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H van Riezen

Publications and source records attributed to H van Riezen.

At least 19 recordsLinked to original sources
PubMed1992

The time course of sigma activity and slow-wave activity during NREMS in cortical and thalamic EEG of the cat during baseline and after 12 hours of wakefulness.

The extrapolation from recent neurophysiological findings concerning the dependency of spindle and slow-wave oscillations of thalamocortical neurons on membrane potential to macroscopic EEG events, predicts a reciprocal relation between spindle activity and slow-wave activity (SWA) in thalamic and cortical EEG during non-rapid-eye-movement sleep (NREMS). To test this hypothesis, the EEG recorded in 8 cats, from the nucleus centralis lateralis of the thalamus and from the skull during a 12-h baseline dark period and during a 12-h recovery dark period, following a 12-h sleep deprivation, were analyzed. Per 12-s epoch, sleep-wake behaviour was determined and spectral power density was computed in the slow-wave frequency range (0.5-4.0 Hz) and in the spindle frequency region (sigma activity: 11.0-14.5 Hz). To analyze the development of EEG power densities in the course of NREMS and during the transition from NREMS to REMS, the last epoch of wakefulness and the first 15 epochs of NREMS, as well as the last epochs of NREMS and the first epoch of REMS were selected from the NREM-REM cycles. For each animal the values were averaged over 4-h intervals. In the cortical EEG, SWA was minimal at NREMS onset and increased progressively in the course of NREMS. SWA declined sharply prior to REMS. sigma Activity increased gradually towards a uniform level after NREMS onset. During the transition to REMS, sigma activity initially increased and then decreased rapidly. In the thalamic EEG, the time course of SWA paralleled that of the cortex. However, the development of sigma activity during the first part of NREMS differed: in the thalamic EEG, sigma activity was maximal during the beginning of NREMS and slightly decreased thereafter. After sleep deprivation, SWA within NREMS was markedly enhanced in both the cortical and the thalamic EEG. Sigma activity was attenuated in the thalamic EEG, whereas in the cortical EEG it was temporarily elevated. The present data show that, in the thalamic EEG, an inverse relation exists between spindle and slow-wave activity during baseline NREMS. This relation is preserved after sleep deprivation. In the cortical EEG, a reciprocal relation between spindling and SWA is less evident.

Animals↗
PubMed1992

Enhanced slow-wave activity within NREM sleep in the cortical and subcortical EEG of the cat after sleep deprivation.

Electroencephalograms (EEGs) of the cortex and of seven subcortical structures were recorded during two baseline days and during a recovery day following a 12-hour period of sleep deprivation (SD) in eight cats. The EEGs were analyzed by visual scoring and by spectral analysis. The following subcortical structures were studied: hippocampus, amygdala, hypothalamus, nucleus centralis lateralis of the thalamus, septum, nucleus caudatus and substantia nigra. The EEGs of all brain structures exhibited sleep state-dependent changes. In general, slow-wave activity (SWA, 0.5-4.0 Hz) during nonrapid eye movement (NREM) sleep exceeded that of REM sleep. The power spectra (0.5-24.5 Hz) in NREM, as well as the relationship between the power spectra of NREM and REM sleep, differed between the recording sites. Moreover, the rate of increase of SWA in the course of an NREM episode and the rate of decrease of SWA at the transition from NREM to REM sleep differed between the brain structures. During the first 12 hours following SD, the duration of NREM increased due to a prolongation of the NREM episodes. REM increased by a rise in the number of REM episodes. During the same period, the NREM EEG power density in the delta and theta frequencies was enhanced in all brain structures. Furthermore, in all structures the enhancement of SWA was most pronounced at the beginning of the recovery period and gradually declined thereafter. SD also induced a rise in the rate of increase of SWA in the NREM episodes in all recording sites. This indicates that the enhancement of EEG power density was not only due to prolongation of the NREM episodes. The EEG activity during REM was barely affected by the SD. It is concluded that, in all brain structures studied, the EEG during NREM is characterized by high levels of SWA. Furthermore, in each brain structure, SWA within NREM sleep is enhanced after a prolonged vigil. These data may indicate that SWA reflects a recovery process in cortical and subcortical structures.

