The modulation of excitatory amino acid responses by serotonin in the cat neocortexin vitro

Nedergaard, Steen; Engberg, I.; Flatman, J. A.

doi:10.1007/bf00733789

Cited by 75 publications

(32 citation statements)

References 26 publications

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“…This suggestion is consistent with evidence showing that blocking phosphatidylinositol turnover or elevating Ca 2ϩ levels affects plasticity in the visual cortex (17). In addition, 5-HT has been shown to facilitate the excitatory actions of N-methyl-Daspartate and glutamate in cat and rat neocortical slices (18,19). The enhanced N-methyl-D-aspartate response evoked by 5-HT application was long lasting and irreversible (19).…”

Section: Discussionsupporting

confidence: 88%

Columnar distribution of serotonin-dependent plasticity within kitten striate cortex

Kojic

Dyck

et al. 2000

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

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Recent studies have identified the potential for an important role for serotonin (5-HT) receptors in the developmental plasticity of the kitten visual cortex. 5-HT 2C receptors are transiently expressed in a patchy fashion in the visual cortex of kittens between 30 -80 days of age complementary to patches demarcated by cytochrome oxidase staining. 5-HT, operating via 5-HT2C receptors, increases cortical synaptic plasticity as assessed both in brain slices and in vivo. Herein, we report that bath application of 5-HT substantially increases the probability of long-term potentiation within 5-HT 2C receptor-rich zones of cortex, but this effect is not observed in the 5-HT 2C receptor-poor zones. Instead, in these zones, 5-HT application increases the probability of long-term depression. These location-specific effects of 5-HT may promote the formation of compartment-specific cortical responses. S pecific, transient, regional, laminar, and columnar changes in the distribution of neurotransmitter-specific afferents and receptors have been shown to occur during the critical period of increased visual cortex plasticity (1-4). Fig. 1 summarizes autoradiographic and histochemical studies showing that, during the critical period, the kitten visual cortex transiently expresses a number of neurochemical markers in a columnar fashion. This columnar, biochemical architecture consists of two sets of complementary columns: one set is enriched in 5-HT 2C and 5-HT 2A receptors along with synaptic zinc, whereas the other expresses increased levels of CO and acetylcholinesterase (3, 4). Among over 30 neurotransmitter receptors that have been studied within the visual cortex (1, 2), only the 5-HT receptors noted above have been found to concentrate into columns within the developing cortex.A special relationship between this 5-HT receptor system and the use-dependent plasticity of visual cortex is reinforced by studies showing that these receptor columns do not form in kittens in which one eye was removed early in life or in animals that were deprived of vision by dark rearing (1, 5). In addition, studies in developing kittens have shown that blockade of 5-HT 2C receptors with mesulergine reduces the activitydependent binocular competition that normally occurs when one eye is deprived of vision (6).Working in brain slices taken from visual cortex of 60-to 80-day-old kittens, we found that low-frequency stimulation (LFS) of the white matter (1 Hz, 15 min) rarely induced long-term potentiation (LTP) or long-term depression (LTD) in layer IV (7). At these ages, however, bath application of 5-HT markedly facilitated the induction of both LTP and LTD. The effects of 5-HT on both LTP and LTD were blocked by the 5-HT 2C antagonist mesulergine (7). Although the general effect of 5-HT application was clearly to increase the probability of long-term changes in response to electrical stimulation, we could not predict the variety of effects that were mediated by 5-HT (sometimes LTP, sometimes LTD, and sometimes no change).We hypothesized that th...

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Section: Discussionsupporting

confidence: 88%

Columnar distribution of serotonin-dependent plasticity within kitten striate cortex

Kojic

Dyck

et al. 2000

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

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“…Serotonin also increased the proportion of glutamate containing neurons in embryonic cortical slices without affecting the proportion of other neuronal or glial cell types [72]. In vitro electrophysiologic studies demonstrated that exogenous application of 5-HT produces enhanced excitatory NMDA-evoked responses in rat [98] and cat [89] neocortical slices. Rodent studies in vivo showed that 5-HT was present during critical periods of postnatal rat [41,78,90] and mouse [59] cortical development and shows a more prevalent peak in male BALB/CbyJ mice [31].…”

