Serotonin (5-HT) release in the dorsal raph� and ventral hippocampus: Raph� control of somatodendritic and terminal 5-HT release

Matos, F. Fátima; Urban, Caitlin; Yocca, Frank D.

doi:10.1007/bf01292626

Cited by 63 publications

(37 citation statements)

References 34 publications

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“…These may release NA in an impulse-dependent manner, as observed in the forebrain (L 'Heureux et al, 1986). Likewise, most previous reports support the notion that the 5-HT release in the DR varies in parallel with serotonergic activity Artigas, 1996, Casanovas et al, 1997;Matos et al, 1996;Celada et al, 2001). As previously reported in the hippocampus of awake rats (Done and Sharp, 1994), 8-OH-DPAT increased NA release in the DR.…”

Section: Methodological Aspectssupporting

confidence: 69%

Control of 5-Hydroxytryptamine Release in the Dorsal Raphe Nucleus by the Noradrenergic System in Rat Brain. Role of α-Adrenoceptors

Bortolozzi

Artigas

2002

Neuropsychopharmacol

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The interactions between the brainstem serotonergic (5-hydroxytryptamine, 5-HT) and noradrenergic (NA) systems are important for the pathophysiology and treatment of affective disorders. We examined the influence of a-adrenoceptors on 5-HT and NA release in the rat dorsal raphe nucleus (DR) using microdialysis. 5-HT and NA concentrations in DR dialysates were virtually suppressed by TTX and increased by veratridine. The local and systemic administration of the a 1 -adrenoceptor antagonist prazosin reduced the DR 5-HT output but not that of NA. The maximal 5-HT reduction induced by local prazosin administration (À78% at 100 mM) was more marked than by its systemic administration (À43% at 0.3 mg/kg). The local application of NA and desipramine, to increase the tone on DR a 1 -adrenoceptors, did not enhance 5-HT release. The local (100 mM) or systemic (0.1-1 mg/kg s.c.) administration of clonidine reduced 5-HT and NA release (À48 and À79%, respectively, at 1 mg/kg), an effect reversed by RX-821002, which by itself increased both amines when given systemically. DSP-4 pretreatment prevented the effects of clonidine on 5-HT, suggesting the participation of a 2 -adrenoceptors on NA elements. Moreover, the systemic effect of clonidine on 5-HT (but not NA) was cancelled by lesion of the lateral habenula and by anesthesia, and was slightly enhanced by cortical transection. These data support the view that a 1 -adrenoceptors in the DR tonically stimulate 5-HT release, possibly at nearly maximal tone. Likewise, the 5-HT release is modulated by a 2 -adrenoceptors in NA neurons and in forebrain areas involved in the distal control of 5-HT neurons.

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Section: Methodological Aspectssupporting

confidence: 69%

Control of 5-Hydroxytryptamine Release in the Dorsal Raphe Nucleus by the Noradrenergic System in Rat Brain. Role of α-Adrenoceptors

Bortolozzi

Artigas

2002

Neuropsychopharmacol

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“…Also, the application of R(ϩ)baclofen in the DRN reduced the striatal 5-HT output. These changes may be attributed to the inhibition of firing activity of serotonergic neurons by GABA A and GABA B receptor activation (Gallager and Aghajanian, 1976;Innis and Aghajanian, 1987) since the 5-HT release in the DRN and forebrain is sensitive to the propagation of nerve impulses (Carboni and Di Chiara, 1989;Sharp et al, 1990;Matos et al, 1996). The remarkable decrease of the 5-HT release in striatum after the application of 1 µM GABA in the DRN suggests a very high sensitivity of serotonergic neurons to the action of this neurotransmitter.…”

Section: Dual Action Of Baclofen On Serotonergic Neuronsmentioning

confidence: 90%

“…Also, the activation of 5-HT 1A receptors, coupled to the same effector system as GABA B receptors (Innis et al, 1988;Williams et al, 1988), results in a reduction of the 5-HT output in the DRN (Matos et al, 1996;Casanovas et al, 1997). This discrepancy could be due to a preferential action of baclofen on GABA B receptors located on inhibitory GABAergic inputs to serotonergic neurons (Wang et al, 1992, Jolas andAghajanian, 1997).…”

Section: Dual Action Of Baclofen On Serotonergic Neuronsmentioning

confidence: 94%

Dual control of dorsal raphe serotonergic neurons by GABAB receptors. Electrophysiological and microdialysis studies