Animals↗
PubMed1991

Effects of circadian phase and duration of sleep deprivation on sleep and EEG power spectra in the cat.

The electroencephalogram (EEG) of cats was recorded under baseline conditions (LD 12:12) and after 4 and 8 h of sleep deprivation (SD). The EEG was analyzed by visual scoring and by spectral analysis. Under baseline conditions the 24-h distribution of sleep was bimodal: the smallest amounts of sleep occurred at the light-dark and dark-light transitions. EEG slow-wave activity (power density in the delta frequency range: 0.5-4.0 Hz) in non-rapid-eye-movement sleep (NREMS) showed a small variation over the 24-h period. When recovery sleep, following 4 h and 8 h of SD, started at the beginning of the dark period, no significant rebound of NREMS and REMS occurred during the 24-h recovery period. When recovery sleep, after 4 h of SD, started at the fifth hour of the light period, the amount of NREMS was increased. In all experiments the EEG power density in NREMS was enhanced after SD in the entire frequency range studied (0.5-31.5 Hz), but more prominently in the delta and theta (4.5-7.0 Hz) frequency bands. The effects dissipated in the course of the recovery period. The magnitude and duration of the enhancements of EEG power densities were dependent on the duration of SD and on the circadian phase at which SD was scheduled. It is concluded that in the cat sleep is a function of both circadian and homeostatic processes and that especially the EEG power density in NREMS is highly responsive to sleep loss.

Analysis of Variance↗
PubMed1990

The competitive NMDA receptor antagonists CGP 37849 and CGP 39551 are potent, orally-active anticonvulsants in rodents.

Anticonvulsant properties of CGP 37849 and CGP 39551, two novel phosphono-amino acids which are competitive NMDA receptor antagonists, were examined in rodents. At optimal pretreatment times CGP 37849 suppressed electroshock-induced seizures in mice and rats with ED50s ranging from 8 to 22 mg/kg after oral administration, and 0.4 to 2.4 mg/kg after i.v. and i.p. injection. Relative to CGP 37849, CGP 39551 was more potent after p.o. (ED50 3.7-8.1 mg/kg), and less potent after i.v. or i.p. treatment (ED50 2.7-8.7 mg/kg). Following oral treatment, the duration of action of CGP 37849 was about 8 h, while CGP 39551 still showed good activity after 24 h (ED50 8.7 mg/kg, mouse; 21 mg/kg, rat). Both compounds were anticonvulsant at doses below those at which overt behavioural side effects were apparent. CGP 39551 delayed the development of kindling in rats at doses of 10 mg/kg p.o. and above, and showed weak anticonvulsant activity against pentylenetetrazol-evoked seizures. CGP 37849 and CGP 39551 are the first competitive NMDA antagonists to show oral anti-convulsant properties in a therapeutically-useful dose-range, and hence are interesting candidates for novel antiepileptic therapy in man.

2-Amino-5-phosphonovalerate↗
PubMed1990

Effects of psychotropic drugs on the behavior and neurochemistry of olfactory bulbectomized rats.

Since its first characterization as a model for the detection of antidepressant drugs (van Riezen et al., 1976) a large body of data now supports the view that olfactory bulbectomy produces changes in animal behavior that are reversed by chronic treatment with antidepressants. The behavioral deficits seen in olfactory bulbectomized rats (such as irritability, deficits in acquisition of avoidance and of appetitive motivated conditioning and hyperactivity in a new environment) are probably the results of a reduced ability to adapt to environmental changes. These behavioral changes, their biochemical consequences and the effects of treatments with psychotropic drugs are reviewed. These studies suggest that the olfactory bulbectomized rat is a model of depression useful to detect antidepressant drugs.

Animals↗
PubMed1988

Enhanced functional responsiveness of the dopaminergic system--the mechanism of anti-immobility effects of antidepressants in the behavioural despair test in the rat.

