Serotonin inhibits the depolarization-evoked release of endogenous glutamate from rat cerebellar nerve endings

Maura, Guido; Ricchetti, Annamaria; Raiteri, Maurizio

doi:10.1016/0304-3940(86)90401-5

Cited by 35 publications

(13 citation statements)

References 14 publications

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“…KC1-evoked glutamate exocytosis from synaptosomes can be inhibited by agonists for GABA (Kato and Fukuda, 1982), serotonin (Maura et al, 1986(Maura et al, , 1991, dopamine (Maura et al, 1988), rc-opiate Terrian, 1991, 1992), muscarine (Marchi et al, 1989) and adenosine agonists Poli et al, 1991 ;Barrie and Nicholls, 1992). In a recent study (Barrie and Nicholls, 19921, we have investigated the ionic basis for the adenosine-mediated inhibition by comparing its effectiveness with KCl-and 4AP-mediated release.…”

Section: Modulation Of Calcium Channelsmentioning

confidence: 99%

The glutamatergic nerve terminal

Nicholls

1993

European Journal of Biochemistry

208

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Glutamate as a neurotransmitterThe human brain has about lolo neurones, each of which, on average, makes about 1000 synaptic contacts with other neurones. Of these l O I 3 synapses perhaps up to 90% utilize amino acids as their neurotransmitter. Glutamate is the major excitatory amino acid (acting predominantly on depolarizing post-synaptic receptors) while 4-aminobutyrate (GABA) and glycine are the major inhibitory transmitters (acting on hyper-polarizing receptors). As well as playing the dominant role in fast information transfer, glutamate is of particular interest in view of its involvement in current models of memory and learning (Bliss and Dolphin, 1982;Cotman et al., 1988;Collingridge and Singer, 1990) and because a pathological release of glutamate in brain ischaemia is neurotoxic and a major contributor to the damage caused under these conditions (Rothman and Olney, 1986;Choi, 1988 ;Meldrum and Garthwaite, 1990).A synapse has a pre-synaptic element responsible for the storage and release of transmitter and a post-synaptic element containing one or more classes of receptor for the transmitter. The potent combination of electrophysiology and molecular cloning has allowed a dramatic advance in our understanding of post-synaptic events. Three classes of post-synaptic ionotropic (possessing an integral ion channel) glutamate receptors have been identified and cloned: the 2-amino-3-hydroxy-5-methyl-4-isoxazole propionatekainate (AMPA/ KA) receptor Nakanishi et al., 1990;Sakmann, 1992), the high-affinity KA receptor (Egebjerg et al., 1991) and the N-methyl D-aSpartate (NMDA) receptor (Moriyoshi et al., 1991 ; Kumar et al., 1991 ;Barnard, 1992). Each can exist in many isoforms by combining subunits formed from distinct genes, by alternative splicing or by post-transcriptional modification (Monyer et al., 1991 ;Burnashev et al., 1992).The AMPNKA receptor is responsible for fast information transfer while the NMDA receptor is only operative when the post-synaptic membrane is independently depolarized by another receptor. This 'associative' behaviour of the latter is believed to underlie aspects of the learning process.

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Section: Modulation Of Calcium Channelsmentioning

confidence: 99%

The glutamatergic nerve terminal

Nicholls

1993

European Journal of Biochemistry

208

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“…Serotonin controls the response within the feedback loop involved in learning processes. Serotonergic fibres form a dense network of the cerebellar cortex, especially in Purkinje cells and granular layer [22,23,34]. Dopamine facilitates learning associated with intentional responses [47] through a cascade of cAMP and dopamine and cyclic AMP regulated phospho-protein-32 (DARP-32), by modifying the sensitivity of Purkinje cells GABA [21].…”

Section: Communicating Authormentioning

confidence: 99%

Original article Morphological and quantitative analysis of cerebellar cortical cells in Alzheimer’s disease

Stępień

Wierzba-Bobrowicz²,

Lewandowska³

et al. 2012

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A b s t r a c t Alzheimer's disease (AD) is a neurodegenerative amyloid disease, although a great deal of research has been done, its aetiology is still unknown. In Khachaturian's hypothesis on the involvement of calcium in the aetiology of Alzheimer's disease, particular attention is paid to the disorder of calcium metabolism. Ludo van Bogaert, describing AD, has drawn attention to the presence of a multi-system damage to the brain and described four forms of the disease, including two cerebellar types: cerebellar-pyramidal and cerebellar. The aim of our study was to analyze the expression of calcium-binding proteins (calbindin, calretinin, parvalbumin) in cortical neurons of the cerebellum in patients diagnosed with Alzheimer's disease (experimental group) and in a control group (patients without Alzheimer's disease). We performed the quantitative analysis of the density of Purkinje cells and Bergmann glial cells in the cerebellar cortex. We observed weak immunoreaction with a calretinin antibody in Lugaro cells, and with parvalbumin in Purkinje cells in the experimental group. A weaker expression of calcium-binding proteins in the experimental

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“…At present, we cannot ascribe the permanent labelling of the ML areas lacking Pc dendrite branches to specific structures. However, taking into consideration that serotonin modulates granule cell activity, which also depends on the presence of both 5-HT1A and 5-HT2A receptors (Maura et al, 1988) and on glutamatergic transmission with mossy fibres, possibly by modulation of glutamate release by 5-HT receptors localized on glutamate terminals (Maura et al, 1986), we can suppose that the labelling in the ML is ascribable to parallel fibres or ectopic mossy fibres. Ectopic mossy fibres in the ML were described in X-ray irradiated rats (Altman, 1982) and we have recently demonstrated the presence of ectopic granule cells in the ML after cisplatin injury (Pisu et al, 2004).…”

Section: Serotonin and Maturation Of The Cytoarchitecture Of The Cerementioning

confidence: 99%

“…Serotoninergic fibre input is the third in size, after the mossy and climbing fibre inputs, and affects all components of the cerebellar circuitry via serotoninergic receptors such as 5-HT1AR and 5-HT2AR. Serotonin has been described to modulate the release of glutamate in granule cells (Maura et al, 1986) and Purkinje cells (Strahlendorf and Hubbard, 1983;Lee et al, 1985), where it has been also reported that short-and long-term increase in GABAergic transmission involves 5-HT1A receptors Konishi, 1996, 1999).…”

Section: Introductionmentioning

confidence: 95%