC implantation of a morphine pellet 4 days earlier 15 micrograms gamma 2-MSH/infusion produced a taste aversion that was comparable to that produced by infusion of a low dose of the competitive opioid receptor antagonist naloxone (0.32 micrograms). The findings confirm with a conditioning procedure and with opiate-dependent animals the naloxone-like effects of gamma 2-MSH. They also suggest that this endogenously-located peptide may acquire an aversive property as a result of chronic morphine treatment.

Animals↗
PubMed1989

Behavioral and neurotrophic activity of ACTH-(7-16)NH2.

The behavioral and neurotrophic effects of ACTH-(7-16)NH2 were assessed in a number of tests in which other ACTH fragments are active. Subcutaneous injection of ACTH-(7-16)NH2 increased motor activity of group-housed rats tested under low light intensity and induced hypokinesia in rats subjected to the mild stress of a nonfunctional "hot" plate. In rats with 6-OHDA lesions in the nucleus accumbens daily subcutaneous treatment with ACTH-(7-16)NH2 during the first week following the lesions reversed the lesion-induced motor hypoactivity. The ED50's for the effects of ACTH-(7-16)NH2 on the environmentally induced changes in motor activity, the stress-induced hypokinesia and the impaired motor activity of 6-OHDA lesioned rats were approximately 8 micrograms/kg. 6.3 micrograms/kg and 0.45 micrograms/kg respectively. It is concluded that ACTH-(7-16)NH2 may mimic the effect of an ACTH-like peptide in the brain involved in brain processes triggered by changes in the environment and by brain damage.

Adrenocorticotropic Hormone↗
PubMed1988

Dopamine release in the nucleus accumbens of freely moving rats determined by on-line dialysis: effects of apomorphine and the neuroleptic-like peptide desenkephalin-gamma-endorphin.

This study examined the effects of apomorphine, sulpiride, desenkephalin-gamma-endorphin (DE gamma E) and a combination of DE gamma E with apomorphine on the release of dopamine (DA) and its main metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the nucleus accumbens of freely moving rats. A fully automated on-line brain dialysis system was used. A small dose of s.c. administered apomorphine induced a decrease in the output of DA and DOPAC. Sulpiride, infused into the nucleus accumbens, induced a 2-fold increase in the output of DA, DOPAC and HVA. DE gamma E hardly modified either the basal release of DA, DOPAC and HVA or the apomorphine-induced attenuation of the release of DA and DOPAC. These results indicate a dissociation between the behavioural effects of DE gamma E and its effect on the release of DA in vivo.

Animals↗
PubMed1988

Scheduled eating increases dopamine release in the nucleus accumbens of food-deprived rats as assessed with on-line brain dialysis.

This study examined the effect of scheduled eating on the in vivo release of dopamine (DA) in the nucleus accumbens of rats that were maintained on a food deprivation schedule. DA release was measured by means of a fully automated on-line brain dialysis system. The initiation of eating increased the release of DA, which remained elevated during the entire eating period. Termination of eating caused a gradual decrease of the release of DA to basal values. Increased motor activities did not change the release of DA. These results indicate a link between eating and DA release and demonstrate the suitability of on-line brain dialysis for behavioural experiments.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Effects of desglycinamide9, (Arg8) vasopressin and vasopressin antiserum on the acquisition of intravenous cocaine self-administration in the rat.

The effect of the vasopressin neuropeptide desglycinamide9, (Arg8) vasopressin (DGAVP) on the acquisition of intravenous cocaine self-administration was studied. Rats were tested under conditions of reduced body weight in a continuous reinforcement operant procedure, during five daily 3 h sessions. Under these conditions, the rate of self-administration obtained with 0.125 and 0.25, but not 0.063 mg.ml-1 cocaine, exceeded the rate obtained with saline. Daily pretreatment with DGAVP (5 micrograms/rat, s.c.) decreased self-administration of 0.125 and 0.25 mg.ml-1 cocaine to the level obtained with saline, but had no effect on self-administration of 0.063 mg.ml-1 cocaine and saline. Using a similar procedure, it was shown that daily intracerebroventricular pretreatment with vasopressin antiserum significantly increased self-administration of 0.125 mg.ml-1 cocaine, without affecting self-administration of 0.063 and 0.25 mg.ml-1 cocaine and saline. The results support previous findings obtained with vasopressin neuropeptides in drug self-administration studies and suggest that DGAVP decreases the acquisition of cocaine self-administration by attenuating the reinforcing effects of cocaine and that endogenous vasopressin may be involved in the acquisition of cocaine self-administration.

