The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Joseph P Huston - One of the best experts on this subject based on the ideXlab platform.
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memory improvement by post trial injection of lidocaine into the Tuberomammillary Nucleus the source of neuronal histamine
Neurobiology of Learning and Memory, 1999Co-Authors: Christian Frisch, R U Hasenohrl, Joseph P HustonAbstract:Brain histamine is exclusively contained within and released from neurons whose cell bodies are clustered in the Tuberomammillary Nucleus (TM) of the posterior hypothalamus. This experiment examined the effects of a transient inactivation of the TM on inhibitory avoidance learning. Rats with chronically implanted cannulae were tested on a 1-trial step-through avoidance task. Immediately following training, the rats received unilateral intra-TM infusions (0.5 μl) of lidocaine (5 or 20 μg). Control groups included vehicle-injected rats and a group given an injection of 20 μg lidocaine 5 h after training. When tested 24 h later, rats treated with 20 μg lidocaine exhibited longer step-through latencies than vehicle-treated controls, indicative of superior learning of the task. The failure of the delayed post-trial injection of lidocaine to significantly influence step-through latencies indicates that the compound influenced learning by modulating memory storage processes rather than by acting on performance variables during retrieval of the task. Thus, inactivation of the TM by lidocaine can exert facilitatory effects on mnemonic processing, which might be related to a temporary reduction of histaminergic activity during the early phase of memory consolidation.
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behavioral asymmetries and neurochemical changes after unilateral lesions of Tuberomammillary Nucleus or substantia nigra
Experimental Brain Research, 1998Co-Authors: Silvia S Maisonnette, Joseph P Huston, Marcus Lira Brandao, Rainer K W SchwartingAbstract:Previous studies in the rat have shown that the hypothalamic Tuberomammillary Nucleus, the major source of neuronal histamine, is related to mechanisms of learning, memory, reinforcement, and functional recovery. These functional relationships were found to be partly lateralized. Therefore, we decided to analyze whether unilateral ibotenic acid lesions aimed at this brain region would acutely lead to asymmetries in open-field behavior, and whether they would affect the biogenic amines dopamine and serotonin in the neostriatum, hippocampus, and tectum. We compared this manipulation with unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta and with unilateral ibotenic acid lesions of the substantia nigra pars reticulata. These lesions were investigated because all three brain areas are anatomically linked to the neostriatum, are related to the neurotransmitters dopamine and serotonin, and play a role in behavioral asymmetry and functional recovery. In support of previous findings, our data show that 6-hydroxydopamine lesions of the substantia nigra pars compacta led to an ipsiversive asymmetry in turning and scanning. Ibotenic acid lesions of the adjacent pars reticulata led to contraversive turning, whereas thigmotactic scanning was reduced bilaterally. In contrast, ibotenic acid lesions of the Tuberomammillary Nucleus did not affect turning, but led to an ipsilateral asymmetry in scanning. Neurochemically, the 6-hydroxydopamine lesion was mainly characterized by the well-known ipsilateral neostriatal dopamine depletion and increased residual dopamine activity. In hippocampus and tectum, these transmitters were not specifically affected, except for an asymmetry of serotonin in the superior colliculus. The ibotenic acid lesions of the pars reticulata did not deplete neostriatal dopamine, indicating that they spared the dopaminergic output of the substantia nigra. In contrast, they affected dopaminergic and serotonergic measures in the colliculi, which may be due to damage of the nigral GABAergic projection to this brain area. In animals with unilateral ibotenic acid lesions of the Tuberomammillary Nucleus, several markers of dopaminergic and serotonergic acitivity were increased in the neostriatum, tectum, and hippocampus. This effect may have been due to the loss of inhibition otherwise provided by the wide-ranging histaminergic output of the Tuberomammillary Nucleus. These results are discussed with respect to the major outputs of the three brain areas, their potential impacts on neurotransmitters in their projection sites, and their role in behavioral asymmetry.
