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Biomedical subjects

J M van Ree

Publications and source records attributed to J M van Ree.

At least 109 records · Page 6Linked to original sources
PubMed1987

Differential effect of desglycinamide9-(Arg8)-vasopressin on cognitive functions of diabetes insipidus and alcoholic patients.

Intranasal treatment with desglycinamide9-(Arg8)-vasopressin (DGAVP) improved certain aspects of cognitive functions of patients with acquired and congenital diabetes insipidus and of alcoholic patients with mild cognitive impairments. Patients with Korsakoff's syndrome, presenting with severe cognitive impairments, were resistent to DGVP treatment. DGAVP treatment did not affect blood pressure and water metabolism. The action of DGAVP on cognitive functions is probably mediated by centrally located target sites and may be expressed only in patients in whom these target sites are unimpaired.

Administration, Intranasal↗
PubMed1987

Structure activity relationship studies with C-terminal fragments of vasopressin and oxytocin on avoidance behaviors of rats.

The potency of various C-terminal fragments of the neurohypophyseal hormone [Arg8]vasopressin [AVP-(1-9)] was determined using different avoidance behavioral test procedures in rats. Passive avoidance behavior was facilitated by these peptides. The fragments [Cyt6]AVP-(5-8) and [Cyt6]AVP-(5-9) were the most potent peptides tested after postlearning injection (consolidation) and preretention treatment (retrieval), respectively, after s.c. treatment. Comparable results were found when the peptides were injected into the lateral brain ventricle, but after this route of administration the peptides were about 3 to 4 order of magnitude more potent as compared to the s.c. route. Pentylenetetrazol-induced retrograde amnesia was reversed by AVP-(1-9) and various C-terminal fragments. In this respect [Cyt6] AVP-(5-9) and [pGlu4,Cyt6]-AVP-(4-9) appeared to be the most potent peptides. Injection of AVP-(1-9) and various C-terminal fragments after the acquisition of pole-jumping avoidance behavior induced resistance to extinction of the behavior. The fragment [pGlu4,Cyt6]AVP-(4-8) was the most potent peptide for this effect. Passive avoidance behavior was attenuated by s.c. administered oxytocin [OXT-(1-9)] and various C-terminal fragments. [pGlu4,Cyt6]-OXT-(4-9), [pGlu4,Cyt6]OXT-(4-8) and [Cyt6]OXT-(5-8) were the most potent of the peptides tested after postlearning administration, whereas [Cyt6]OXT-(5-9) was the most potent sequence after preretention injection. In all experiments the effects of the peptides were dose-dependent and of a long term nature. The results show that C-terminal fragments of the neurohypophyseal hormones potently modulate various aspects of memory processes, as assessed with different avoidance behaviors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The interaction between gamma-type endorphins and HLA class I antigens.

The clinical response of schizophrenic patients to treatment with gamma-type endorphins was found to be associated with certain HLA class I antigens (Bw22, B15, B13). Moreover, pretreatment of lymphocytes from healthy donors with des-Tyr1-gamma-endorphin (DT gamma E) inhibits the complement-dependent cytotoxicity between alloantisera and those HLA antigens, of which the frequency was increased among schizophrenic patients, who respond well to the gamma-endorphin therapy. Also for the opiate antagonist, naloxon interactions with HLA class I antigens could be demonstrated. Using the inhibition assay with DT gamma E it was possible to detect a subtype of HLA-A2, which, until now, was only defined by cytotoxic T lymphocytes and biochemistry. These data suggest an interaction between the HLA class I antigens and the receptor(s) for DT gamma E and naloxon, which may support the hypothesis that HLA class I antigens play a role in many recognition processes. Their role in immunological recognition would then be only a specialized form of a more general function.

Antigen-Antibody Reactions↗
PubMed1986

Intracerebroventricular injection of anti-prolactin serum suppresses excessive grooming of pituitary homografted rats.