Section: Discussionmentioning

confidence: 92%

Modeling early cortical serotonergic deficits in autism

Boylan

Blue

Höhmann

2007

Behavioural Brain Research

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Autism is a developmental brain disorder characterized by deficits in social interaction, language and behavior. Brain imaging studies demonstrate increased cerebral cortical volumes and micro-and macroscopic neuroanatomic changes in children with this disorder. Alterations in forebrain serotonergic function may underlie the neuroanatomic and behavioral features of autism. Serotonin is involved in neuronal growth and plasticity and these actions are likely mediated via serotonergic and glutamatergic receptors. Few animal models of autism have been described that replicate both etiology and pathophysiology. We report here on a selective serotonin (5-HT) depletion model of this disorder in neonatal mice that mimics neurochemical and structural changes in cortex and, in addition, displays a behavioral phenotype consistent with autism. Newborn male and female mice were depleted of forebrain 5-HT with injections of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the bilateral medial forebrain bundle (mfb). Behavioral testing of these animals as adults revealed alterations in social, sensory and stereotypic behaviors. Lesioned mice showed significantly increased cortical width. Serotonin immunocytochemistry showed a dramatic long-lasting depletion of 5-HT containing fibers in cerebral cortex until postnatal day (PND) 60. Autoradiographic binding to high affinity 5-HT transporters was significantly but transiently reduced in cerebral cortex of 5,7-DHT-depleted mice. AMPA glutamate receptor binding was decreased at PND 15. We hypothesize that increased cerebral cortical volume and sensorimotor, cognitive and social deficits observed in both 5-HT-depleted animals and in individuals with autism, may be the result of deficiencies in timely axonal pruning to key cerebral cortical areas.

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“…Activation of G-protein complexes requires Mg2+ (Birnbaumer et al, 1990;Litosch, 1991); removal of extracellular Mg2 + which presumably lowers the concentration of Mg2+ in the cytosol (Heinonen & Akerman, 1986), is sufficient to depress the muscarinic AChR-evoked depolarization of neocortical neurones (El-Beheiry & Puil, 1990). Thus, it is plausible that the Mg2+-dependence of the facilitation induced by G-protein coupled receptors reflects the regulatory role of Mg2+ in signal transduction associated with these receptors, rather than loss of voltage-dependence at the NMDA receptor-gated ion channel (Chen & Huang, 1992; see also Nedergaard et al, 1987). Such a mechanism would account for the insensitivity of the calcimycin facilitation to the reduction in Mg2+.…”

Section: Discussionmentioning

confidence: 99%

Action of 5‐hydroxytryptamine in facilitating N‐methyl‐D‐aspartate depolarization of cortical neurones mimicked by calcimycin, cyclopiazonic acid and thapsigargin

Rahman

Neuman

1996

British J Pharmacology

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1 The ability of calcimycin, cyclopiazonic acid and thapsigargin to facilitate the N-methyl-D-aspartate (NMDA)-mediated depolarization of cortical projection neurones was investigated by use of grease-gap recording and the results compared with the facilitation that results from activation of 5-hydroxytryptamine2A receptors.2 Calcimycin (0.25 to 3 gM), cyclopiazonic acid (5 to 30 gM), and thapsigargin (10 to 300 nM) reversibly facilitated the NMDA (50 gM)-induced depolarization in the presence of tetrodotoxin. The concentration-response relationships were bell-shaped with a mean enhancement of 550% for calcimycin(1 gM) and approximately 400% for cyclopiazonic acid (20 gM) and thapsigargin (100 nM). At the highest concentration of each agent tested, no facilitation was observed.3 Chlorpromazine (1 gM) partially restored a facilitation at 3 gM calcimycin and 300 nM thapsigargin.Myo-inositol (10 mM) and 100 nM staurosporine were both ineffective in this regard. 4 The depolarization elicited by 10 gM quisqualate or 5 gM kainate was not facilitated by 10 pM cyclopiazonic acid.5 Calcimycin (0.5 gM), cyclopiazonic acid (20 gM), and thapsigargin (100 nM) elicited a significant facilitation in the presence of an antagonist cocktail consisting of D,L-2-amino-3-phosphonopropionic acid, prazosin, ritanserin, and scopolamine, although the magnitude of the facilitation was reduced. 6 Facilitation of the NMDA depolarization elicited by both 30 gM 5-hydroxytryptamine and 10 pM phenylephrine was eliminated in nominally Mg2"-free medium. In contrast, the facilitation induced by 0.5 gM calcimycin remained intact.7 Bis-(o-aminophenoxy)-ethane-N,N,N,N, tetraacetic acid aminoethoxy (50 gM) or perfusion with nominally Ca2+-free medium eliminated facilitation of the NMDA depolarization induced by 30 gM 5-hydroxytryptamine and 100 nM thapsigargin. 8 The facilitation induced by both 30 gM 5-hydroxytryptamine and 1 guM calcimycin was reduced in a concentration-dependent manner by nifedipine (1 to 10 gM).9 Calcimycin, cyclopiazonic acid and thapsigargin facilitate the NMDA depolarization in a manner which closely mimics the facilitation induced by 5-hydroxytryptamine. It is concluded that enhancement of the NMDA depolarization at cortical projection neurones results from an elevation of Ca2+ in the cytosol and that several sources of Ca2+ contribute to the facilitation.

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The modulation of excitatory amino acid responses by serotonin in the cat neocortexin vitro

Cited by 75 publications

References 26 publications

Columnar distribution of serotonin-dependent plasticity within kitten striate cortex

Columnar distribution of serotonin-dependent plasticity within kitten striate cortex

Modeling early cortical serotonergic deficits in autism

Action of 5‐hydroxytryptamine in facilitating N‐methyl‐D‐aspartate depolarization of cortical neurones mimicked by calcimycin, cyclopiazonic acid and thapsigargin

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