Abstract. Vasopressin and oxytocin exert pronounced effects on behaviour by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behaviour, delays extinction of appetitive discrimination tasks, affects approach behaviour to an imprinting stimulus in ducklings, improves copulation rewarded behaviour of male rats in a T-maze, prevents or reverses amnesia induced by electroconvulsive shoch. CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects of vasopressin in the various and sometimes relatively complex tasks may be explained by stimulatory influences of this neuropeptide on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Various limbic system structures seem to act as the anatomical substrate for the bevavioural effects of vasopressin. In particular the amygdala, the dentate gyrus of the hippocampal complex, the ventral hippocampus and the dorsal septum seem to be involved. Evidence has been obtained from experiments with homozygous diabetes insipidus rats and from experiments in which antisera were applied that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. It appears that highly active fragments can be generated from vasopressin and experiments in which a fragment of vasopressin ([pGlu4, Cyt6]AVP-(4–8)) as well as an AVP-antagonist were used, reveal that the vasopressin receptors mediating the behavioural effects are situated in the brain and differ in specificity from the peripheral (blood pressure) vasopressin receptors. Generally the clinical data obtained so far with vasopressin treatment are in agreement with the results from animal experiments and they support the notion on the involvement of vasopressin in memory function. The sometimes reported conflicting results on vasopressin effects in certain patients (Korsakoff or Alzheimer) may have to do with the wide-spread pathology in these diseases.
Tj. B. van Wimersma Greidanus, J. P. H. Burbach and H. D. Veldhuis
L. J. Hellebrekers, E. Lagerweij, H. W. de Vries and Tj. B. Van Wimersma Greidanus
Abstract. Experiments were performed in conscious dogs, in order to study the possibility of dopaminergic or opioid modulation of the osmolality-regulated release of AVP. Hypertonic saline (20%), infused during a period of 2 h at a rate of 0.03 ml· kg−1 · min−1, induced a significant AVP response, which was not influenced by prior administration of bromocriptine or naloxone. Data presented in this report, therefore, are not in support of a dopaminergic or opioid modulation of the osmolality-regulated AVP release in dogs. The results demonstrate a great consistency in individual plasma osmolality-plasma AVP relationships, next to a large inter-individual variation.
A. A. De Rotte, J. Verhoef, E. A. D. Andringa-Bakker and Tj. B. Van Wimersma Greidanus
Abstract. We have investigated the nature of the α-melanocyte stimulating hormone-like immunoreactivity (α-MSH-LI) in blood and cerebrospinal fluid (CSF) of the rat. Blood and CSF from intact animals were subjected to high pressure liquid chromatography (HPLC) followed by a radioimmunoassay (RIA) specific for the C-terminal part of the α-MSH molecule. It appeared that in both body fluids the predomiant α-MSH-LI co-migrated with synthetic α-MSH and not with its des-acetyl or di-acetyl analogues. We conclude that α-MSH is the predominant form of α-MSH-LI circulating in plasma and CSF of rats from our Wistar strain.
L.J. Hellebrekers, E. Lagerweij, H W. de Vries and Tj. B. van Wimersma Greidanus
Abstract. The possibility of a dopaminergic and/or opioid modulation of the volume-regulated release of AVP was investigated in conscious dogs. Either bromocriptine, 10 μg/kg body weight po, or naloxone, 0.1 mg/kg body weight iv, was administered prior to induction of nonhypotensive hypovolemia. Volume contraction of 15 ml/kg body weight was induced gradually, over a period of 30 min. Basal plasma AVP levels in the bromocriptine group were not significantly different from control group values. Bromocriptine administration significantly augmented AVP release following volume contraction. Mean arterial pressure in the bromocriptine group decreased to a slightly, but significantly, lower level than that in the control group. Mean arterial pressures, however, did not adequately explain the magnitude of the AVP response in the bromocriptine group. In the naloxone group, neither baseline levels, nor AVP values following volume contraction, differed significantly from respective control group values. In conclusion, the results suggest the possibility of a stimulatory role for endogenous dopamine in the volume-regulated, but not the basal, release of AVP in conscious dogs.