Abellán¹,

Jolas

Aghajanian

et al. 2000

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We assessed the role of GABA(B) receptors in the control of serotonergic (5-HT) neurons of the dorsal raphe nucleus (DRN) by using microdialysis in vivo and intra- and extracellular recording in vitro in the rat. The GABA(B) agonist R(+)baclofen (but not the inactive S(-)enantiomer) enhanced the 5-HT output in the DRN (4. 7-fold at 15 mg/kg s.c.) and, to a much lesser extent, striatum of unanesthetized rats. Phaclofen (2 mg/kg s.c.) antagonized the effects of 6 mg/kg R(+)baclofen in dorsal striatum. Using dual-probe microdialysis, R(+)baclofen (0.1-100 microM) applied in the DRN enhanced the local 5-HT output (4.5-fold at 100 microM) but decreased that in striatum at 100 microM. At concentrations higher than 100 microM there was a moderate decrement in the elevation of 5-HT in the DRN. In midbrain slices, bath R(+)baclofen exerted a biphasic effect on DRN 5-HT neurons. Consistent with a reduced striatal 5-HT release when infused in the DRN, R(+)baclofen (0.1-30 microM) induced an outward current in 5-HT neurons (IC(50) = 1.4 microM). Lower R(+)baclofen concentrations (0.01-1 microM) preferentially reduced GABAergic inhibitory postsynaptic currents induced by N-methyl-D-aspartate (20 microM) in 5-HT neurons (IC(50) = 72 nM). Using extracellular recordings, R(+)baclofen (300 nM) enhanced the ability of NMDA to induce firing in a subpopulation of serotonergic neurons. These results are consistent with a preferential activation by a low concentration of R(+)baclofen of presynaptic GABA(B) receptors on GABAergic afferents that could disinhibit 5-HT neurons and increase 5-HT release.

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“…However, recent studies have shown that dendritic dopamine and serotonin release are also fully TTX-and calcium-dependent (Matos et al, 1996;Santiago and Westerink, 1992).…”

Section: Ttx-dependencymentioning

confidence: 99%

Brain microdialysis of GABA and glutamate: What does it signify?

Timmerman

Westerink

1997

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376

194

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Microdialysis has become a frequently used method to study extracellular levels of GABA and glutamate in the central nervous system. However, the fact that the major part of GABA and glutamate as measured by microdialysis does not fulfill the classical criteria for exocytotic release questions the vesicular origin of the amino acids in dialysates. Glial metabolism or reversal of the (re)uptake sites has been suggested to be responsible for the pool of nonexocytotically released amino-acid transmitters that seem to predominate over the neuronal exocytotic pool. The origin of extracellular GABA and glutamate levels and, as a consequence, the implications of changes in these levels upon manipulations are therefore obscure. This review critically analyzes what microdialysis data signify, i.e., whether amino-acid neurotransmitters sampled by microdialysis represent synaptic release, carrier-mediated release, or glial metabolism. The basal levels of GABA and glutamate are virtually tetrodotoxin- and calcium-independent. Given the fact that evidence for nonexocytotic release mediated by reversal of the uptake sites as a release mechanism relevant for normal neurotransmission is so far limited to conditions of "excessive stimulation," basal levels most likely reflect a nonneuronal pool of amino acids. Extracellular GABA and glutamate concentrations can be enhanced by a wide variety of pharmacological and physiological manipulations. However, it is presently impossible to ascertain that the stimulated GABA and glutamate in dialysates are of neuronal origin. On the other hand, under certain stimulatory conditions, increases in amino-acid transmitters can be obtained in the presence of tetrodotoxin, again suggesting that aspecific factors not directly related to neurotransmission underlie these changes in extracellular levels. It is concluded that synaptic transmission of GABA and glutamate is strictly compartmentalized and as a result, these amino acids can hardly leak out of the synaptic cleft and reach the extracellular space where the dialysis probe samples.

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Serotonin (5-HT) release in the dorsal raph� and ventral hippocampus: Raph� control of somatodendritic and terminal 5-HT release

Cited by 63 publications

References 34 publications

Control of 5-Hydroxytryptamine Release in the Dorsal Raphe Nucleus by the Noradrenergic System in Rat Brain. Role of α-Adrenoceptors

Control of 5-Hydroxytryptamine Release in the Dorsal Raphe Nucleus by the Noradrenergic System in Rat Brain. Role of α-Adrenoceptors

Dual control of dorsal raphe serotonergic neurons by GABAB receptors. Electrophysiological and microdialysis studies

Brain microdialysis of GABA and glutamate: What does it signify?

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