Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Prell, George D.; Khandelwal, J. K.; Burns, R. S.; Green, J. P.

doi:10.1007/bf01967291

Cited by 30 publications

(30 citation statements)

References 54 publications

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“…Since amplification of the reward after hypothalamic stimulation was demonstrated following bilateral lesions of the tuberomammillary nucleus [63], one might suggest that tuberomammillary nucleus lesions facilitated cognition by enhancing the function of the reinforcement system. Interestingly, the implication of these studies, that the histaminergic system might exert an inhibitory tone on cognitive processes, could be readily integrated with findings that brain histaminergic activity was higher in the elderly [109,110], and histamine content of rat brain increased with age [92]. In conclusion, a role of his- [80][81][82].…”

Section: Histamine and Cognitionmentioning

confidence: 87%

Interactions between histaminergic and cholinergic systems in learning and memory

Bacciottini

Passani

Mannaioni

et al. 2001

Behavioural Brain Research

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The aim of this review is to survey biochemical, electrophysiological and behavioral evidence of the interactions between the cholinergic and histaminergic systems and evaluate their possible involvement in cognitive processes. The cholinergic system has long been implicated in cognition, and there is a plethora of data showing that cholinergic deficits parallel cognitive impairments in animal models and those accompanying neurodegenerative diseases or normal aging in humans. Several other neurotransmitters, though, are clearly implicated in cognitive processes and interact with the cholinergic system. The neuromodulatory effect that histamine exerts on acetylcholine release is complex and multifarious. There is clear evidence indicating that histamine controls the release of central acetylcholine (ACh) locally in the cortex and amygdala, and activating cholinergic neurones in the nucleus basalis magnocellularis (NBM) and the medial septal area-diagonal band that project to the cortex and to the hippocampus, respectively. Extensive experimental evidence supports the involvement of histamine in learning and memory and the procognitive effects of H 3 receptor antagonists. However, any attempt to strictly correlate cholinergic/histaminergic interactions with behavioral outcomes without taking into account the contribution of other neurotransmitter systems is illegitimate. Our understanding of the role of histamine in learning and memory is still at its dawn, but progresses are being made to the point of suggesting potential treatment strategies that may produce beneficial effects on neurodegenerative disorders associated with impaired cholinergic function.

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Section: Histamine and Cognitionmentioning

confidence: 87%

Interactions between histaminergic and cholinergic systems in learning and memory

Bacciottini

Passani

Mannaioni

et al. 2001

Behavioural Brain Research

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“…The relative paucity of complex molecules led to the idea of CSF acting as a 'sink' [42] into which brain metabolites and waste products could flow down their concentration gradient and be removed with the normal drainage of CSF. Examples include metabolites of serotonin and histamine flowing from brain into CSF for disposal [10,140].…”