Rats with endogenous hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, displayed increased grooming behavior as compared to that of sham-operated animals. Twelve days after surgery, intracerebroventricular injection of anti-prolactin serum (dilution 1:100, 1 microliter) suppressed the excessive grooming of homografted rats. These observations suggest that prolactin from a peripheral source may reach the central nervous system to affect brain mechanisms involved in grooming behavior.

Adrenocorticotropic Hormone↗
PubMed1986

A comparative study on the antipsychotic properties of desenkephalin-gamma-endorphin and ceruletide in schizophrenic patients.

The neuropeptides desenkephalin-gamma-endorphin (DE gamma E) and ceruletide were administered intramuscularly to patients with schizophrenic psychoses following a double-blind placebo-controlled design, including a total of 44 subjects. Neuroleptic medication was continued during the experimental period, which was started with one placebo injection for all patients. One week later subjects received a single intramuscular injection with 3 mg DE gamma E, 40 micrograms ceruletide or placebo. After an interval of 10 days, the patients received six similar injections over a period of 2 weeks. Treatment with either peptides resulted in a decrease of psychotic symptomatology as compared to placebo treatment. The beneficial effect of the peptides lasted at least 2 weeks after the experimental treatment period. Of the 14 patients treated with placebo only, three showed a slight response. Of the 30 patients treated with the neuropeptides, eight did not respond (DE gamma E: 3; ceruletide: 5), eight had a slight response (DE gamma E: 6; ceruletide: 2) and 14 responded moderately or markedly (DE gamma E: 6; ceruletide: 8). No obvious difference between the effects of the two neuropeptides was found, besides a somewhat earlier onset of the effect of ceruletide. Patients presenting relatively less negative psychotic symptoms were particularly susceptible to treatment with either peptide. Apart from slight and short-lasting gastrointestinal complaints after the first injections with ceruletide in some patients, no side effects were observed.

Adult↗
PubMed1986

Behavioral interaction between endogenous opioids, CCK-8 and dopaminergic systems in the nucleus accumbens of rats.

Injection of apomorphine into the nucleus accumbens of rats elicits hypermotility, presumably by activating postsynaptically located dopamine receptor systems. This behavioral response is inhibited by local treatment with CCK-8 or gamma-endorphin. The action of both peptides is antagonized by intra-accumbal treatment with naloxone. These findings suggest that endogenous opioids are implicated in certain neuroleptic-like effects of CCK-8 and that in the nucleus accumbens a functional interaction exists between CCK-8, endogenous opioids and dopaminergic systems.

Animals↗
PubMed1985

Site of rewarding action of morphine in the mesolimbic system determined by intracranial electrical self-stimulation.

Systemic treatment with morphine has been shown to facilitate intracranial electrical self-stimulation reward elicited from the ventral tegmental area (VTA) as was determined using a response rate-insensitive threshold measurement. In the present experiment graded doses of morphine were microinjected into the mesolimbic system to determine the site of this morphine action. Morphine injected into the nucleus accumbens did not affect the threshold and response rate of self-stimulation by electrodes in the VTA, while relatively high doses of morphine injected into the VTA produced a long-lasting decrease of the threshold of self-stimulation by electrodes in the nucleus accumbens. It is concluded that morphine can facilitate self-stimulation when injected into the VTA, and that a concerted action of morphine on multiple brain sites may be involved in the interaction of the drug with brain reward.

Animals↗
PubMed1985

Beta-endorphin-(10-16) antagonizes behavioral responses elicited by melatonin following injection into the nucleus accumbens of rats.

The behavioral changes induced by low doses of melatonin bilaterally injected into the nucleus accumbens of rats (decrease of locomotor activity and rearing and increase of grooming and sniffing behavior) were not affected by local pretreatment with beta-endorphin, but could be completely antagonized by alpha-type and gamma-type endorphins. Structure activity relationship studies revealed that the peptide beta-endorphin-(10-16) contains the essential information in this respect. The lowest effective dose of this peptide was 10 pg. The peptide, in contrast to gamma-type endorphins, did not interfere with the decrease of locomotor activity and rearing induced by injection of low doses of apomorphine into the nucleus accumbens. It is concluded that the described action of beta-endorphin-(10-16) resembles that of serotonin and various antidepressant drugs.