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anxiolytic like behavior after lesion of the Tuberomammillary Nucleus e2 region
Experimental Brain Research, 1998Co-Authors: Christian Frisch, R U Hasenohrl, J Krauth, Joseph P HustonAbstract:The Tuberomammillary Nucleus (TM), located in the posterior hypothalamic region, consists of five subgroups and is the only known source of brain histamine. In the present experiment, rats received bilateral ibotenic acid or sham lesions in the rostroventral part of the TM (E2-region). Three weeks later they were tested on the elevated plus-maze test of fear and anxiety. Lesions in the Tuberomammillary E2-region elevated the time spent on the open arms, as well as excursions into the end of the open arms, increased scanning over the edge of an open arm, and decreased risk-assessment from an enclosed arm. Thus, partial destruction of TM intrinsic neurons can induce anxiolytic-like effects which are possibly related to a lesion-induced reduction of histaminergic activity.
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facilitation of learning after lesions of the Tuberomammillary Nucleus region in adult and aged rats
Experimental Brain Research, 1998Co-Authors: Christian Frisch, R U Hasenohrl, H T Weiler, Helmut L Haas, H W M Steinbusch, Joseph P HustonAbstract:The Tuberomammillary Nucleus (TM) located in the posterior part of the hypothalamus is the main source of neuronal histamine in the central nervous system. Recent work from our laboratories has indicated an involvement of the TM region in neuronal plasticity and reinforcement processes. In the present study, we investigated the effects of TM lesions on the performance of adult and aged Wistar rats in a set of learning tasks, which differed in terms of complexity and reward contingencies (habituation learning, inhibitory avoidance, discrimination learning, Morris water maze). An improvement was found in every test applied, indicating that TM lesions seem to generally enhance learning and memory capacities independent of the special demands of a given task. Age-related learning deficits were strongly diminished. Immunohistochemistry revealed that the excitotoxic lesions used to destroy the TM region led to a marked decrease in the number of histamine-positive neurons in the vicinity of the injection site, indicating an involvement of the brain histaminergic system in the observed behavioral changes.
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the Tuberomammillary Nucleus projections in the control of learning memory and reinforcement processes evidence for an inhibitory role
Behavioural Brain Research, 1997Co-Authors: Joseph P Huston, Uwe Wagner, R U HasenohrlAbstract:Abstract The Tuberomammillary Nucleus (TM), a cluster of magnocellular cells in the posterior hypothalamus, is the main source of neuronal histamine in the brain. Although this Nucleus is well described in terms of anatomy and neurochemistry, only little is known about its function. Our earlier work showed that the TM projection system may be involved in behavioral asymmetries and behavioral recovery after unilateral manipulations of the brain. Using horseradish peroxidase (HRP) labeling we found an increase in strength (structure and/or activity) in the crossed and uncrossed Tuberomammillary-striatal projections in the course of recovery from behavioral asymmetries produced by unilateral removal of the rats' vibrissae, which were in the same direction as the asymmetries found in projections from the substantia nigra to the striatum. Experiments performed with unilateral lesions of the TM region provide evidence for an involvement of the TM system in reinforcement mechanisms. Unilateral destruction of the TM with direct current (DC) or ibotenic acid was found to increase the rate of lateral hypothalamic self-stimulation ipsilateral to the lesion site, suggesting that the TM (particularly the E2 subgroup in its rostra] part: may function as a reinforcement inhibiting neural substrate. Experiments performed with bilateral DC or ibotenic acid lesions of the TM region suggest a role of the Nucleus in learning and mnemonic processes. A bilateral electrolytic or neurotoxic lesion of the TM region was found to facilitate the performance of adult and behaviorally impaired aged rats in a variety of learning tasks, including a habituation paradigm, aversively motivated learning tasks and water mazes. Examination of the site of the neurotoxic lesion in the TM region with immunohistochemical techniques revealed a marked decline of histamine-staining neurons mainly in the rostral part of the TM Nucleus, suggesting that the facilitatory effects on reinforcement and mnemonic processes might be related to the destruction of TM intrinsic histaminergic cells. In summary, the present results indicate that the TM Nucleus is involved in neural plasticity and functional recovery following damage to the CNS and may function as an inhibitory neural substrate in the control of reinforcement and mnemonic processes.