Section: History Of Csf Generation and Flowmentioning

confidence: 99%

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

et al. 2018

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Brain fluids are rigidly regulated to provide stable environments for neuronal function, e.g., low K + , Ca 2+ , and protein to optimise signalling and minimise neurotoxicity. At the same time, neuronal and astroglial waste must be promptly removed. The interstitial fluid (ISF) of the brain tissue and the cerebrospinal fluid (CSF) bathing the CNS are integral to this homeostasis and the idea of a glia-lymph or 'glymphatic' system for waste clearance from brain has developed over the last 5 years. This links bulk (convective) flow of CSF into brain along the outside of penetrating arteries, glia-mediated convective transport of fluid and solutes through the brain extracellular space (ECS) involving the aquaporin-4 (AQP4) water channel, and finally delivery of fluid to venules for clearance along peri-venous spaces. However, recent evidence favours important amendments to the 'glymphatic' hypothesis, particularly concerning the role of glia and transfer of solutes within the ECS. This review discusses studies which question the role of AQP4 in ISF flow and the lack of evidence for its ability to transport solutes; summarizes attributes of brain ECS that strongly favour the diffusion of small and large molecules without ISF flow; discusses work on hydraulic conductivity and the nature of the extracellular matrix which may impede fluid movement; and reconsiders the roles of the perivascular space (PVS) in CSF-ISF exchange and drainage. We also consider the extent to which CSF-ISF exchange is possible and desirable, the impact of neuropathology on fluid drainage, and why using CSF as a proxy measure of brain components or drug delivery is problematic. We propose that new work and key historical studies both support the concept of a perivascular fluid system, whereby CSF enters the brain via PVS convective flow or dispersion along larger caliber arteries/arterioles, diffusion predominantly regulates CSF/ISF exchange at the level of the neurovascular unit associated with CNS microvessels, and, finally, a mixture of CSF/ISF/waste products is normally cleared along the PVS of venules/veins as well as other pathways; such a system may or may not constitute a true 'circulation', but, at the least, suggests a comprehensive re-evaluation of the previously proposed 'glymphatic' concepts in favour of a new system better taking into account basic cerebrovascular physiology and fluid transport considerations.

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“…Brain histaminergic activity is higher in the elderly (Prell et al, 1988;, and histamine content of the rat brain increases with age (Onodera et al, 1992). These observations could be readily integrated: decreased choline uptake in the elderly may be due to feed-back inhibition produced by decreased ACh release, to which high histaminergic activity may be contributing.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of cortical acetylcholine release and cognitive performance by histamine H₃ receptor activation in rats

Blandina

Giorgetti

Bartolini

et al. 1996

British J Pharmacology

216

151

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1 The effects of histamine and agents acting at histamine receptors on spontaneous and 100 mM K+-evoked release of acetylcholine, measured by microdialysis from the cortex of freely moving rats, and on cognitive tests are described. 2 Local administration of histamine (0.1-100 pM) failed to affect spontaneous but inhibited 100 mM K+-stimulated release of acetylcholine up to about 50%. The H3 receptor agonists (R)-ca-methylhistamine (RAMH) (0.1-10 yM), imetit (0.01-10 yM) and immepip (0.01-10 yM) mimicked the effect of histamine.3 Neither 2-thiazolylethylamine (TEA), an agonist showing some selectivity for H, receptors, nor the H2 receptor agonist, dimaprit, modified 100 mM K+-evoked release of acetylcholine. 4 The inhibitory effect of 100 pM histamine was completely prevented by the highly selective histamine H3 receptor antagonist, clobenpropit but was resistant to antagonism by triprolidine and cimetidine, antagonists at histamine H, and H2 but not H3 receptors.5 The H3 receptor-induced inhibition of K+-evoked release of acetylcholine was fully sensitive to tetrodotoxin (TTX).6 The effects of intraperitoneal (i.p.) injection of imetit (5 mg kg-') and RAMH (5 mg kg-') were tested on acetylcholine release and short term memory paradigms. Both drugs reduced 100 mM K+-evoked release of cortical acetylcholine, and impaired object recognition and a passive avoidance response.7 These observations provide the first evidence of a regulatory role of histamine H3 receptors on cortical acetylcholine release in vivo. Moreover, they suggest a role for histamine in learning and memory and may have implications for the treatment of degenerative disorders associated with impaired cholinergic function.

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Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Cited by 30 publications

References 54 publications

Interactions between histaminergic and cholinergic systems in learning and memory

Interactions between histaminergic and cholinergic systems in learning and memory

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

Inhibition of cortical acetylcholine release and cognitive performance by histamine H₃ receptor activation in rats

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Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey

Cited by 30 publications

References 54 publications

Interactions between histaminergic and cholinergic systems in learning and memory

Interactions between histaminergic and cholinergic systems in learning and memory

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

Inhibition of cortical acetylcholine release and cognitive performance by histamine H3 receptor activation in rats

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Inhibition of cortical acetylcholine release and cognitive performance by histamine H₃ receptor activation in rats