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M Garbarg

Publications and source records attributed to M Garbarg.

28 records · Page 2Linked to original sources
PubMed1977

Histamine synthesizing afferents within the amygdaloid complex and bed nucleus of the stria terminalis of the rat.

The regional distribution of histidine decarboxylase (HD) activity has been studied in the amygdaloid complex and the bed nucleus of the stria terminalis (BST) of the rat. The central and medial nuclei of the amygdala had 2-fold higher HD activity levels than the remaining nuclei of the complex. HD activity was exceptionally high in the BST, particularly in its ventral part. A lesion of the stria terminalis had no effect on this distribution whereas a combined lesion of the stria terminalis and the so-called ventral pathway induced a decrease of approximately 60% in all the amygdaloid nuclei, but not in the BST. On the other hand, a lesion of the medial forebrain bundle (MFB) induced a similar decrease in both the amygdaloid nuclei and the BST. These results confirm that HD-containing fibres are present in the MFB. On the one hand these project massively to the BST and on the other penetrate in the amygdala ventromedially along the ansa peduncularis and preferentially innervate the more medially located nuclei.

Afferent Pathways↗
PubMed1976

Dual localization of histamine in an ascending neuronal pathway and in non-neuronal cells evidenced by lesions in the lateral hypothalamic area.

The effects of lesions placed in the lateral hypothalamic area, i.e., interrupting the MFB (as evidenced by a 65% decrease in cortical noradrenaline and serotonin) suggest a pluricompartmentation of brain histamine (HA). The existence of an ascending histaminergic system is indicated by the reductions in l-histidine decarboxylase (H.D.) activity, in [3H]histamine synthesis and in HA content, in the cortex of lesioned rats. Moreover, the decrease in H.D. activity was restricted to the regions rostral to the lesion, without modification caudally. The time-course of the alterations in H.D. activity and in HA content is compatible with a process of anterograde degeneration. In subcellular fractionation studies, the reduction in cortical HA content was found to be mainly confined to the P2 fraction, which contains the synaptosomes. Although the widespread ipsilateral distribution of HA synthesizing terminals resembles that of monoaminergic ones, the absence of reduction in H.D. activity after selective destruction of catecholaminergic and serotoninergic neurons, by 6-hydroxydopamine or 5,6-dihydroxytryptamine respectively, renders likely the existence of specific HA-containing neurons. That the release of the amine from these neurons might be related to the nerve impulse flow is suggested by the transient effects of the lesions which preceded the degenerative process (elevated endogenous HA level and slowed rate of [3H]HA synthesis). In addition, the discrepancy between the reduction in H.D. activity and in HA level after the lesions could be explained by the presence of the amine in another neuronal system and/or in non-neuronal cells, not affected by the lesion. This additional compartment is characterized by a high HA content and a low H.D. activity and could therefore be localized in mast-cells. The respective sizes of these two compartments, estimated by several methods, appear to be approximately the same.

5-Hydroxytryptophan↗