“…In agreement with anatomical data, most of the reports on this subject indicate that striatal cells are predominantly affected by dorsal raphe (DR) stimulation, with the median raphe stimulation being unable to alter striatal cell activity directly (Olpe and Koella, 1977;Davies and Tongroach, 1978). In addition, it has been found that suppression of spontaneous firing activity is the main response of cultured striatal cells (Yakel et al, 1988) in vivo following DRN stimulation, and excitation being observed in only about 10% of them.…”
Section: -Ht Modulation Of Striatal Activitysupporting
confidence: 68%
“…Nevertheless, a rebound excitation was observed in some cells that were initially inhibited. Local application of 5-HT was found to produce changes similar to that caused by raphe stimulation, and most of the cells responsive to the raphe stimulation were also affected by nigral stimulation (Davies and Tongroach, 1978). However, using intracellular recording techniques, Kitai and co-workers (Vandermaelen et al, 1979) found that DRN stimulation was consistently capable of generating excitatory postsynaptic potentials.…”
Section: -Ht Modulation Of Striatal Activitymentioning
Several recent studies have emphasized a crucial role for the interactions between serotonergic and dopaminergic systems in movement control and the pathophysiology of basal ganglia. These observations are supported by anatomical evidence demonstrating large serotonergic innervation of all the basal ganglia nuclei. In fact, serotonergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high concentration of serotonin (5-HT), with the substantia nigra pars reticulata receiving the greatest input. In this chapter, the distribution of different 5-HT receptor subtypes in the basal ganglia nuclei will be described. Furthermore, evidence demonstrating the serotonergic control of basal ganglia activity will be reviewed and the contribution of the different 5-HT receptor subtypes examined. The new avenues that the increasing knowledge of 5-HT in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. It is clear that these avenues will be fruitful, despite the disappointing results so far obtained by clinical studies with selective 5-HT ligands. Nevertheless, these studies have led to a great increase in the attention given to the neurotransmitters of the basal ganglia and their connections.
“…In agreement with anatomical data, most of the reports on this subject indicate that striatal cells are predominantly affected by dorsal raphe (DR) stimulation, with the median raphe stimulation being unable to alter striatal cell activity directly (Olpe and Koella, 1977;Davies and Tongroach, 1978). In addition, it has been found that suppression of spontaneous firing activity is the main response of cultured striatal cells (Yakel et al, 1988) in vivo following DRN stimulation, and excitation being observed in only about 10% of them.…”
Section: -Ht Modulation Of Striatal Activitysupporting
confidence: 68%
“…Nevertheless, a rebound excitation was observed in some cells that were initially inhibited. Local application of 5-HT was found to produce changes similar to that caused by raphe stimulation, and most of the cells responsive to the raphe stimulation were also affected by nigral stimulation (Davies and Tongroach, 1978). However, using intracellular recording techniques, Kitai and co-workers (Vandermaelen et al, 1979) found that DRN stimulation was consistently capable of generating excitatory postsynaptic potentials.…”
Section: -Ht Modulation Of Striatal Activitymentioning
Several recent studies have emphasized a crucial role for the interactions between serotonergic and dopaminergic systems in movement control and the pathophysiology of basal ganglia. These observations are supported by anatomical evidence demonstrating large serotonergic innervation of all the basal ganglia nuclei. In fact, serotonergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high concentration of serotonin (5-HT), with the substantia nigra pars reticulata receiving the greatest input. In this chapter, the distribution of different 5-HT receptor subtypes in the basal ganglia nuclei will be described. Furthermore, evidence demonstrating the serotonergic control of basal ganglia activity will be reviewed and the contribution of the different 5-HT receptor subtypes examined. The new avenues that the increasing knowledge of 5-HT in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. It is clear that these avenues will be fruitful, despite the disappointing results so far obtained by clinical studies with selective 5-HT ligands. Nevertheless, these studies have led to a great increase in the attention given to the neurotransmitters of the basal ganglia and their connections.
