A. Björklund

Adrenergic innervation of the human uterus

The uterine adrenergic transmitter is in many animal species dramatically reduced during pregnancy, probably leading to a functional denervation near term. In order to clarify whether similar changes also occur in the human uterus, the adrenergic innervation of the isthmic myometrium during nonpregnant and pregnant conditions was analyzed by fluorescence histochemistry for demonstration of adrenergic nerves, and by quantitative measurements of norepinephrine and its synthesizing enzymes, tyrosine hydroxylase and dopa decarboxylase. At term pregnancy all fluorescent adrenergic nerves in the myometrium had disappeared, and the norepinephrine concentration had been reduced to almost zero. Parallel to this the activities of tyrosine hydroxylase and dopa decarboxylase were markedly reduced. By contrast, the activity of the acetylcholine-synthesizing enzyme, choline acetyltransferase, was unchanged, indicating that the adrenergic system was selectively affected. The results confirm that the adrenergic nerves in the human uterus, like those in uterine horns of laboratory animals, undergo fundamental changes in the course of pregnancy. This probably reflects entirely different conditions for a sympathetic influence on the myometrium during the last two trimesters of pregnancy compared to the non-pregnant situation.

Compensation of Lesion-Induced Changes in Cerebral Metabolism and Behaviour by Striatal Neural Implants in a Rat Model of Huntington’s Disease

There now exists ample evidence that the capacity of the adult CNS for functional recovery after large long-term lesions can be promoted by implants of foetal brain tissue (see, e.g., Bjorklund and Stenevi, 1979; Bjorklund et al., 1980; Dunnett et al., 1981a,b, 1982; Perlow et al., 1979; Gash and Sladek, 1979; Freed et al., 1980; Krieger et al., 1980; Gage et al., 1983, 1984; Deckel et al., 1983; Labbe et al., 1983; Isacson et al., 1984; Fine et al., this volume). The use of neural grafting as an experimental technique complements lesion and stimulation experiments in neurobiology. In the assessment of lesion-induced changes in the rat it has been investigated to what extent the grafting of neural tissue to the young lesioned or aged impaired animal can create a sufficient condition for functional recovery (see Bjorklund et al., 1983; Gage et al., 1983, 1984). Functional recovery after lesion-induced changes has been correlated with histological, neurochemical, physiological and metabolic parameters sometimes giving new insights into the mode of operation of certain neural circuitries or transmitter systems.

Long-term Locomotor and Cognitive Deficits in Rats with 6-OHDA Lesions of the VTA: A Model for Transplantation Studies

In Parkinson’s disease there is a reduction of dopamine (DA)-levels not only in the neostriatum, but also in cortical and limbic regions. The mesolimbocortical DA-neurons which originate in the ventral tegmental area (VTA, A10 of Dahlstrom and Fuxe) and project, e.g. to the nucleus accumbens, olfactory tubercle, amygdala, prefrontal cortex, anteromedial striatum and septum have been implicated in, i.a., stress and cognitive behaviours and the regulation of locomotor activity in rats. Extensive bilateral 6-OHDA lesions of the VTA have, for example, been shown to produce a persistent reduction of spontaneous locomotor activity, a blockade of amphetamine-induced activation and hyperactivity in response to apomorphine (Koob et al. 1981), however no significant effects have previously been seen on spatial learning ability in the watermaze (Hagan et al. 1983). Recent studies have demonstrated behavioural effects of DA-rich transplants in rats with 6-OHDA lesions in the VTA (S.B. Dunnett et al., 1984, N. Nadaud et al., 1984). We report here of significant changes in open field activity, somatosensory reactivity and watermaze performance after 6OHDA lesions of the VTA. Subsequently, the amelioration of the lesion-induced behavioural syndrome by DA-rich transplants is described.