Histaminergic neurons in the tuberomammillary nucleus as a control centre for wakefulness

2020 ◽  
Author(s):  
Takeo Yoshikawa ◽  
Tadaho Nakamura ◽  
Kazuhiko Yanai
Keyword(s):  
Tuberomammillary Nucleus ◽  
Histaminergic Neurons ◽  
Control Centre

scholarly journals Thyrotropin-releasing hormone-containing axons innervate histaminergic neurons in the tuberomammillary nucleus

2012 ◽  
Vol 1488 ◽  
pp. 72-80 ◽  
Author(s):  
Anna Sárvári ◽  
Erzsébet Farkas ◽  
Andrea Kádár ◽  
Györgyi Zséli ◽  
Tamás Füzesi ◽  
...  
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Tuberomammillary Nucleus ◽  
Histaminergic Neurons

scholarly journals Chemogenetic modulation of histaminergic neurons in the tuberomammillary nucleus alters territorial aggression and wakefulness

2021 ◽  
Author(s):  
Fumito Naganuma ◽  
Tadaho Nakamura ◽  
Hiroshi Kuroyanagi ◽  
Masato Tanaka ◽  
Takeo Yoshikawa ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Nrem Sleep ◽  
Cre Recombinase ◽  
Designer Drugs ◽  
Brain Histamine ◽  
Tuberomammillary Nucleus ◽  
Territorial Aggression ◽  
Neuronal Populations ◽  
Histaminergic Neurons ◽  
Aggressive Behaviours

Abstract Designer receptor activated by designer drugs (DREADDs) techniques are widely used to modulate the activities of specific neuronal populations during behavioural tasks. However, DREADDs-induced modulation of histaminergic neurons in the tuberomammillary nucleus (HATMN neurons) has produced inconsistent effects on the sleep–wake cycle, possibly due to the use of Hdc-Cre mice driving Cre recombinase and DREADDs activity outside the targeted region. Moreover, previous DREADDs studies have not examined locomotor activity and aggressive behaviours, which are also regulated by brain histamine levels. In the present study, we investigated the effects of HATMN activation and inhibition on the locomotor activity, aggressive behaviours and sleep–wake cycle of Hdc-Cre mice with minimal non-target expression of Cre-recombinase. Chemoactivation of HATMN moderately enhanced locomotor activity in a novel open field. Activation of HATMN neurons significantly enhanced aggressive behaviour in the resident–intruder test. Wakefulness was increased and non-rapid eye movement (NREM) sleep decreased for an hour by HATMN chemoactivation. Conversely HATMN chemoinhibition decreased wakefulness and increased NREM sleep for 6 hours. These changes in wakefulness induced by HATMN modulation were related to vigilance status transition. These results indicate the influences of HATMN neurons on exploratory activity, territorial aggression, and wake maintenance.

scholarly journals Orexin/Hypocretin Excites the Histaminergic Neurons of the Tuberomammillary Nucleus

2001 ◽  
Vol 21 (23) ◽  
pp. 9273-9279 ◽  
Author(s):  
Krister S. Eriksson ◽  
Olga Sergeeva ◽  
Ritchie E. Brown ◽  
Helmut L. Haas
Keyword(s):  
Tuberomammillary Nucleus ◽  
Histaminergic Neurons

scholarly journals Histamine modulation of the basal ganglia circuitry in the development of pathological grooming

2017 ◽  
Vol 114 (25) ◽  
pp. 6599-6604 ◽  
Author(s):  
Maximiliano Rapanelli ◽  
Luciana Frick ◽  
Haruhiko Bito ◽  
Christopher Pittenger
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Histidine Decarboxylase ◽  
Dorsal Striatum ◽  
Tic Disorders ◽  
Rare Mutation ◽  
Tuberomammillary Nucleus ◽  
Histaminergic Neurons ◽  
Plausible Model ◽  
Behavioral Pathology

Aberrant histaminergic function has been proposed as a cause of tic disorders. A rare mutation in the enzyme that produces histamine (HA), histidine decarboxylase (HDC), has been identified in patients with Tourette syndrome (TS). Hdc knockout mice exhibit repetitive behavioral pathology and neurochemical characteristics of TS, establishing them as a plausible model of tic pathophysiology. Where, when, and how HA deficiency produces these effects has remained unclear: whether the contribution of HA deficiency to pathogenesis is acute or developmental, and where in the brain the relevant consequences of HA deficiency occur. Here, we address these key pathophysiological questions, using anatomically and cellularly targeted manipulations in mice. We report that specific ablation or chemogenetic silencing of histaminergic neurons in the tuberomammillary nucleus (TMN) of the hypothalamus leads to markedly elevated grooming, a form of repetitive behavioral pathology, and to elevated markers of neuronal activity in both dorsal striatum and medial prefrontal cortex. Infusion of HA directly into the striatum reverses this behavioral pathology, confirming that acute HA deficiency mediates the effect. Bidirectional chemogenetic regulation reveals that dorsal striatum neurons activated after TMN silencing are both sufficient to produce repetitive behavioral pathology and necessary for the full expression of the effect. Chemogenetic activation of TMN-regulated medial prefrontal cortex neurons, in contrast, increases locomotion and not grooming. These data confirm the centrality of striatal regulation by neurotransmitter HA in the adult in the production of pathological grooming.

The role of the central histaminergic system in emergence from propofol anesthesia

2021 ◽  
Vol 18 ◽  
Author(s):  
Chenzhong Xia ◽  
Zexian Zhao ◽  
Lina Yu ◽  
Min Yan
Keyword(s):  
Critical Role ◽  
State Transitions ◽  
Dependent Manner ◽  
Emergence Time ◽  
Firing Activity ◽  
Excitatory Effect ◽  
Histaminergic System ◽  
Tuberomammillary Nucleus ◽  
Histaminergic Neurons

Background: The mechanisms of emergence from general anesthesia remain to be elucidated. Recent studies indicate that the central histaminergic system plays a critical role in maintaining wakefulness. Methods: Role of the central histaminergic system in emergence from propofol anesthesia using microinjections and single-unit recordings in rats was evaluated. Results: Intracerebroventricular (icv) microinjections of histamine decreased the emergence time in a dose-dependent manner and had an excitatory effect on the firing activity of medial prefrontal cortex (mPFC) neurons, while the decrease of emergence time was completely reversed by the pre-treatment with triprolidine (80 μg/5 μl) but not cimetidine (100 μg/5 μl). Moreover, the presumed histaminergic neurons fired in a state-dependent manner, and there was a dramatic increase in firing activity before regain of righting reflex. Furthermore, bidirectional manipulations of emergence were achieved through the microinjection of GABA (10 μg/side) and a potent H3 receptor inverse agonist ciproxian (1 μg/side) into the posterior hypothalamus, where the tuberomammillary nucleus (TMN) resides. Conclusion: Combining the behavioral and neurophysiologic evidence, the central histaminergic system promotes emergence from propofol anesthesia in rats. Our findings suggest an important role of the central histaminergic system in a broader field of state transitions, such as emergence from propofol anesthesia.

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