Ilsung Jang - One of the best experts on this subject based on the ideXlab platform.
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α2a adrenoceptor mediated presynaptic inhibition of gabaergic transmission in rat Tuberomammillary Nucleus neurons
Journal of Neurochemistry, 2013Co-Authors: Michiko Nakamura, Ilsung JangAbstract:Histaminergic neurons within the Tuberomammillary Nucleus (TMN) play an important role in the regulation of sleep-wakefulness. Here, we report the adrenergic modulation of GABAergic transmission in rat TMN histaminergic neurons using a conventional whole-cell patch clamp technique. Norepinephrine (NE) reversibly decreased the amplitude of action potential-dependent GABAergic inhibitory post-synaptic currents (IPSCs) and increased the paired pulse ratio. The NE-induced inhibition of GABAergic IPSCs was mimicked by clonidine, a selective α2 adrenoceptor agonist. However, cirazoline and isoproterenol, nonselective α1 and β adrenoceptor agonists, respectively, had no effect on GABAergic IPSCs. The NE-induced inhibition of GABAergic IPSCs was significantly blocked by BRL44408, a selective α2A adrenoceptor antagonist, but not imiloxan or JP1302, a selective α2B and α2C adrenoceptor antagonists. The extent of NE-induced inhibition of GABAergic IPSCs was inversely proportional to the extracellular Ca2+ concentration. Pharmacological agents affecting the activities of adenylyl cyclase or G-protein-coupled inwardly rectifying K+ channels did not affect the NE-induced inhibition of GABAergic IPSCs. However, NE had no effect on the frequency and amplitude of GABAergic miniature IPSCs. These results suggest that NE acts on presynaptic α2A adrenoceptor to inhibit action potential-dependent GABA release via the inhibition of Ca2+ influx from the extracellular space to GABAergic nerve terminals, and that this α2A adrenoceptor-mediated modulation of GABAergic transmission may be involved in regulating the excitability of TMN histaminergic neurons.
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muscarinic m4 receptors regulate gabaergic transmission in rat Tuberomammillary Nucleus neurons
Neuropharmacology, 2012Co-Authors: Michiko Nakamura, Ilsung JangAbstract:Abstract Histaminergic neurons within the Tuberomammillary Nucleus (TMN) play an important role in sleep-wakefulness regulation. Here, we report the muscarinic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) in mechanically dissociated rat histaminergic neurons using a conventional whole-cell patch clamp technique. Muscarine, a nonselective muscarinic acetylcholine (mACh) receptor agonist, reversibly decreased mIPSC frequency without affecting the current amplitude, indicating that muscarine acts presynaptically to decrease the probability of spontaneous GABA release. The muscarine action on GABAergic mIPSC frequency was completely blocked by atropine, a nonselective mACh receptor antagonist, and tropicamide, an M4 receptor antagonist. The muscarine-induced decrease in mIPSC frequency was completely occluded in the presence of Cd2+, a general voltage-dependent Ca2+ channel blocker, or in a Ca2+-free external solution. However, pharmacological agents affecting adenylyl cyclase or G-protein coupled inwardly rectifying K+ channel activity did not prevent the inhibitory action of muscarine on GABAergic mIPSCs. These results suggest that muscarine acts on M4 receptors on GABAergic nerve terminals projecting to histaminergic neurons to inhibit spontaneous GABA release via the inhibition of Ca2+ influx from the extracellular space. Muscarine also inhibited action potential-dependent GABA release by activating presynaptic M4 receptors in more physiological conditions. The M4 receptor-mediated modulation of GABAergic transmission onto TMN neurons may contribute to the regulation of sleep-wakefulness.
