Effects of stimulating the dorsal raphe nucleus of the rat on neuronal activity in the dorsal lateral geniculate nucleus

Kayama, Yukihiko; Shimada, Soukichi; Hishikawa, Yasuo; Ogawa, Tetsuro

doi:10.1016/0006-8993(89)90002-4

Cited by 53 publications

(28 citation statements)

References 42 publications

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“…Our results show that 5-HT activates presynaptic receptors and decreases the strength of the sensory afferent input. Taken together, the combination of these multiple actions can result in a net decrease in relay neuron response to optic tract stimulation in certain situations, consistent with previous in vivo studies (Yoshida et al, 1984;Marks et al, 1987;Kayama et al, 1989).…”

Section: -Ht Receptor-mediated Presynaptic Modulation Of Retinogenicsupporting

confidence: 74%

“…Presynaptic inhibition may help to explain the observed effects of neuromodulators on visually evoked responses of relay neurons that are not accounted for by the known mechanisms of postsynaptic modulation. For example, in rats, stimulation of serotonergic inputs from the dorsal raphe nucleus or iontophoretic application of serotonin (5-HT) in the LGN in vivo decreases the response of relay neurons evoked by light or optic tract stimulation (Yoshida et al, 1984;Marks et al, 1987;Kayama et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Presynaptic Modulation of the Retinogeniculate Synapse

2003

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Modulatory projections from brainstem nuclei and intrinsic thalamic interneurons play a significant role in modifying sensory information as it is relayed from the thalamus to the cortex. In the lateral geniculate nucleus (LGN), neurotransmitters released from these modulatory inputs can affect the intrinsic conductances of thalamocortical relay neurons, thus altering their firing properties. Here, we show that in addition to postsynaptic effects, neuromodulators such as serotonin (5-HT) and GABA can act presynaptically to regulate neurotransmitter release at the synapse between retinal ganglion cells (RGCs) and relay neurons in the LGN, the retinogeniculate synapse. Activation of 5HT 1 and GABA B receptors significantly decreased EPSC amplitude. This inhibition was accompanied by a decrease in the extent of paired-pulse depression, suggesting that it is presynaptic in origin. In addition, fluorometric calcium measurements from retinal axon terminals labeled with Calcium Green-1 dextran revealed that 5HT 1 and GABA B receptor agonists decreased presynaptic calcium influx. Taken together, our data indicate that serotonin and GABA can act presynaptically to decrease calcium influx at the retinogeniculate synapse and modify transmission of visual information in the LGN.

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Section: -Ht Receptor-mediated Presynaptic Modulation Of Retinogenicsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Presynaptic Modulation of the Retinogeniculate Synapse

2003

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“…These fmdings to gether with our present results lead us to believe that 5-HT may now be confldently viewed as an inhibitory modulator of PGO activity. Furthermore, iontophoretic and raphe stimulation studies based on extracellular recordings in vivo have shown inhibitory effects of 5-HT on LGB neurons (Yoshida et al 1984;Marks et al 1987;Kayama et al 1989). More recently, intracellular studies in vitro have shown that the response of thalamocorti cal relay LGB neurons to 5-HT is a slow depolarizing cation current, the response being blocked by methyser gide, a 5-HT1,2 antagonist (McCormick and Pape 1990).…”

Section: Discussionmentioning

confidence: 99%

Dose-Related Suppression of REM Sleep and PGO Waves by the Serotonin-1 Agonist Eltoprazine

Quattrochi

Mamelak

Binder

et al. 1993

Neuropsychopharmacol

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Parenteral administration of the serotonin-1 agonist eltoprazine (0.0625 to 4.0 mglkg [0.0002 to 0.016 mmollkgJ) in freely moving cats produced significant suppression of electrophysiologic rapid eye movement (REM) sleep signs, ponto-geniculo-occipital (PGG) activity, and REM sleep behavior. The virtual total suppression of REM sleep (0.4%, 4.0 mglkg) and PGG wave activity (2 to 4 mglkg) in exchange for increasing amounts of non-REM (NREM) slow-wave sleep was a dose-dependent function of the amount of eltoprazine KEY WORDS: REM sleep; PGG waves; Serotonin; Eltoprazine Despite the large number of studies implicating sero tonin (5-HT) in the modulation of behavioral state, its exact role in the regulation of sleep and waking remains unclear. Pharmacological studies designed to elucidate the mechanism by which 5-HT neurotransmission aff ects behavioral state have reported paradoxical or contradictory results. While the listing of multiple 5-HT receptor subtypes (Glennon 1986;Peroutka 1988) has elucidated many of the pharmacological properties of ser otonin and underscores the complexity of its modula tory influences, this research has failed to provide a detailed understanding of behavioral state control and administered. Wakefulness was unaffected by eltoprazine regardless of dose. Concurrent with this dose-dependent suppression of REM was a dose-dependent increase in electroencephalographic synchrony and mean electromyographic amplitude. Since eltoprazine was found to shift the balance between REM and NREM sleep but did not change the balance between sleep and waking, it is a potentially useful tool for the investigation of serotonergic-cholinergic interaction.lNeuropsychopharmacology 8:7-13, 1993J neurophysiological phenomena. One reason for this failure is that surprisingly few studies have focused on how administration of receptor-specifIc 5-HT agonists affects sleep, particularly rapid eye movement (REM) sleep.We have previously observed suppression of REM sleep by the parenteral administration of the 5-HTl agonist eltoprazine (Quattrochi et al. 1990) and docu mented the REM rebound that followed discontinua tion of the drug. These findings support the hypothe sis that REM sleep is under the inhibitory control of serotonin (Hobson and Steriade 1986). We now dem onstrate that the suppression of REM sleep is dose de pendent and show that the dose-response properties of one relatively specifIc REM sleep sign, ponto geniculo-occipital (PGO) waves, are quantitatively sen sitive to eltoprazine.PGO waves are of particular interest because they are highly specifIc phenomena of REM sleep. Early studies by Jouvet (1969), Delorme et al. (1965), and De ment et al. (1973) indicated that PGO activity was sus ceptible to serotonergic inhibition; successive studies