Animals↗
PubMed1985

Long-term changes in self-stimulation threshold by repeated morphine and naloxone treatment.

To analyse the interaction between endogenous opioid systems and brain reward, the influence of repeated treatment for 3 weeks with morphine and the opioid antagonist naloxone was investigated in rats with self-stimulation electrodes in the ventral tegmental area. Changes in threshold of self-stimulation determined by a response rate insensitive two lever method were considered as changes in reward. Morphine induced a temporary decrease of the response rate which lasted 3 days, and decreased the threshold for self-stimulation. The effect on threshold remained present till morphine treatment was discontinued, indicating that tolerance does not develop to this effect of morphine. Repeated naloxone treatment gradually increased the threshold for self-stimulation. This effect persisted after discontinuation of naloxone treatment. It is concluded that blockade of opioid receptors induces long term changes in the setpoint of self-stimulation reward.

Animals↗
PubMed1985

Beneficial effect of gamma-endorphin-type peptides in anaphylactic shock.

gamma-Endorphin-type peptides (i.e. gamma-endorphin, des-tyr'-gamma-endorphin [DT gamma E]) result from the processing of the opioid peptide, beta-endorphin. Previous studies have implicated the involvement of beta-endorphin in various types of shock, including anaphylactic shock. In the present experiments the intracerebroventricular (i.c.v.) administration of gamma-endorphin (10 micrograms) or DT gamma E (3.3-10 micrograms) significantly improved survival in anaphylactic shock in mice. Moreover, DT gamma E (10 micrograms) reversed the effect of i.c.v. beta-endorphin (3.3 micrograms) to exacerbate shock. A similar dose of DT gamma E was ineffective in antagonizing beta-endorphin-induced analgesia. The anti-anaphylactic action of DT gamma E as well as its effect to block the pro-anaphylactic action of beta-endorphin were prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride. The results suggest that gamma-endorphin-type peptides may act in the central nervous system (CNS) to physiologically oppose the autonomic pathophysiologic influences of beta-endorphin.

Anaphylaxis↗
PubMed1985

[Pain and endorphins].

Various stimuli may evoke the symptom pain. These stimuli activate sensory receptors and this information is transmitted to the spinal cord and a number of cerebral centres. Various endogenous analgesic systems are present in the body, which can modulate and control the consequences of pain stimuli to some extent. Endogenous morphine-like substances (endorphins) are an essential factor in some of these systems. Endorphins may be released in the body during stress or by acupuncture and other pain-relieving procedures (e.g. the twitch in horses). The significance of endorphins is not confined to pain, but they are also involved in reward systems of the brain may therefore play a role in eating, sexual, social and addictive behaviour among others.

Analgesia↗
PubMed1985

Effects of morphine and naloxone on thresholds of ventral tegmental electrical self-stimulation.

The involvement of opioid systems in self-stimulation reward was investigated by studying the effects of the opioid antagonist naloxone (10 mg/kg s.c.) and graded doses of morphine (0.3-5.0 mg/kg s.c.) on intracranial electrical self-stimulation (ICSS) in rats with electrodes in the ventral tegmental area. Lever pressing for ICSS was analyzed using three different procedures: determination of response rate i.e. the number of responses to high and threshold currents, measuring threshold current when response rate was kept low and relatively constant, determination of 'behavioural' threshold using a two-lever procedure in which a response on one lever resulted in a reset of the decreasing current to a high current contingent on a response to the other lever. It was found that low doses of morphine increased the response rate of ICSS behaviour and decreased the threshold whereas the higher doses decreased the response rate but also decreased the threshold current when measured with a rate insensitive procedure. Naloxone raised the threshold for ICSS and caused a corresponding decrease of response rate. In a second series of experiments in which the behaviour of rats which had been tested in one procedure was analysed using one of the other methods, it was observed that naloxone caused smaller changes, while the effects of morphine were at least comparable to those observed in the first series of experiments. The present data suggest that response rate insensitive procedures to analyse ICSS should be preferred to response rate sensitive ones, especially when the interaction of depressant drugs such as morphine with reward mechanisms is investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Disrupting circadian rhythms in rats induces retrograde amnesia.