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adenosine a1 receptors inhibit gabaergic transmission in rat Tuberomammillary Nucleus neurons
Journal of Neurochemistry, 2008Co-Authors: Insun Choi, Michiko Nakamura, Byungju Choi, Jaekap Choi, Ilsung JangAbstract:The adenosinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) was investigated in mechanically dissociated rat Tuberomammillary Nucleus (TMN) neurons using a conventional whole-cell patch clamp technique. Adenosine (100 μM) reversibly decreased mIPSC frequency without affecting the current amplitude, indicating that adenosine acts presynaptically to decrease the probability of spontaneous GABA release. The adenosine action on GABAergic mIPSC frequency was completely blocked by 1 μM DPCPX, a selective A1 receptor antagonist, and mimicked by 1 μM CPA, a selective A1 receptor agonist. This suggests that presynaptic A1 receptors were responsible for the adenosine-mediated inhibition of GABAergic mIPSC frequency. CPA still decreased GABAergic mIPSC frequency even either in the presence of 200 μM Cd2+, a general voltage-dependent Ca2+ channel blocker, or in the Ca2+-free external solution. However, the inhibitory effect of CPA on GABAergic mIPSC frequency was completely occluded by 1 mM Ba2+, a G-protein coupled inwardly rectifying K+ (GIRK) channel blocker. In addition, the CPA-induced decrease in mIPSC frequency was completely occluded by either 100 μM SQ22536, an adenylyl cyclase (AC) inhibitor, or 1 μM KT5720, a specific protein kinase A (PKA) inhibitor. The results suggest that the activation of presynaptic A1 receptors decreases spontaneous GABAergic transmission onto TMN neurons via the modulation of GIRK channels as well as the AC/cAMP/PKA signal transduction pathway. This adenosine A1 receptor-mediated modulation of GABAergic transmission onto TMN neurons may play an important role in the fine modulation of the excitability of TMN histaminergic neurons as well as the regulation of sleep-wakefulness.
Zhong Chen - One of the best experts on this subject based on the ideXlab platform.
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low frequency stimulation of the Tuberomammillary Nucleus facilitates electrical amygdaloid kindling acquisition in sprague dawley rats
Neurobiology of Disease, 2008Co-Authors: Deng Chang Wu, Zheng Bing Zhuge, Shuang Wang, Chao Yang Yu, Qi Fang, Shihong Zhang, Zhong ChenAbstract:Histamine plays a suppressive role in seizure. The Tuberomammillary Nucleus (TM) is the only locus of histaminergic neurons in the brain. To determine whether deep brain stimulation (DBS) of the TM provides protection against seizures, we tested the effects of low-frequency stimulation (LFS, 1 Hz), high frequency stimulation (HFS, 100 Hz), and electrolytic lesions of the TM on seizures generated by amygdaloid kindling, pentylenetetrazol (PTZ) and maximal electroshock (MES) in rats. LFS of TM accelerated the progression of behavioral seizure stage and increased the mean afterdischarge duration (ADD) during acquisition of amygdaloid-kindling seizures, but had no considerable anticonvulsive effect in fully kindled animals. It augmented the MES-induced seizures as well, but had no appreciable effects on PTZ-kindled seizures. In addition, both HFS and bilateral lesions of the TM exacerbated the progression of amygdaloid-kindling seizures. These results suggest that specific negative sites for DBS exist in the brain, such as the TM. This study indicates that it is crucial to choose a suitable target for DBS in the clinical treatment of epilepsy.