Animals↗
PubMed1988

Vasopressin neuropeptides and acquisition of heroin and cocaine self-administration in rats.

The effect of the vasopressin neuropeptide des-glycinamide (Arg8)-vasopressin (DGAVP) on reducing the acquisition of intravenous heroin self-administration in rats was analyzed. When rats reduced in body weight were allowed to self-administer heroin for 1 h per day in the presence of a fixed time, non contingent food delivery schedule, it appeared that heroin intake was related in an orderly way to the unit dose of heroin delivered. DGAVP decreased heroin intake during days 4 and 5 of acquisition, especially when a high dose of heroin was delivered. DGAVP decreased heroin intake more effectively when rats were tested without the food delivery schedule and for 6 h instead of 1 h sessions per day. Structure activity relationship studies revealed that the peptide (pGlu4, Cyt6)AVP-(4-8) was the shortest active sequence mimicking the effect of DGAVP and that this peptide was somewhat more potent than DGAVP in this respect. The peptide (pGlu4,Cyt6)AVP-(4-9) increased the heroin intake of the rats. DGAVP and (pGlu4,Cyt6)-AVP-(4-8) also decreased cocaine intake of body weight reduced rats given the opportunity to self-administer cocaine intravenously in daily 6 h sessions. It is concluded that vasopressin neuropeptides may decrease the reinforcing efficacy of heroin and cocaine during acquisition of drug self-administration rather than interact with nutritional and environmental factors influencing drug taking behavior.

Animals↗
PubMed1988

The response of apomorphine administered into the accumbens in rats with bilateral lesions of the nucleus accumbens, induced with 6-hydroxydopamine.

Bilateral lesions of the nucleus accumbens, induced with 6-hydroxydopamine, reduced motor activity and produced a 20-35% depletion of the concentrations of dopamine (DA) and its main metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Small doses of apomorphine (1-10 ng), injected into the nucleus accumbens of sham-lesioned rats, decreased motor activity, while larger doses (1-10 micrograms) produced hyperactivity. In rats lesioned with 6-hydroxydopamine, apomorphine caused hyperactivity only, and this apomorphine-induced response was more pronounced than in sham-lesioned rats. Large doses of apomorphine decreased, only in sham-lesioned animals, the levels of DOPAC and HVA. These data suggest that the apomorphine-induced hypomotility is mediated by presynaptically located DA receptor systems in the nucleus accumbens, whereas the apomorphine-induced hypermotility is likely to be mediated by postsynaptically located DA receptor systems.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Catecholamines and endogenous opioids in ventral tegmental self-stimulation reward.

Midbrain dopaminergic pathways and opioid receptor systems have been implicated in the reward experienced in electrical intracranial self-stimulation behavior. In the present experiment, the influence of graded doses of the dopamine antagonist haloperidol and of the agonist cocaine were investigated on electrical self-stimulation reward, elicited by electrodes located in the ventral tegmental area. A threshold method, which is rather insensitive for aspecific motor effects, was applied to determine the reward of self-stimulation. The method allowed to determine simultaneously the rate of lever pressing for self-stimulation. All doses of haloperidol and cocaine were administered with and without the opioid antagonist naloxone, in order to investigate the interaction between dopaminergic and opioid modulation of reward. Haloperidol lowered and cocaine tended to increase the response rate, whereas cocaine but also haloperidol lowered the self-stimulation threshold. The effects appear to be dose-dependent. Naloxone did not interact with the effect of the drugs on threshold and it lowered the response rate, but in the haloperidol-treated rats only. It is concluded that dopamine is involved in the reward of electrical self-stimulation elicited from the ventral tegmental area and that this involvement is independent of endorphin systems, suggesting the existence of separate catecholamine and opioid mechanisms modulating brain reward.

