Lateral habenular influence on dorsal raphe neurons

Ferraro, Giuseppe; Montalbano, Maria; Sardo, Pierangelo; Grutta, V La

doi:10.1016/0361-9230(96)00170-0

Cited by 91 publications

(35 citation statements)

References 27 publications

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“…In agreement with the anatomical circuitry, the electrical activity of the habenula has been shown to exert a powerful control over the activity of serotonin cells in the nucleus of dorsal raphe and dopamine cells in the ventral tegmental area and substantia nigra (Matsuda and Fujimura, 1992;Ferraro et al, 1996;Morris et al, 1999;Conley et al, 2002).…”

Section: The Maintenance and Termination Of The Ldapmentioning

confidence: 67%

“…For instance, a change in habenular activity in response to either local electrical stimulation or a local injection of substance P antagonist resulted in alterations in the activity of serotonin cells in the dorsal raphe nucleus (Matsuda and Eaton, 1990;Ferraro et al, 1996;Conley et al, 2002). Because the projections to the dorsal raphe nucleus arise mainly from the medial part of the lateral habenula, and this habenular area receives its input mainly from the limbic regions of the forebrain Nauta, 1977, 1979), it is probable that the medial part of the lateral habenula signals the activity change in the limbic forebrain to the dorsal raphe nucleus for regulating serotonin cell activity.…”

Section: Introductionmentioning

confidence: 99%

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Ionic Mechanism of Long-Lasting Discharges of Action Potentials Triggered by Membrane Hyperpolarization in the Medial Lateral Habenula

Su¹,

Kim²

2004

J. Neurosci.

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The activation of inhibitory synapses typically suppresses the generation of action potentials by hyperpolarizing the membrane of postsynaptic cells. In contrast to such conventional action of inhibitory synapses, we report here the ionic mechanism through which hyperpolarizing synapses trigger long-lasting discharges of action potentials that persist up to several tens of seconds. By using extracellular and intracellular recordings in slice preparations, we demonstrate that the activation of synaptic input from the limbic forebrain generates transient hyperpolarizing postsynaptic potentials in neurons of the medial part of the lateral habenular nucleus of the epithalamus. The synaptic hyperpolarization then sets off the coordinated activation of a distinct set of membrane ion channels and intracellular Ca 2ϩ mobilization by internal stores. The activation of these cellular events in distinct temporal order drives a persistent depolarization of habenular cells and promotes long-lasting discharges of tonic action potentials. The cells in the medial division of the lateral habenula project to dopamine and serotonin cells in the midbrain. We suggest that these habenular cells, by generating persistent action potentials in response to a transient increase in the activity of the limbic forebrain, may contribute to the regulation of the serotonergic and dopaminergic activity in the brain.

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Section: The Maintenance and Termination Of The Ldapmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Ionic Mechanism of Long-Lasting Discharges of Action Potentials Triggered by Membrane Hyperpolarization in the Medial Lateral Habenula

Su¹,

Kim²

2004

J. Neurosci.

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“…Thus, GABA inhibits serotonergic systems as it decreases the turnover rate of 5-HT in the raphe nuclei and it has also been reported that serotonergic neural activity was blocked by local application of GABA agonists in the raphe nuclei [58]. Besides the autoreceptor characteristics of 5-HT 1 receptor subtypes, these receptors may also serve as heteroreceptors expressed on GABA interneurons and serotonergic neurons also possess GABA heteroreceptors, which are involved in mediation of GABAergic inhibition [158].…”

Section: Reciprocal Innervation Between Serotonergic and Gabaergic Nementioning

confidence: 97%

The Pharmacology of the Neurochemical Transmission in the Midbrain Raphe Nuclei of the Rat

Hársing

2006

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3 H]5-HT taken up by raphe tissue indicated various pools where the neurotransmitter release may originate from these stores differed both in size and rate constant. 5-HT release originates not only from vesicles but also from cytoplasmic stores via a transporter-dependent exchange process establishing synaptic and non-synaptic neurochemical transmission in the serotonergic somatodendritic area. Manipulation of 5-HT transporter function modulates extracellular 5-HT concentrations in the raphe nuclei: of the SSRIs, fluoxetine was found 5-HT releaser, whereas citalopram did not exhibit this effect. Serotonergic projection neurons in the raphe nuclei possess inhibitory 5-HT 1A and 5-HT 1B/1D receptors and facilitatory 5-HT 3 receptors, which regulate 5-HT release in an opposing fashion. This observation indicates that somatodendritic 5-HT release in the raphe nuclei is under the control of several 5-HT homoreceptors. 5-HT 7 receptors located on glutamatergic axon terminals indirectly inhibit 5-HT release by reducing glutamatergic facilitation of serotonergic projection neurons. An opposite regulation of glutamatergic axon terminals was also found by involvement of the inhibitory 5-HT 7 and the stimulatory 5-HT 2 receptors as these receptors inhibit and stimulate glutamate release in raphe slice preparation, respectively, Furthermore, postsynaptic 5-HT 1B/1D heteroreceptors interact with release of GABA in inhibitory fashion in raphe GABAergic interneurons. Serotonergic projection neurons also possess glutamate and GABA heteroreceptors; NMDA and AMPA receptors release 5-HT, whereas both GABA A and GABA B receptors inhibit somatodendritic 5-HT release. Evidence was found for reciprocal interactions between serotonergic and glutamatergic as well as serotonergic and GABAergic innervations in the raphe nuclei. Serotonergic neurons in the raphe nuclei also receive noradrenergic innervation arising from the locus coeruleus and alpha-1 and alpha-2 adrenoceptors inhibited [3 H]5-HT release in our experimental conditions. The close relation between 5-HT transporter and release-mediating 5-HT autoreceptors was also shown by addition of L-deprenyl, a drug possessing inhibition of type B monoamine oxidase and 5-HT reuptake. L-Deprenyl selectively desensitizes 5-HT 1B but not 5-HT 1A receptors and these effects are not related to inhibition of 5-HT metabolism but rather to inhibition of 5-HT transporter.

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“…Although not as well characterized as other inputs to midbrain and hindbrain monoaminergic neurons, cells in the lateral habenula (LHb) project to the SN, VTA, and raphe nuclei (Bunney and Aghajanian, 1976;Herkenham and Nauta, 1979;Ferraro et al, 1996;Lecourtier and Kelly, 2007). Biochemical and electrophysiological studies indicate that the habenulomesencephalic pathway is capable of altering the activity of DA-containing neurons at a population level.…”

Section: Introductionmentioning

confidence: 99%

Lateral Habenula Stimulation Inhibits Rat Midbrain Dopamine Neurons through a GABAA Receptor-Mediated Mechanism

Shepard²

2007

Journal of Neuroscience

353

306

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Lateral habenular influence on dorsal raphe neurons

Cited by 91 publications

References 27 publications

Ionic Mechanism of Long-Lasting Discharges of Action Potentials Triggered by Membrane Hyperpolarization in the Medial Lateral Habenula

Ionic Mechanism of Long-Lasting Discharges of Action Potentials Triggered by Membrane Hyperpolarization in the Medial Lateral Habenula

The Pharmacology of the Neurochemical Transmission in the Midbrain Raphe Nuclei of the Rat

Lateral Habenula Stimulation Inhibits Rat Midbrain Dopamine Neurons through a GABAA Receptor-Mediated Mechanism

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