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Low-frequency stimulation of the Tuberomammillary Nucleus facilitates electrical amygdaloid-kindling acquisition in Sprague–Dawley rats
Neurobiology of Disease, 2008Co-Authors: Deng Chang Wu, Shuang Wang, Chao Yang Yu, Qi Fang, Shihong Zhang, Zhong ChenAbstract:Histamine plays a suppressive role in seizure. The Tuberomammillary Nucleus (TM) is the only locus of histaminergic neurons in the brain. To determine whether deep brain stimulation (DBS) of the TM provides protection against seizures, we tested the effects of low-frequency stimulation (LFS, 1 Hz), high frequency stimulation (HFS, 100 Hz), and electrolytic lesions of the TM on seizures generated by amygdaloid kindling, pentylenetetrazol (PTZ) and maximal electroshock (MES) in rats. LFS of TM accelerated the progression of behavioral seizure stage and increased the mean afterdischarge duration (ADD) during acquisition of amygdaloid-kindling seizures, but had no considerable anticonvulsive effect in fully kindled animals. It augmented the MES-induced seizures as well, but had no appreciable effects on PTZ-kindled seizures. In addition, both HFS and bilateral lesions of the TM exacerbated the progression of amygdaloid-kindling seizures. These results suggest that specific negative sites for DBS exist in the brain, such as the TM. This study indicates that it is crucial to choose a suitable target for DBS in the clinical treatment of epilepsy.
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lesion of the Tuberomammillary Nucleus e2 region attenuates postictal seizure protection in rats
Epilepsy Research, 2007Co-Authors: Zheng Bing Zhuge, Deng Chang Wu, Shuang Wang, Zhong ChenAbstract:Summary Postictal seizure protection (PSP) is an endogenous anticonvulsant phenomenon that follows an epileptic seizure and inhibits the induction of further seizures. The Tuberomammillary Nucleus (TM), located in the posterior hypothalamus, consists of five subregions and is the sole source of histaminergic neurons in the brain. To determine whether the TM is involved in PSP in rats, we tested the effects of bilateral electrolytic lesions of the TM E2-region on seizures induced by intermittent maximal electroshock (MES). The TM E2-region lesions significantly attenuated PSP during the intermittent MES procedure. Furthermore, intracerebroventricular injection of α-fluoromethylhistidine (100 μg), a selective and irreversible histidine decarboxylase inhibitor, mimicked the attenuation of PSP induced by the lesion of TM E2-region. In addition, neurochemical experiments revealed that the TM E2-region lesions markedly decreased basal histamine levels in the cortex, hippocampus, brainstem and hypothalamus, but had no significant effect on basal glutamate and GABA levels. Moreover, intermittent MES induced a persistent decrease of brain histamine levels in both sham-operated and lesioned rats. These results indicate that through its intrinsic histaminergic system, the TM may exert powerful inhibitory function during the intermittent MES procedure and actively participate in the mechanisms of PSP.
Uwe Wagner - One of the best experts on this subject based on the ideXlab platform.
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the Tuberomammillary Nucleus projections in the control of learning memory and reinforcement processes evidence for an inhibitory role
Behavioural Brain Research, 1997Co-Authors: Joseph P Huston, Uwe Wagner, R U HasenohrlAbstract:Abstract The Tuberomammillary Nucleus (TM), a cluster of magnocellular cells in the posterior hypothalamus, is the main source of neuronal histamine in the brain. Although this Nucleus is well described in terms of anatomy and neurochemistry, only little is known about its function. Our earlier work showed that the TM projection system may be involved in behavioral asymmetries and behavioral recovery after unilateral manipulations of the brain. Using horseradish peroxidase (HRP) labeling we found an increase in strength (structure and/or activity) in the crossed and uncrossed Tuberomammillary-striatal projections in the course of recovery from behavioral asymmetries produced by unilateral removal of the rats' vibrissae, which were in the same direction as the asymmetries found in projections from the substantia nigra to the striatum. Experiments performed with unilateral lesions of the TM region provide evidence for an involvement of the TM system in reinforcement mechanisms. Unilateral destruction of the TM with direct current (DC) or ibotenic acid was found to increase the rate of lateral hypothalamic self-stimulation ipsilateral to the lesion site, suggesting that the TM (particularly the E2 subgroup in its rostra] part: may function as a reinforcement inhibiting neural substrate. Experiments performed with bilateral DC or ibotenic acid lesions of the TM region suggest a role of the Nucleus in learning and mnemonic processes. A bilateral electrolytic or neurotoxic lesion of the TM region was found to facilitate the performance of adult and behaviorally impaired aged rats in a variety of learning tasks, including a habituation paradigm, aversively motivated learning tasks and water mazes. Examination of the site of the neurotoxic lesion in the TM region with immunohistochemical techniques revealed a marked decline of histamine-staining neurons mainly in the rostral part of the TM Nucleus, suggesting that the facilitatory effects on reinforcement and mnemonic processes might be related to the destruction of TM intrinsic histaminergic cells. In summary, the present results indicate that the TM Nucleus is involved in neural plasticity and functional recovery following damage to the CNS and may function as an inhibitory neural substrate in the control of reinforcement and mnemonic processes.
