Feedback Stimulation of Somatodendritic Serotonin Release: A 5-HT3 Receptor-Mediated Effect in the Raphe Nuclei of the Rat

Bagdy, Erzsébet; Sólyom, Sándor; Hársing, László G.

doi:10.1016/s0361-9230(97)00340-7

Cited by 34 publications

(22 citation statements)

References 31 publications

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“…The other way is through the reversal of dopamine carriers (Falkenburger et al, 2001). In the raphe nucleus, it is not clear whether vesicular release is contributing to somatodendritic release, but the occurrence of carrier-mediated release of serotonin has been reported previously (Bagdy et al, 1998). Increases in membrane capacitance in response to calcium influx have been found in isolated somata of dorsal root ganglia (Huang and Neher, 1996), indicating that, in these neurons, somatic release is vesicular and calcium dependent.…”

Section: Somatodendritic Secretion Of Retrograde Transmittersmentioning

confidence: 96%

“…Interestingly, dopamine acts on presynaptic GABAergic terminals (Radnikow and Misgeld, 1998). Also, in the raphe nucleus, somatodendritic release of serotonin (5-HT) affects presynaptic release of GABA (Bagdy et al, 1998;Bunin and Wightman, 1998;Liu et al, 2000). Although it is unknown whether in these nuclei changes in dopamine and serotonin release underlie changes in excitability and synchronous firing, retrograde signaling that leads to short-term synaptic plasticity may be a general concept.…”

Section: Somatodendritic Secretion Of Retrograde Transmittersmentioning

confidence: 99%

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Somatodendritic Secretion in Oxytocin Neurons Is Upregulated during the Female Reproductive Cycle

Kock¹,

Wierda²,

Bosman³

et al. 2003

J. Neurosci.

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During the female reproductive cycle, hypothalamic oxytocin (OT) neurons undergo sharp changes in excitability. In lactating mammals, bursts of electrical activity of OT neurons result in the release of large amounts of OT in the bloodstream, which causes milk ejection. One hypothesis is that OT neurons regulate their own firing activity and that of nearby OT neurons by somatodendritic release of OT. In this study, we show that OT neuron activity strongly reduces inhibitory synaptic transmission to these neurons. This effect is blocked by antagonists of both adenosine and OT receptors and is mimicked by OT application. Inhibition of soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex formation by tetanus toxin completely blocked the stimulation-induced reduction in inhibitory input, as did the calcium chelator BAPTA. During lactation, the readily releasable pool of secretory vesicles in OT cell bodies was doubled, and calcium currents were upregulated. This resulted in an increased inhibition of GABAergic synaptic transmission by somatodendritic release during lactation compared with the adult virgin stage. These results demonstrate that somatodendritic release is augmented during lactation, which is a novel form of plasticity to change the strength of synaptic transmission.

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Section: Somatodendritic Secretion Of Retrograde Transmittersmentioning

confidence: 96%

Section: Somatodendritic Secretion Of Retrograde Transmittersmentioning

confidence: 99%

Somatodendritic Secretion in Oxytocin Neurons Is Upregulated during the Female Reproductive Cycle

Kock¹,

Wierda²,

Bosman³

et al. 2003

J. Neurosci.

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show abstract

“…These are the spontaneous, slow firing activity of 5-HT neurons, the 5-HT release-mediated autoinhibition of the neurons and the excitatory and inhibitory afferent inputs mediated by non-5-HT receptors [126]. The autoinhibitory properties of serotonergic neurons, which include regulation of transmitter release and synthesis and neural firing, are determined by various metabotropic (5-HT 1A/1B/1D , 5-HT 2A/2C , 5-HT 7 ) and ionotropic (5-HT 3 ) 5-HT receptors [11,15,180]. Different 5-HT 1 receptor subtypes are present on 5-HT-containing neurons in the raphe nuclei and they inhibit 5-HT release [49,125,149,153] albeit their regulatory function in this process is different.…”

Section: Serotonergic Projection Neuronsmentioning

confidence: 99%

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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“…In spite of this promising perspective, experiments to demonstrate 5-HT 3 receptor-mediated 5-HT release in the amygdala do not appear to have been carried out. By contrast, a 5-HT 3 receptor-mediated enhancement of 5-HT release has been reported from other brain regions, for example, hippocampus, frontal cortex, hypothalamus, and raphé nucleus [22][23][24][25] . However, the presence of 5-HT 3 receptors on serotonergic nerve endings in these brain regions has not been demonstrated thus far.…”

Section: -Ht Releasementioning

confidence: 81%

5-HT3 receptors and neurotransmitter release in the CNS: a nerve ending story?

Hooft

2000

Trends in Neurosciences

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Feedback Stimulation of Somatodendritic Serotonin Release: A 5-HT3 Receptor-Mediated Effect in the Raphe Nuclei of the Rat

Cited by 34 publications

References 31 publications

Somatodendritic Secretion in Oxytocin Neurons Is Upregulated during the Female Reproductive Cycle

Somatodendritic Secretion in Oxytocin Neurons Is Upregulated during the Female Reproductive Cycle

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

5-HT3 receptors and neurotransmitter release in the CNS: a nerve ending story?

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