Imipramine, desipramine, maprotiline and atypical antidepressants such as mianserin, trimipramine and levoprotiline were tested in the behavioural despair test in rats. After chronic treatment (twice daily for 7 days), all the drugs, including trimipramine and levoprotiline, significantly reduced the immobility of rats subjected to forced swimming. Of particular interest are the findings with levoprotiline, which in contrast to other antidepressant drugs did not exert any direct or indirect influence on the metabolism of catecholamines and does not seem to interact with the known receptor systems, except the H1 receptors. However, antihistaminics, such as mepyramine and promethazine (5 and 10 mg/kg i.p.) reduced immobility after single doses but were, in contrast to levoprotiline, inactive after chronic treatment. The anti-immobility effect of levoprotiline, as reported for other antidepressants, appears to be related to enhanced dopaminergic function, since it was antagonised by haloperidol and sulpiride, but not by prazosin. The findings of this study therefore support the assumption that dopaminergic activation is critically involved in the anti-immobility effects of antidepressants. Further, the findings support the predictive value of the test since antidepressant properties of levoprotiline have been observed clinically.

Animals↗
PubMed1984

Response changes after repeated low apomorphine: dopamine autoreceptor desensitization or learning?

Repeated injection of rats with low doses of apomorphine (APO), which selectively interact with dopamine (DA) autoreceptors, caused a change in yawning responses that suggests initial low-APO-induced desensitization of DA autoreceptors, followed by a long-lasting rebound hypersensitivity. Repeated treatment with low APO followed by open-field testing, however, yielded totally different results. APO accelerated intrasession response decrement and upon repeated administration enhanced the intersession response decrement. Both for yawning and open-field behavior, the response change after the second dose of APO was only evident when the first as well as the second APO injection were followed by exposure of the rat to the same test situation. These results indicate that response changes after repeated treatment with low APO are not due to a simple DA-agonist-induced change in receptor sensitivity but that drug experience combined with environmental influences play a decisive role.

Animals↗
PubMed1981

[Effects of synthetic neuropeptides in psycho-organic brain syndrome. Results with ACTH4-10 and ACTH4-9-analog (author's transl)].

The effects of ACTH4-10 (Org O163) and of the ACTH4-9 analog (Org 2766) were tested in 20 male patients suffering from a mild to moderate cerebroorganic impairment. Patients were aged between 51-72 years (mean 60.9). Org 2766 was given in dosages of 0.05 mg, 0.5 mg and 5 mg, Org O163 in a dosage of 30 mg. The investigation was based on a randomized incomplete crossover design. By means of psychological tests the effects of the synthetic neuropeptides on memory, state of well-being, attention, vigilance and psychomotor function were investigated. The statistical analysis of the results did not reveal any effects of both substances on the functions tested. These results are in agreement with those of other studies in man using similar methods and acute administration of ACTH4-10 and/or Org 2766. In such studies only effects of reactive inhibition of attention and motivation could be demonstrated consistently.

Adrenocorticotropic Hormone↗
PubMed1978

[Possible consequence of ACTH-like peptides for human mental performance (author's transl)].

ACTH affects behavior of rats. The results of the reported experiments suggest that ACTH effects on conditioned behavior are the result of an improved motivation or attention. The ACTH fragments, ACTH 4--10 and ACTH 4--9, have the behavioral effects of ACTH but are devoid of endocrine activities. The ACTH 4--9 analog H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) has behavioral activity after oral administration. ACTH-like-peptides restore the behavioral deficiencies of hypophysectomised rats and delay extinction of conditioned behavior of normal rats independent of the type of conditioning. So is extinction of pole jump avoidance and extinction of conditioned tast aversion delayed after Org 2766. Moreover ACTH-like peptides reduce the behavioral deficit in rats with amnesia even when the treatment is given two weeks after the induction of amnesia. In man the administration of a single dose of ACTH 4--10 on Org 2766 reduces the duration of lapses as well as the number of errors of volunteers in a continuous performance task. These and similar observations suggest that ACTH-like peptides may be of practical consequence for the therapy of patients with impairments of cognitive processes.

Adrenocorticotropic Hormone↗
PubMed1977

A new animal model for the prediction of antidepressant activity.

