By Neville N. Osborne (eds.)
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Extra resources for Current Aspects of the Neurosciences: Volume 1
1986c). , 1986d) revealed that after transsection of the dorsal (noradrenergic) bundle GAL-ir fine fibres were almost completely depleted in the hippocampal formation, with the exception of fine fibres in proximity to the pyramidal and granule cell layers (contained in cholinergic fibres). Coarse and punctate fibres in the hippocampus appeared to be unaffected, with the exception of the most lateral area of the dentate gyrus, where the normally dense fine punctate fibres seemed to be depleted.
The quantitative distribution of GAL-ir in discrete areas of the rat brain is presented in Table 1. Perusal of these values reveals that GAL-ir is unevenly distributed in individual nuclei of the rat CNS. The highest concentrations of GAL-ir (>2000 fmoVmg protein) were observed in the amygdaloid nuclei, the lateral septum, the globus pallidus, the bed nuclei of the stria terminalis, especially the ventral bed nucleus, all diencephalic nuclei investigated, the superior colliculus, the locus coeruleus, the nucleus of the solitary tract and the neurointermediate lobe of the pituitary.
This effect, however, was abolished by the addition of neurotensin (Meister and Hulting, 1987). Fuxe et a/. (1985) suggested that dopamine released from the medial palisade zone of the median eminence acts as a prolactin inhibiting factor. , 1986c), some of which presumably belong to the A12 dopamine cell group of Dahlstrom and Fuxe (1964) and send processes to the external layers of the median eminence. , 1987). In fact, Nordstrom eta/. (1987) showed a dose-dependent inhibition of dopamine release by GAL from the median eminence in vitro.