“…An inhibitory regulation of dopamine synthesis may occur directly through presynaptic receptors since 5-HT inhibits the synthesis of dopamine from tyrosine in striatal synaptosomes (de Belleroche and Bradford, 1980). The inhibitory effect of both 5-HT and dorsal raph6 stimulation on cell firing in the striatum is reversed by the peripheral 5-HT antagonist, methysergide (Davies and Tongroach, 1978) as well as the inhibition of dopamine synthesis by 5-HT seen i n vitro (de Belleroche and Bradford, 1980). However, although these and other reports (Segal, 1976) point to an antagonist action of drugs such as methysergide and cyproheptadine at central 5-HT receptors, an agonist effect is also seen in electrophysiological studies (Haigler and Aghajanian, 1974) and at high drug concentrations i n vitro (de Belleroche and Bradford, 1980).…”
SummaryThe interaction between 5-hydroxytryptamine (5-HT) and the release of dopamine and acetylcholine in the nucleus accumbens of rat was investigated. 5-HT (20/~M) significantly decreased levels of [3H]-dopamine synthesized from [3H]-tyrosine. 5-HT also enhanced the release of [~4C]-dopamine at all concentrations of K + tested (up to 34 raM). The maximal effect of 5-HT occurred at 15 mM K + and was reversed by methysergide (3/zM). Increasing concentrations of Ca 2+ facilitated the releasing effect of 5-HT up to 1.2 mM Ca 2+. In contrast, 5-HT had an inhibitory effect on the K+-evoked release of [3H]-acetylcholine synthesized from [3H]-choline. 5-HT was not effective at non-depolarizing concentrations of K +. Increasing the external Ca 2+ concentration to 2.5 mM overcame the inhibition of [3H]-acetylcholine release due to 5-HT. These results indicate that 5-HT has at least two actions in the nucleus accumbens, one which is a methysergidesensitive facilitatory action on dopamine release promoted by Ca 2+ entry and a second, inhibitory effect on the K+-evoked release of acetylcholine, which is not blocked by methysergide and appears to operate by reducing Ca 2+ influx.
“…Although there have been a number ofelectrophysiological studies using extracellular recording where excitatory amino acids have been applied by micro-ionophoresis to neurones in the caudate nucleus, most of these agents were used in order to create a background of firing against which inhibitory drugs could be tested (Ben-Ari & Kelly, 1976;Davies & Tongroach, 1978, 1979Fry, Zieglgaensberger & Herz, 1980;Jones, 1981;McLennan & York, 1966;Norcross & Spehlmann, 1981;Woodruff, McCarthy & Walker, 1976). Only a few authors directly addressed the question of the specificity of the effects of excitatory amino acids (Spencer, 1976;Stone, 1979).…”
SUMMARY1. The electrical activity of caudate neurones was recorded with intracellular electrodes in halothane anaesthetized cats. Agonists and antagonists of excitatory amino acid receptors were applied by micro-ionophoresis and their effects on membrane-and action potentials and on cortically evoked synaptic potentials evaluated.2. The agonists, L-aspartate (asp), L-glutamate (glu), N-methyl-DL-aspartate (NMA), quinolinate and quisqualate all depolarized the membrane, caused repetitive firing, reduced the apparent amplitude of the cortically evoked excitatory postsynaptic potentials (e.p.s.p.s) and increased the amplitude of the associated inhibitory post-synaptic potential. Two of the agonists, NMA and quinolinate, additionally caused the appearance of up to 500 ms long depolarizations (plateaus) on the falling phase of action potentials. These plateaus were seen in about two-thirds of the cells in this sample while in the other third the excitatory effects of NMA and quinolinate were indistinguishable from those of glu and quisqualate.3. The N-methyl-D-aspartate (NMDA) receptor antagonist D-a-aminoadipate (DAA) reversibly inhibited the effects of NMA and quinolinate but only on those cells where these two agents evoked action potential plateaus while on the same cells the effects of asp, glu and quisqualate were either only weakly antagonized or not affected. On cells not displaying plateaus to NMA or quinolinate none of the effects of the agonists could be antagonized by DAA. DAA applications that completely antagonized the effects of NMA never reduced the amplitudes of cortically evoked e.p.s.p.s.4. Cis-2,3-piperidine dicarboxylate also blocked the effects of NMA and asp at low application currents while at higher currents it enhanced the effects of glu or asp although still retaining its NMA antagonistic activity.5. High-frequency stimulation of the cortico-caudate pathway resulted in longlasting depolarizations and repetitive firing, but plateaus of the type caused by NMA or quinolinate were not seen.
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