Animals↗
PubMed1987

The neuroleptic-like peptide desenkephalin-gamma-endorphin does not antagonize the dopamine receptor agonist-induced inhibition of the release of [3H]dopamine from rat nucleus accumbens slices in vitro.

In rats, the non-opioid beta-endorphin (beta E) fragment desenkephalin-gamma-endorphin (DE gamma E, beta E6-17) antagonizes the hypomotility induced by a small dose of dopamine (DA) receptor agonists. It has been suggested that DE gamma E might act in this respect by a direct or indirect blockade of presynaptically located DA receptors in the nucleus accumbens, thereby causing an increase of DA release. Therefore in the present study the effect of DE gamma E was examined on DA receptor agonist-induced inhibition of the electrically evoked release of previously accumulated [3H]DA from rat nucleus accumbens slices in vitro. The DA receptor agonists apomorphine, LY 171555 and n,n-di-n-propyl-7-hydroxy-2-aminotetralin (DP-7-AT) inhibited in a concentration-dependent manner the electrically evoked release of [3H]DA. The selective D2 receptor antagonist (-)-sulpiride blocked the effects of apomorphine, corroborating that the DA receptor involved is of a D2 type. DE gamma E was tested at several concentrations (10(-9)-10(-6) M) and under various experimental conditions. DE gamma E, by itself, did not affect either the electrically stimulated or the basal release of [3H]DA. The inhibiting effect of DA receptor agonists was slightly reduced by DE gamma E, but this effect was present in some experiments only. It is concluded that DE gamma E does not function as an antagonist for the DA receptor mediating DA release and that the interaction observed in behavioural experiments between DA agonists and DE gamma E does not occur at the level of this receptor.

Animals↗
PubMed1987

Enhancement of human lymphocyte natural killing function by non-opioid fragments of beta-endorphin.

Opioid peptides have been shown to enhance peripheral blood lymphocyte natural killer (NK) cell function. In this study, we report that certain non-opioid fragments of beta-endorphin (2-16, 2-17, and 6-17) enhance NK activity with peak dose responses seen at 10(-12) to 10(-15) concentrations. This effect can be inhibited by naloxone. We conclude that non-opioid fragments of beta-endorphin are more potent than either beta- or gamma-endorphin in enhancing human lymphocyte NK activity.

Endorphins↗
PubMed1987

The dexamethasone and cortisol suppression test in depression: beta-endorphin as a useful marker.

To investigate the mechanism underlying disturbances in hypothalamopituitary-adrenal (HPA) function in depressed patients, the dexamethasone suppression test (DST) was compared with a cortisol suppression test (CST) and placebo treatment in depressed patients and control subjects. Plasma levels of cortisol, ACTH and beta-endorphin were assessed at 3 times during the day after treatment with a single dose of exogenous steroid. Both dexamethasone and cortisol treatment resulted in suppression of cortisol, ACTH and beta-endorphin in control subjects, while neither treatment had any effect on the hormone levels in those depressed patients who showed cortisol nonsuppression after dexamethasone. In the depressed patients who were cortisol suppressors after dexamethasone, cortisol treatment only slightly changed plasma levels of beta-endorphin, although they were suppressed after dexamethasone treatment. In addition, high levels of both cortisol and beta-endorphin were observed after placebo treatment in all depressed patients compared to control subjects, probably due to the absence of the normally occurring decrease of these hormones during the day in these patients. Cortisol treatment, but not dexamethasone treatment, discriminated depressed patients from controls with respect to their beta-endorphin plasma levels. However, it is not yet clear whether these different effects of the two steroids are related to a different mode of action of these steroids in depressed patients. beta-Endorphin seems to be a useful marker in detecting disturbances in HPA function among depressed patients.

Adrenocorticotropic Hormone↗