Abstract
There is increasing evidence that non-synaptic communication by volume transmission in the flowing CSF plays an important role in neural mechanisms, especially for extending the duration of behavioral effects. In the present review, we explore the mechanisms involved in the behavioral and physiological effects of β-endorphin (β-END), especially those involving the cerebrospinal fluid (CSF), as a message transport system to reach distant brain areas. The major source of β-END are the pro-opio-melano-cortin (POMC) neurons, located in the arcuate hypothalamic nucleus (ARH), bordering the 3rd ventricle. In addition, numerous varicose β-END-immunoreactive fibers are situated close to the ventricular surfaces. In the present paper we surveyed the evidence that volume transmission via the CSF can be considered as an option for messages to reach remote brain areas. Some of the points discussed in the present review are: release mechanisms of β-END, independence of peripheral versus central levels, central β-END migration over considerable distances, behavioral effects of β-END depend on location of ventricular administration, and abundance of mu and delta opioid receptors in the periventricular regions of the brain.
Highlights
There is increasing evidence that non-synaptic communication by volume transmission in the flowing cerebrospinal fluid (CSF) plays an important role in neural mechanisms, especially for extending the duration of behavioral effects [1,2,3,4]
Beta-Endorphin (β-END) is a neuropeptide, produced by pro-opio-melanocortin (POMC) neurons as well as by pituitary cells mainly located in the intermediate lobe [5,6], by cleavage from a larger precursor molecule, beta-lipotropin. β-END is its C-fragment and was characterized by Guillemin et al, in 1977 [7,8], in combination with its sister peptides, α-melanocyte-stimulating hormone (α-MSH), adrenocorticotropic hormone, (ACTH) and other substances [9,10,11,12,13]
The present review explores the existence of a special central and brain-directed β-END system and the possibility that the cerebrospinal fluid (CSF) plays a special role in the propagation of these brain-directed β-END messages
Summary
There is increasing evidence that non-synaptic communication by volume transmission in the flowing CSF plays an important role in neural mechanisms, especially for extending the duration of behavioral effects [1,2,3,4]. On the basis of the evidence presented here, we propose the following: There are two functionally different systems for the release of β-END, one for the peripheral effects via the systemic circulation and one directed to the central nervous system The latter system uses synaptic communication and additional volume transport mechanisms provided by the flowing CSF. In addition to tolerance effects, hormonal factors, so far mainly controlling energy homeostasis, may induce changes in the composition of the peptide cocktail which may have serious consequences for the different activation/inhibition patterns in the projection areas of the opiocortin neurons Such plastic changes are even region-specific to some extent, because certain hormonal conditions induced changes in local hypothalamic β-END levels only, without affecting other hypothalamic nuclei [203]. This enables the target circuitry to be programmed in a flexible way: a different cocktail of neuropeptides could induce different functionalities of the circuit, by modifying simultaneously a relevant set of parameters
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