Disrupting circadian organization in rats by phase-shifting the illumination cycle or by exposure to a reversed day/night cycle or to continuous light, resulted in retrograde amnesia for passive avoidance behavior. This retrograde amnesia induced by phase-shifting lasted at least 2 days, and gradually diminished the longer the rats were exposed to the new illumination cycle. Retention performance was not impaired when rats were exposed to phase-shifting for 3-5 days before the learning trial. The retrograde amnesia due to changing the illumination cycle is probably due to retrieval disturbances. Extinction of active avoidance behavior was facilitated in rats exposed to a phase-shifted illumination cycle, but social and explorative behavior of rats tested in dyadic encounters were not affected by changing the normal illumination cycle. It is concluded that phase-shifting may result in amnesia for newly learned behavioral responses, but not for more innate behavioral patterns.

Amnesia↗
PubMed1985

Differential effect of naloxone on food and self-stimulation rewarded acquisition of a behavioral response pattern.

The involvement of endogenous opioids in self-stimulation reward was investigated by repeated administration of the opioid antagonist naloxone to rats during acquisition of a behavioral response pattern that was rewarded with electrical (self-)stimulation of the ventral tegmental area. A control experiment was performed using food deprived rats in which a comparable response pattern was rewarded with food pellets. The response patterns consisted of gradually decreasing amounts of reward per response, which could be reset to maximal reward by another response. It was found that naloxone disrupted the acquisition of the stimulation rewarded response pattern, while it did not influence the food rewarded behavior. It is suggested that endorphin systems are actively involved in the acquisition of self-stimulation reward procedures, and that this involvement may be specific for self-stimulation reward.

Animals↗
PubMed1985

Endogenous opioids are involved in abnormal stereotyped behaviours of tethered sows.

Tethered sows continuously performed stereotypies during a substantial part of the day time. A single subcutaneous injection with naloxone significantly decreased the profound stereotypies, while explorative behaviours of pigs were not affected by naloxone. In addition a long-term effect of naloxone was noticed. It is suggested that performing the seemingly purposeless stereotypies may function as an effective strategy in order to cope with the conflict-inducing housing conditions. The present data implicate endorphins in this strategy. The involvement of endorphins in the stereotypies of the sows may be related to the calming, rewarding and dependency-inducing effects of the endorphins.

Animals↗
PubMed1985

Behavioral effects of non-opioid fragments of beta-endorphin.

The opioid peptide beta-endorphin (beta E) is converted by brain enzymes to a variety of non-opioid peptide molecules. Several of these peptides specifically affect brain processes in a different manner as assessed in behavioral test procedures. The peptide beta E-(2-9) exhibits behavioral effects resembling psychostimulant drugs in certain aspects and potentiates apomorphine-induced stereotypy following peripheral and intrastriatal treatment. The peptide beta E-(10-16), like serotonin and antidepressant drugs antagonizes the behavioral effects of intra-accumbens injected melatonin. The peptide beta E-(6-17) induces several effects which resemble those of neuroleptic drugs, including an antipsychotic action, and may control the activity of specific dopaminergic systems present in the nucleus accumbens. Thus, non-opioid fragments of beta-endorphin may be involved in the modulation of neurotransmitter systems and consequently in brain homeostasis and possibly in psychopathological syndromes.

Animals↗