PubMed Health⌕ Search

Biomedical subjects

J M van Ree

Publications and source records attributed to J M van Ree.

189 records · Page 11Linked to original sources
PubMedDate not supplied

Behavioral effects of the beta-endorphin fragment 2-9.

The non-opiate beta-endorphin (beta E) fragment des-Tyr-alpha-endorphin (beta E 2-16) delays extinction of pole jumping avoidance behavior and potentiates apomorphine-induced stereotyped sniffing. Structure-activity relationship studies revealed that the active moiety mediating these psychostimulant effects resides in the sequence beta E 2-9. The interaction between beta E 2-9 and apomorphine was also present following intrastriatal injection of both substances. These data provide evidence for a selective interference of the fragment beta E 2-9 with brain mechanisms, which can be distinguished from the opiate- and neuroleptic-like activity of beta-endorphin fragments. This further demonstrates the importance of beta-endorphin and its fragments for modulation of behavioral processes.

Animals↗
PubMedDate not supplied

des-Tyr1-gamma-endorphin and haloperidol increase pineal gland melatonin levels in rats.

The effect of subcutaneously injected DT gamma E (beta-endorphin, (beta E)2-17) on the pineal melatonin level was compared with that of closely related peptides and the neuroleptic drug haloperidol. As found previously, DT gamma E (3 ng/rat and 300 ng/rat) increased the melatonin levels. Similar doses of DT alpha E (beta E 2-16), DT beta E (beta E 2-31), gamma E (beta E 1-17), alpha E (beta E 1-16) and beta E failed to significantly change the melatonin levels in both the dark and the light phase. Haloperidol in a dose of 300 ng/rat exhibited a similar effect as DT gamma E.

Animals↗
PubMedDate not supplied

Behavioral support for an ACTH receptor in the CNS.

In this report we present a series of experiments which have led us to support the notion of the presence of an ACTH receptor in the CNS. A short intense heat-stress (hot-plate) applied to the paws of rats will temporarily reduce activity. During the course of experimentation we were able to eliminate a number of logical mediators. Neither adrenalectomy, adrenal-medullectomy, naloxone administration, nor alpha-MSH-(1-12) were able to affect the observed akinesia. Hypophysectomy, however, was able to abolish or mask the behavior and the reduction in activity could be reinstated by the administration of ACTH-(4-10) to hypophysectomised rats. These data support the notion that a short intense stressor can release ACTH and that this ACTH can be responsible for mediating the short term reduction in activity. In addition, the fact that ACTH-(4-10) has only minimal steroidogenic properties and was able to reinstate the behavior led us to speculate that these effects were of central origin. Furthermore, since naloxone was not capable of altering the behavior, the suggestion is that ACTH in this paradigm acted at a receptor site apart from the naloxone sensitive receptor. This site may in fact be an ACTH specific receptor.

Adrenal Medulla↗
PubMedDate not supplied

Central target for the behavioural effects of vasopressin neuropeptides.

The neurohypophysial hormone vasopressin exerts antidiuretic, vasopressor and behavioural effects (for example, facilitation of memory processes). Vasopressin may alter animal behaviour via direct effect on brain processes. Recently, however, it has been suggested that vasopressin acts mainly at peripheral receptor systems and influences behavioural mechanisms by altering visceral afferent signals. We now present data showing that (1) central administration of [Arg8]vasopressin (AVP) and more potently [pGlu, Cyt]AVP(4-8), the desglycinamide derivative of a peptide generated from AVP by brain synaptic membranes, produce the behavioural effect (promotion of passive avoidance behaviour) without the pressor effect; (2) central administration of a vasopressor antagonist blocks the behavioural but not the pressor effect of systemically administered AVP; and (3) [pGlu, Cyt]AVP(4-8) induces the behavioural effect in the absence of the pressor effect. The results indicate that AVP and related peptides affect passive avoidance behaviour by a direct central action and that the structural requirement for activation of central vasopressin receptors differs from that of the peripheral cardiovascular receptors, although both can be blocked by the same vasopressor antagonist.

Animals↗
PubMedDate not supplied

Recognition cue in the rat's social memory paradigm.

The cue used by an adult resident rat for recognition of a just met juvenile in the social memory paradigm was assessed by manipulating the amount of olfactory information and enhancing the recognition with arginine8-vasopressin (AVP). Social recognition was impaired in anosmic resident rats, suggesting that the recognition cue is olfactory in nature. Washed juveniles were recognized by AVP but not placebo treated residents, independently of whether after washing they were marked with previously collected urine of the residents or not. Preputialectomized juveniles were recognized neither by placebo nor by AVP treated residents. The results suggest that the scents originating from the preputial gland of the juvenile serve as the recognition cue in the social memory paradigm of rats.

Animals↗
PubMedDate not supplied

Social play in juvenile rats after in utero exposure to morphine.

Changes in analgesia, play behavior, sexual behavior and responsiveness to stress and stimulants have been reported in rodents treated in utero with opiates. During development the endogenous opioids and opioid receptors are present in a tonic balance in the mammalian nervous system. The development of this balance is particularly sensitive to prenatal administration of opioid agonists and antagonists. The motivational and rewarding aspects of play behavior are probably controlled by endogenous opioid systems; low doses of opioids stimulate play behavior, whereas administration of opioid antagonists attenuates play behavior. We have analyzed the effect of morphine administration during the prenatal development of endogenous opioid systems on play behavior in juvenile rats. The doses of morphine used neither affected gestation of pregnant mother rats nor sensorimotor development of the juvenile rats. Levels of social play were elevated in juvenile rats after prenatal exposure to morphine. Social behaviors not related to play and non-social activities were not affected by the prenatal treatment procedure. To study these changes in more detail, social play was investigated using a sequential analysis in prenatally morphine-and saline-exposed pairs. The sequential structure of behavior was not altered by the in utero exposure to morphine. Quantitatively, increases in behavioral transitions were found between behaviors related to play. The prenatal morphine treatment did not affect transitions between behaviors not related to play. It is concluded that the prenatal exposure to morphine did not affect mechanisms underlying play behavior itself, but is probably affecting more general phenomena like reward or motivation to play.

Animals↗