Animal models presently in use for the screening of potential antidepressant drugs yield numerous false positives and false negatives. In search of a more specific model, we have studied the effects of psychotropic compounds on the behavioural changes induced in rats by the removal of the olfactory bulbs. We have observed that subchronic treatment with antidepressants in general reverses the behavioural alterations displayed by bulbectomized rats in tests of conditioned behaviour. The present paper describes a brief test, the so-called anxiosoif test, which may be used to assess the effects of drugs on the behaviour of bulbectomized rats. Removal of the olfactory bulbs leads to increased water intake in the anxiosoif test and to an attenuation of avoidance when the drinking spout is electrified. This latter effect can be reversed by subchronic treatment with the antidepressant drugs amitriptyline and mianserine (Org GB 94). It is suggested that the behavior of bulbectomized rats may be used as a specific tool in the prediction of antidepressant activity of novel compounds.

Animals↗
PubMed1977

Olfactory bulb ablation in the rat: behavioural changes and their reversal by antidepressant drugs.

1. The effects of bilateral olfactory bulbectomy, sham-operation and inducement of peripheral anosmia were studied on locomotor activity, passive avoidance acquisition and irritability. 2. Bulbectomized rats were hyperactive, deficient at learning a step-down passive avoidance response and hyperirritable. Peripheral anosmia, induced by intranasal infusion of ZnSO4 solution resulted in no behavioural changes. 3. Chronic pretreatment with amitriptyline (3 and 10 mg/kg) and a tetracyclic antidepressant mianserin (Org GB 94, 5 and 15 mg/kg) reversed the hyperactivity and reduced the learning deficit of bulbectomized rats. These drugs had no significant effects on sham-operated animals. 4. Neither amitriptyline nor mianserin reduced the exaggerated responses of bulbectomized rats to external stimuli. 5. (+)-Amphetamine (1 and 3 mg/kg) accelerated the acquisition of the passive avoidance response, greatly enhanced the locomotor activity and slightly increased the irritability score of both sham-operated and bulbectomized rats. 6. Chlorpromazine (1 and 3 mg/kg) and chlordiazepoxide (10 mg/kg) significantly reduced the acquisition, locomotor activity and irritability of experimental and control rats. 7. Lithium sulphate (1 and 3 mg/kg) had no effect on activity or irritability but produced a small impairment in acquistion of bulbectomized rats. 8. It is concluded that the reversal by antidepressant drugs of the behavioural syndrome seen after olfactory bulb ablation could constitute a new model for the detection of this group of centrally acting compounds.

Animals↗
PubMed1977

Changes in muscle action potentials of patients with diseases of motor units following the infusion of a peptide fragment of ACTH.

The polypeptides ACTH and ATCH4-10 (OI 63) witha sequence of amino acids H-Met-Glu-His-Phe-Arg-Trp-Gly-OH, have similar stimulating effects on motor units in lower mammals. Their actions differ primarily in that ACTH4-10 is not corticotropic. Since the corticotropic action of ACTH frequently presents a problem during its clinical use in treatment of motor unit diseases, the action of ACTH4-10 was studied in two patients with muscular atrophy. Prior to administration of ACTH4-10, stimulation of M. oppenens pollicis through the median nerve evoked muscle action potentials in both patients which progressively declined in amplitude. This decline was not observed subsequent to the infuscion of ACTH4-10 (3, 6 and 15 mg). The effect lasted partially in excess of at least 2 h. It is suggested that ACTH4-10 produces this effect by direct action on a peripheral component of the motor unit and/or indirectly by an action on the central nervous system.

Action Potentials↗
PubMed1975

Enhancement of attention in man with ACTH/MSH 4-10.

Normal men were infused for 4 hr with ACTH/MSH 4-10 or a control solution. Behavioral testing after the infusion indicated that subjects who received ACTH/MSH 4-10 were less anxious and had better visual memory than control subjects but the predominant effect of the heptapeptide was to increase visual attention. It was speculated that ACTH/MSH 4-10 may be uniquely coded for attentional functioning.

Adrenocorticotropic Hormone↗