Literature DB >> 11578594

Axon terminals containing tyrosine hydroxylase- and dopamine-beta-hydroxylase immunoreactivity form synapses with galanin immunoreactive neurons in the lateral division of the bed nucleus of the stria terminalis in the rat.

T Kozicz1.   

Abstract

Catecholaminergic projections from brainstem sources to the bed nucleus of the stria terminalis play a central role in the neurochemically mediated modulation/regulation of stress response. The lateral division of the bed nucleus of the stria terminalis (BSTL) exhibits several galanin immunoreactive (ir) neurons that are also central in the modulatory control of acute stress responses. The distribution of galaninergic nervous structures overlaps with that of the dopaminergic and noradrenergic axon terminals in the BSTL. Since both monoamines and galanin regulate/modulate the central regulatory pathways of endocrine, behavioral and physiological responses during stress, the aim of this study was to demonstrate synaptic interaction between galanin-ir nervous structures and fiber terminals immunopositive for dopamine or noradrenaline in the BSTL, thereby providing morphological data to understand better the significance of catecholamine-galanin interactions in brain areas responding to stressful stimuli. Double-labeling immunohistochemistry applied both at light and electron microscopic levels made it possible to demonstrate synaptic interactions between galanin-ir nervous structures and axon terminals immunopositive for either dopamine or noradrenaline. The dopaminergic fiber terminals innervated galanin-ir cells and dendrites in the laterodorsal division of the bed nucleus of the stria terminalis (BST), whereas the noradrenergic axons contacted galaninergic neurons and dendrites in the lateroventral BST. In this study, interactions between monoamines and galanin-ir structures were demonstrated in the BSTL which can be central in the modulatory control of the major stress regulatory pathway of the limbic-hypothalamo-pituitary-adrenal axis.

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Year:  2001        PMID: 11578594     DOI: 10.1016/s0006-8993(01)02770-6

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


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