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Tuberomammillary Nucleus lesion facilitates two way active avoidance retention in rats
Behavioural Brain Research, 1996Co-Authors: Pilar Seguratorres, Uwe Wagner, Ester Massanesrotger, Laura Aldavertvera, Margarita Martinicolovius, Ignacio MorgadobernalAbstract:Abstract To evaluate whether the Tuberomammillary Nucleus might be involved in the acquisition and/or retention of a two-way active avoidance conditioning, rats were given a unilateral lesion of the Tuberomammillary Nucleus (E2 region) 24 h prior to the first conditioning session. Four learning sessions were performed: one acquisition and 3 retention sessions (short-term, 24 h; and longterm, 8 and 18 days). Results showed that the lesion facilitated the long-term retention of conditioning, but no effects were observed on acquisition and short-term retention. Since rewarding intracranial electrical stimulation seems to be a consistent way to facilitate learning and memory processes, and Tuberomammillary lesion has been shown to improve intracranial self-stimulation behavior (ICSS), we suggest that lesions in the present experiment could have facilitated two-way active avoidance retention by enhancing the function of brain reward mechanisms.
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the Tuberomammillary Nucleus region as a reinforcement inhibiting substrate facilitation of ipsihypothalamic self stimulation by unilateral ibotenic acid lesions
Brain Research, 1993Co-Authors: Uwe Wagner, Pilar Seguratorres, Theo Weiler, Joseph P HustonAbstract:Abstract The Tuberomammillary Nucleus (TM), located in the posterior hypothalamic region, consists of five subgroups and is the only known source of brain histamine. Knowledge about the function of this Nucleus is still scarce. In a previous study we found an increase in the rate of ipsihemispheric hypothalamic self-stimulation following a dc lesion in the rostroventral part of this Nucleus, suggesting that this region has an inhibitory action on a neuronal reward system or on the brain's reinforcement mechanism. In the present study we examined whether this facilitating effect on reinforcement was due to the destruction of fibers passing through the lesion area or of intrinsic cells, by lesioning subgroups of the TM with ibotenic acid, an excitatory amino acid, that selectively destroys neural cell bodies, leaving fibers largely intact. Following such lesions in the rostroventral part of the TM the operant response rates increased over the six days of testing when the animals stimulated themselves in the lateral hypothalamus in the hemisphere located ipsilateral but not contralateral to the lesion. No significant changes in response rate occurred following the lesion in the caudal part of the ventral TM. The results indicate that the region influenced by the lesion exerts inhibitory control over lateral hypothalamic self-stimulation, and that it is possible that histamine-containing neurons are involved in this effect.