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“…In most cells, the number ofpeaks of EPSPs did not change if stimulus frequency was increased. But in 5 of the 34 cells, EPSPs were unimodal at low stimulus frequencies (0.3-0.5 Hz) and bimodal (a second, later peak was evident) at higher stimulus frequencies (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). In terms of waveform and voltage sensitivity (see below), the first component of the bimodal EPSPs closely resembled unimodal EPSPs, but we have not yet categorized unimodal EPSPs in detail and therefore consider only bimodal EPSPs in the analysis below.…”

Section: Methodsmentioning

confidence: 99%

N-methyl-D-aspartate receptors contribute to excitatory postsynaptic potentials of cat lateral geniculate neurons recorded in thalamic slices.

Scharfman

Guido

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

146

102

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Neurons of the cat's dorsal lateral geniculate nucleus were recorded intracellularly to study the contribution of N-methyl-D-aspartate (NMDA) receptors to excitatory posty tic potentials (EPSPs) and low-threshold calcium spikes. EPSPs were evoked by stimulation of retinogeniculate axons in the optic tract and/or corticogeniculate axons in the optic radiations; EPSPs from both sources were similar. These EPSPs had one or two components, and the second component had several characteristics of NMDA receptor-mediated events. For example, EPSP amplitude decreased when neurons were hyperpolarized and increased when stimulus frequency was increased; these EPSPs could also be blocked reversibly by application of the selective NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV). We also studied the influence of NMDA receptors on low-threshold calcium spikes, which are large, voltage-and calcium-dependent depolarizations that are often accompanied by high-frequency action potential discharge. APV blocked synaptically activated lowthreshold calcium spikes, but APV had no effect on lowthreshold calcium spikes that were elicited by current i 'ection. Therefore, APV does not appear to have a direct effect on the T-type calcium channel that is involved in generation of low-threshold calcium spikes. The voltage and frequency dependence of the NMDA receptor-mediated component of the EPSPs, as well as its ability to trigger low-threshold calcium spikes, provide for complex signal processing in the lateral geniculate nucleus.To examine mechanisms underlying retinogeniculate and corticogeniculate transmission, we used a slice preparation to record from geniculate neurons intracellularly while stimulating the retinal or cortical input. Of specific interest was the possible role of N-methyl-D-aspartate (NMDA) receptors in generating excitatory postsynaptic potentials (EPSPs), since activation of this receptor is associated with complex events (5-7). Thus, we compared EPSPs of geniculate neurons with the distinctive characteristics of NMDA-mediated EPSPs that have been described in other preparations. For example, in rat neocortex (8, 9) and hippocampus (10-12), NMDA receptor-mediated EPSPs contribute a component to the EPSP that peaks at a relatively long latency after the stimulus. This late component decreases in amplitude upon membrane hyperpolarization, a phenomenon attributed to the voltage-dependent block by magnesium ions of the ion channel that is coupled to the NMDA receptor (13,14). It has also been shown that NMDA receptor-mediated EPSPs are enhanced by increasing frequency of stimulation (8,12). In addition, NMDA receptor-mediated events may be identified by use of the selective NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV). Our results suggest that NMDA receptors contribute to retinogeniculate and corticogeniculate transmission and may be one of the factors that provides the lateral geniculate nucleus with the capacity for complex information processing in response to both retina...

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Effects of stimulating the dorsal raphe nucleus of the rat on neuronal activity in the dorsal lateral geniculate nucleus

Cited by 53 publications

References 42 publications

Presynaptic Modulation of the Retinogeniculate Synapse

Presynaptic Modulation of the Retinogeniculate Synapse

Dose-Related Suppression of REM Sleep and PGO Waves by the Serotonin-1 Agonist Eltoprazine

N-methyl-D-aspartate receptors contribute to excitatory postsynaptic potentials of cat lateral geniculate neurons recorded in thalamic slices.

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