TY  - JOUR
A1  - ,  
T1  - Axonal and terminal degeneration in the mediobasal forebrain after lesions of brainstem pathways
JO  - Eur. J. Anat.
SN  - 1136-4890
Y1  - 2005
VL  - 9
SP  - 35
EP  - 48
UR  - http://www.eurjanat.com/web/paper.php?id=05010035
KW  - gonadorelin
KW  - animal experiment
KW  - animal model
KW  - animal tissue
KW  - article
KW  - brain edema
KW  - brain hemorrhage
KW  - brain necrosis
KW  - brain nerve cell
KW  - brain region
KW  - brain stem injury
KW  - catecholaminergic system
KW  - controlled study
KW  - efferent nerve
KW  - female
KW  - Fink Heimer method
KW  - forebrain
KW  - gonadorelin release
KW  - histopathology
KW  - hypothalamus
KW  - locus ceruleus
KW  - mesencephalon
KW  - nerve ending
KW  - nerve fiber degeneration
KW  - nerve fiber transection
KW  - nerve projection
KW  - neuropil
KW  - nonhuman
KW  - noradrenergic nerve
KW  - parameter
KW  - rat
KW  - sensory nerve
KW  - supraoptic nucleus
KW  - technique
KW  - tegmentum
KW  - tissue structure
N2  - Lesion studies in animals are widely used for evaluating physiological parameters. However, changes in anatomical structures of the neuropil have often been neglected in the interpretation of the physiological results. Our study shows that anatomical data should also be considered. Here, the Fink-Heimer-method was used to demonstrate degeneration patterns after lesions in the rat brain. In detail, the ascending noradrenergic fibres were incised at the level of the dorsal tegmental area of the mesencephalon. The resulting degeneration pattern corresponds largely with the noradrenergic projection. The extent of degeneration is less than the physiological results in the literature predict. The interruption of the medial forebrain bundle at the posterolateral hypothalamic level led to a degeneration of the supraoptic decussation, where, according to physiological data, locus coeruleus fibres had been assumed to cross to the contralateral hemisphere. Beside axotomy, the lesions caused edema, hemorrhage and necrosis. They were not restricted to the width of the blade and did not only affect the catecholaminergic system but led to degeneration in mediobasal forebrain sites where gonadotropin-releasing hormone-neurons are present, in fibre systems which carry afferents and efferents of these neurons and in hypothalamic and extrahypothalamic structures that influence the release of the gonadotropin-releasing hormone. Thus, both anatomical and physiological aspects are important for a correct evaluation of lesion studies in brain/behavior research.
ER  -