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amplification of rewarding hypothalamic stimulation following a unilateral lesion in the region of the Tuberomammillary Nucleus
Neuroscience, 1993Co-Authors: Uwe Wagner, H T Weiler, Joseph P HustonAbstract:Abstract The Tuberomammillary Nucleus, a cluster of cells in the posterior hypothalamus, is the only known source of brain histamine. Although this Nucleus is well described in terms of anatomy and neurochemistry, only little is known about its function. In the present study, the effect of a lesion in the region of this Nucleus on intracranial self-stimulation was examined. Rats were implanted bilaterally with stimulating electrodes in the lateral hypothalamus and unilaterally with one lesion electrode in the region of this Nucleus. After three days of baseline testing, half of the animals were given an electrolytic lesion. The animals were retested for six consecutive days, and thereafter weekly for another seven weeks. From the second day postlesion on, we unexpectedly found a gradual increase in response rate, which peaked on day 13 in the ipsilateral hemisphere only. Although there was no further increase over subsequent days, response rates remained elevated during the following seven weekly tests. The observed increase in lateral hypothalamic self-stimulation after an electrolytic lesion of the Tuberomammillary Nucleus is discussed in terms of an inhibitory system, possibly located in the region of this Nucleus which, when removed by the lesion, increased reinforcing effects of the electrical brain stimulation. The fact that the effects on self-stimulation were lateralized to one hemisphere rules out an interpretation in terms of unspecific “performance” variables that could influence rate of lever pressing.
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unilateral lesion in the Tuberomammillary Nucleus region behavioral asymmetries and effects of histamine precursor
Behavioural Brain Research, 1992Co-Authors: Hanstheo Weiler, Uwe Wagner, Joseph P HustonAbstract:The subnuclei of Tuberomammillary Nucleus are located in the posterior part of the hypothalamus adjacent to the basolateral surface of the mammillary bodies. The neurons of this Nucleus innervate extensive parts of the brain with transmitters, particularly with histamine. In fact, they represent the only source of histaminergic projections in the brain. The present study deals with the effects of a lesions in this region on behavior. Unilateral electrolytic direct current (DC) lesions in the Tuberomammillary Nucleus led to an asymmetry in thigmotactic scanning; i.e., at 11 days, but not 1 day postlesion, the rats scanned the walls of an open field more with the vibrissae contralateral to the lesion than with those of the ipsilateral side. Furthermore, they emitted more ipsiversive than contraversive wide angle turns. The behavioral asymmetries are, in general, opposite in direction to those induced by lesion of the neighboring lateral hypothalmus and substantia nigra, indicating that they are specific to the Tuberomammillary region destroyed. Application of the histamine precursor histidine led to a compensation of these asymmetries, suggesting that the Tuberomammillary's histaminergic efferents are functionally related to the lesion-induced behavioral effects.
R U Hasenohrl - One of the best experts on this subject based on the ideXlab platform.
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memory improvement by post trial injection of lidocaine into the Tuberomammillary Nucleus the source of neuronal histamine
Neurobiology of Learning and Memory, 1999Co-Authors: Christian Frisch, R U Hasenohrl, Joseph P HustonAbstract:Brain histamine is exclusively contained within and released from neurons whose cell bodies are clustered in the Tuberomammillary Nucleus (TM) of the posterior hypothalamus. This experiment examined the effects of a transient inactivation of the TM on inhibitory avoidance learning. Rats with chronically implanted cannulae were tested on a 1-trial step-through avoidance task. Immediately following training, the rats received unilateral intra-TM infusions (0.5 μl) of lidocaine (5 or 20 μg). Control groups included vehicle-injected rats and a group given an injection of 20 μg lidocaine 5 h after training. When tested 24 h later, rats treated with 20 μg lidocaine exhibited longer step-through latencies than vehicle-treated controls, indicative of superior learning of the task. The failure of the delayed post-trial injection of lidocaine to significantly influence step-through latencies indicates that the compound influenced learning by modulating memory storage processes rather than by acting on performance variables during retrieval of the task. Thus, inactivation of the TM by lidocaine can exert facilitatory effects on mnemonic processing, which might be related to a temporary reduction of histaminergic activity during the early phase of memory consolidation.
