Regulation of the Release of Coexisting Neurotransmitters

Bartfai, Tamás; Iverfeldt, Kerstin; Fisone, Gilberto; Serfózó, Péter

doi:10.1146/annurev.pa.28.040188.001441

Cited by 280 publications

(129 citation statements)

References 6 publications

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“…This scenario probably is not realized at the lower 5 Hz frequency, because this stimulation may be insufficient to initiate significant endogenous CCK release from cortical neurons. This is in line with previous studies showing that in neurons in which classical neurotransmitters coexist with peptides, there exists a sort of "frequency code" because the neurotransmitter is released either alone (low frequency) or in combination with the peptide (high frequency) (Bartfai et al, 1988;Millhorn and Hök-felt, 1988). Furthermore, as the exogenous CCK-8S and CCK4 fragments enhance electrically evoked cortical GABA release even at the 10 Hz stimulation frequency, it seems likely that, under this experimental condition, endogenous CCK peptide is coreleased only to a small extent with GABA and thus does not fully occupy all the available CCK B receptors.…”

Section: Figsupporting

confidence: 91%

Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Ferraro

Beani²,

Trist³

et al. 1999

Journal of Neurochemistry

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Abstract:The effects of cholecystokinin (CCK) agonists and antagonists on spontaneous and electrically evoked endogenous GABA release from rat cerebral cortex slices were evaluated. Neither the nonselective and CCK B -selective receptor agonists CCK-8S (3-1,000 nM) and CCK-4 (3-1,000 nM), respectively, nor the selective CCK B and CCK A receptor antagonists GV 150013 (3-30 nM) and L-364,718 (10 -100 nM), respectively, significantly affected spontaneous GABA release. CCK-8S (1-1,000 nM) and CCK-4 (1-1,000 nM) increased the electrically (5 and 10 Hz)-evoked GABA release. On the contrary, GV 150013 (10 and 30 nM) significantly decreased the electrically evoked GABA release only when the slices were stimulated at the higher 10 Hz frequency. The CCK-8S-and CCK-4-induced increases in electrically evoked GABA release were counteracted by GV 150013, but not by L-364,718. Furthermore, GV 150013 at 3 nM shifted to the right the CCK-4 concentration-response curve, whereas at the higher 10 nM concentration it dramatically flattened the curve. Finally, in cortical slices obtained from rats chronically treated with GV 150013, the concentration-response curve of CCK-4 was shifted to the left and the peak effect of the peptide was significantly higher than that observed in naive animals. These results suggest that CCK increases electrically evoked, but not spontaneous, endogenous GABA release from rat cortical slices, possibly by activating local CCK B receptors. In addition, chronic treatment with the novel CCK B receptor antagonist GV 150013 leads to an enhanced responsiveness of cortical slices to CCK-4 application.

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Section: Figsupporting

confidence: 91%

Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Ferraro

Beani²,

Trist³

et al. 1999

Journal of Neurochemistry

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“…This model is in agreement with the frequency-dependent nature of galanin release. In contrast to classical neurotransmitters, which are released at low neuronal firing rates, neuropeptides such as galanin are released only during high neuronal firing, as might be expected under high stress provocation (Bartfai et al, 1988;Consolo et al, 1994;Hökfelt et al, 2000). Interestingly in this regard, GAL-R1 +/À mice demonstrated normal anxietylike behaviors on all tests.…”

Section: Discussionmentioning

confidence: 72%

Galanin GAL-R1 Receptor Null Mutant Mice Display Increased Anxiety-Like Behavior Specific to the Elevated Plus-Maze

Holmes

Kinney

Wrenn

et al. 2003

Neuropsychopharmacol

189

137

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The neuropeptide galanin coexists with norepinephrine and serotonin in neural systems mediating emotion. Previous findings suggested that galanin modulates anxiety-related behaviors in rodents. Three galanin receptor subtypes have been cloned; however, understanding their functions has been limited by the lack of galanin receptor subtype-selective ligands. To study the role of the galanin GAL-R1 receptor subtype in mediating anxiety-related behavior, we generated mice with a null mutation in the Galr1 gene. GAL-R1 À/À are viable and show no abnormalities in health, neurological reflexes, motoric functions, or sensory abilities. On a battery of tests for anxietylike behavior, GAL-R1 À/À showed increased anxiety-like behavior on the elevated plus-maze test. Anxiety-related behaviors on the light/dark exploration, emergence, and open field tests were normal in GAL-R1 À/À. This test-specific anxiety-like phenotype was confirmed in a second, independent cohort of GAL-R1 null mutant mice and +/+ controls. Principal components factor analysis of behavioral scores from 279 mice suggested that anxiety-like behavior on the elevated plus-maze was qualitatively distinct from behavior on other tests in the battery. In addition, exposure to the elevated plus-maze produced a significantly greater neuroendocrine response than exposure to the light/dark exploration test, as analyzed in normal C57BL/6J mice. These behavioral findings in the first galanin receptor null mutant mouse are consistent with the hypothesis that galanin exerts anxiolytic actions via the GAL-R1 receptor under conditions of relatively high stress.

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“…In preparations where electrically evoked release of co-existing transmitters can be quantified, it is found that increasing the frequency of electrical stimulation of terminals containing co-stored classical and neuropeptide transmitters causes a disproportionate increase in neuropeptide release relative to that of classical transmitter (Bartfai et al, 1988;Agoston et al, 1988). Since the terminal stores of the classical transmitter may be several orders of magnitude higher than the neuropeptide, and since the latter can only be replenished by axonal transport, the neuropeptide can therefore be used more sparingly than the classical transmitter.…”

Section: Differential Release Of Amino Acids and Rzeuropeptidesmentioning

confidence: 99%

“…Since the terminal stores of the classical transmitter may be several orders of magnitude higher than the neuropeptide, and since the latter can only be replenished by axonal transport, the neuropeptide can therefore be used more sparingly than the classical transmitter. This also implies that the mix of transmitters may vary not only by the acute stimulation frequency, but also chronically due to temporary depletion of peptide stores in the terminal (Bartfai et al, 1988).…”

Section: Differential Release Of Amino Acids and Rzeuropeptidesmentioning

confidence: 99%

The glutamatergic nerve terminal

Nicholls

1993

European Journal of Biochemistry

207

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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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Regulation of the Release of Coexisting Neurotransmitters

Cited by 280 publications

References 6 publications

Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Galanin GAL-R1 Receptor Null Mutant Mice Display Increased Anxiety-Like Behavior Specific to the Elevated Plus-Maze

The glutamatergic nerve terminal

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Regulation of the Release of Coexisting Neurotransmitters

Cited by 280 publications

References 6 publications

Effects of Cholecystokinin Peptides and GV 150013, a Selective CholecystokininB Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Effects of Cholecystokinin Peptides and GV 150013, a Selective CholecystokininB Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Galanin GAL-R1 Receptor Null Mutant Mice Display Increased Anxiety-Like Behavior Specific to the Elevated Plus-Maze

The glutamatergic nerve terminal

Contact Info

Product

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Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices

Effects of Cholecystokinin Peptides and GV 150013, a Selective Cholecystokinin_B Receptor Antagonist, on Electrically Evoked Endogenous GABA Release from Rat Cortical Slices