The tuberomammillary nucleus projections in the control of learning, memory and reinforcement processes: evidence for an inhibitory role

Huston, Joseph P.; Wagner, Uwe; Hasenöhrl, Rüdiger U.

doi:10.1016/s0166-4328(97)86052-4

Cited by 121 publications

(57 citation statements)

References 49 publications

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“…Our findings provide supportive evidence for the hypothesis that the endocannabinoid system is involved in the inhibitory control of associative processing in a way similar to endogenous opiates (Izquierdo, 1982) and neuronal histamine (Huston, Wagner & Hasenöhrl, 1997). CB 1 R -/-mice displayed enhanced acquisition and prolonged retention of the habituation task compared to wild-type controls and this inability to forget may result in behavioral perseveration evidenced in more complex learning paradigms like the Morris water maze .…”

Section: Discussionsupporting

confidence: 82%

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

Thiemann¹,

Fletcher²,

Ledent³

et al. 2007

Neurobiology of Learning and Memory

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The endocannabinoid CB1 receptor has been implicated in the inhibitory control of learning and memory. In the present experiment, we compared the behavioral response of CB1 receptor knockout mice (CB1R-/-) with animals administered CB1 receptor antagonist/inverse agonist SR141716A (rimonabant; 3 mg/kg IP, 30 min pre-trial) in terms of acquisition and retention of a habituation task and changes in cerebral monoamines. The results can be summarized as follows: (i.) The acute and chronic invalidation of the CB1 receptor resulted in an increase of behavioral habituation during the first exposure to an open field, indicative of enhanced acquisition of the task; (ii.) CB1R-/-mice, but not rimonabant-treated animals, showed enhanced long-term retention of the habituation task when tested 48 hours and 1 week subsequent to the first exposure to the open field, respectively; (iii.) The facilitation of long-term retention of the habituation task in CB1R-/-mice was accompanied by a selective and site-specific increase in serotonin activity in hippocampus; and (iv.) Rimonabant-treated animals displayed 'antidepressant-like' alterations of cerebral monoamines, that is, most parameters of monoaminergic activity were increased especially in dorsal striatum and hippocampus. Taken together, the present findings demonstrate that the genetic disruption of the CB1 receptor gene can cause an improvement of behavioral habituation, which is considered to represent a form of 'non-associative' learning. Furthermore, the data support our assumption of a rimonabant-sensitive cannabinoid receptive site that is different from the 'classical' CB1 receptor and which, under physiological conditions, might be involved in the inhibitory control of the acquisition but not retention of non-associative learning tasks. Furthermore, the data support our assumption of a rimonabant-sensitive cannabinoid receptive site that is different from the 'classical' CB 1 receptor and which, under physiological conditions, might be involved in the inhibitory control of the acquisition but not retention of non-associative learning tasks. U nive r s it y o f H e r t f o r d s hir e S C H O O L O F P S Y C H O L O G Y

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Section: Discussionsupporting

confidence: 82%

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

Thiemann¹,

Fletcher²,

Ledent³

et al. 2007

Neurobiology of Learning and Memory

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“…Recently, the effects of lesions of the tuberomammillary nucleus on the performance of adult and aged rats in a set of cognitive tasks have been reported; in addition to a marked decrease in the number of histaminergic neurons, these lesions produced an improvement in every cognition test applied, and strongly diminished the age-related learning deficits [43]. 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].…”

Section: Histamine and Cognitionmentioning

confidence: 99%

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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“…To verify this hypothesis, pharmacological experiments using receptor-gene knockout mice should be conducted. Previous studies have shown that histaminergic neurons have inhibitory effects on behavioral sensitization and rewarding using histamine H 1 /H 2 receptor-gene doubleknockout mice (10,11), histidine decarboxylase-gene knockout mice (12), and brain-lesion methods in rats (13). However, further studies are needed to clearly determine whether the histaminergic neuron system has inhibitory effects on behavioral sensitization and rewarding.…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine- and 3,4-Methylenedioxymethamphetamine–Induced Behavioral Changes in Histamine H3–Receptor Knockout Mice

et al. 2009

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Abstract. Histamine H 3 receptors inhibit the release of not only histamine itself, but also other neurotransmitters including dopamine. Previous papers have reported that histaminergic neurons inhibit psychostimulant-induced behavioral changes. To examine whether deficiency in histamine H 3 receptors influences psychostimulant-induced behavioral sensitization and reward, we examined locomotor activity, conditioned place preference (CPP), and c-Fos expression in histamine H 3 receptor-gene knockout mice (H3KO) and their wild-type (WT) counterparts before and after treatment with methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA). The increase in locomotion induced by treatment with METH or MDMA was lower in histamine H3KO mice than in WT mice, while the locomotor sensitization was developed by METH or MDMA in both strains. However, no significant difference in METH-and MDMA-induced preference scores of CPP between histamine H3KO mice and WT mice was observed. Following treatment with METH, the number of c-Fos-positive neurons in the the caudate-putamen of histamine H3KO mice was lower than that in the caudate-putamen of WT mice. In contrast, there was no significant difference in the number of the psychostimulant-induced c-Fos-positive cells in the nucleus accumbens between the two strains of mice. These findings suggest that deficiency in histamine H 3 receptors may have inhibitory effects on psychostimulant-induced increase in locomotion, but insignificant effects on the reward.

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The tuberomammillary nucleus projections in the control of learning, memory and reinforcement processes: evidence for an inhibitory role

Cited by 121 publications

References 49 publications

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

Interactions between histaminergic and cholinergic systems in learning and memory

Methamphetamine- and 3,4-Methylenedioxymethamphetamine–Induced Behavioral Changes in Histamine H3–Receptor Knockout Mice

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