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anxiolytic like behavior after lesion of the Tuberomammillary Nucleus e2 region
Experimental Brain Research, 1998Co-Authors: Christian Frisch, R U Hasenohrl, J Krauth, Joseph P HustonAbstract:The Tuberomammillary Nucleus (TM), located in the posterior hypothalamic region, consists of five subgroups and is the only known source of brain histamine. In the present experiment, rats received bilateral ibotenic acid or sham lesions in the rostroventral part of the TM (E2-region). Three weeks later they were tested on the elevated plus-maze test of fear and anxiety. Lesions in the Tuberomammillary E2-region elevated the time spent on the open arms, as well as excursions into the end of the open arms, increased scanning over the edge of an open arm, and decreased risk-assessment from an enclosed arm. Thus, partial destruction of TM intrinsic neurons can induce anxiolytic-like effects which are possibly related to a lesion-induced reduction of histaminergic activity.
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facilitation of learning after lesions of the Tuberomammillary Nucleus region in adult and aged rats
Experimental Brain Research, 1998Co-Authors: Christian Frisch, R U Hasenohrl, H T Weiler, Helmut L Haas, H W M Steinbusch, Joseph P HustonAbstract:The Tuberomammillary Nucleus (TM) located in the posterior part of the hypothalamus is the main source of neuronal histamine in the central nervous system. Recent work from our laboratories has indicated an involvement of the TM region in neuronal plasticity and reinforcement processes. In the present study, we investigated the effects of TM lesions on the performance of adult and aged Wistar rats in a set of learning tasks, which differed in terms of complexity and reward contingencies (habituation learning, inhibitory avoidance, discrimination learning, Morris water maze). An improvement was found in every test applied, indicating that TM lesions seem to generally enhance learning and memory capacities independent of the special demands of a given task. Age-related learning deficits were strongly diminished. Immunohistochemistry revealed that the excitotoxic lesions used to destroy the TM region led to a marked decrease in the number of histamine-positive neurons in the vicinity of the injection site, indicating an involvement of the brain histaminergic system in the observed behavioral changes.
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the Tuberomammillary Nucleus projections in the control of learning memory and reinforcement processes evidence for an inhibitory role
Behavioural Brain Research, 1997Co-Authors: Joseph P Huston, Uwe Wagner, R U HasenohrlAbstract:Abstract The Tuberomammillary Nucleus (TM), a cluster of magnocellular cells in the posterior hypothalamus, is the main source of neuronal histamine in the brain. Although this Nucleus is well described in terms of anatomy and neurochemistry, only little is known about its function. Our earlier work showed that the TM projection system may be involved in behavioral asymmetries and behavioral recovery after unilateral manipulations of the brain. Using horseradish peroxidase (HRP) labeling we found an increase in strength (structure and/or activity) in the crossed and uncrossed Tuberomammillary-striatal projections in the course of recovery from behavioral asymmetries produced by unilateral removal of the rats' vibrissae, which were in the same direction as the asymmetries found in projections from the substantia nigra to the striatum. Experiments performed with unilateral lesions of the TM region provide evidence for an involvement of the TM system in reinforcement mechanisms. Unilateral destruction of the TM with direct current (DC) or ibotenic acid was found to increase the rate of lateral hypothalamic self-stimulation ipsilateral to the lesion site, suggesting that the TM (particularly the E2 subgroup in its rostra] part: may function as a reinforcement inhibiting neural substrate. Experiments performed with bilateral DC or ibotenic acid lesions of the TM region suggest a role of the Nucleus in learning and mnemonic processes. A bilateral electrolytic or neurotoxic lesion of the TM region was found to facilitate the performance of adult and behaviorally impaired aged rats in a variety of learning tasks, including a habituation paradigm, aversively motivated learning tasks and water mazes. Examination of the site of the neurotoxic lesion in the TM region with immunohistochemical techniques revealed a marked decline of histamine-staining neurons mainly in the rostral part of the TM Nucleus, suggesting that the facilitatory effects on reinforcement and mnemonic processes might be related to the destruction of TM intrinsic histaminergic cells. In summary, the present results indicate that the TM Nucleus is involved in neural plasticity and functional recovery following damage to the CNS and may function as an inhibitory neural substrate in the control of reinforcement and mnemonic processes.