Effect of local cholecystokinin-8 administration on extracellular levels of amino acids and glycolytic products monitored by in vivo microdialysis in the fronto-parietal cortex of the rat

Godukhin, O. V.; You, Zhi‐Bing; Herrera‐Marschitz, Mario; Goiny, Michel; Pettersson, Elisabeth; Hökfelt, Tomas; Ungerstedt, Urban

doi:10.1016/0304-3940(95)11711-5

Cited by 15 publications

(8 citation statements)

References 19 publications

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“…CCK-8S also increased extracellular Glu and GABA levels, but the effect on the latter was minor and not reproduced following administration of the solvent for CCK antagonists. As previously reported (Godukhin et al 1995), the effect of CCK-8S on Glu levels was inhibited by both CCK B and CCK A receptor antagonists. These results give further evidence for the hypothesis that CCK may act as a neurotransmitter/neuromodulator in the neocortex of the rat where CCK peptides are found at high concentration (Dockray 1980;Goltermann et al 1980), and are released in the form of CCK-8S following K + -depolarisation (Yaksh et al 1987;Meana et al 1991; see also You et al 1994c).…”

Section: Discussionsupporting

confidence: 59%

Cholecystokinin-8S increases dynorphin B, aspartate and glutamate release in the fronto-parietal cortex of the rat via different receptor subtypes

You

Godukhin

Goiny

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The effect of sulphated cholecystokinin-8 (CCK-8S) on extracellular dynorphin B, aspartate, glutamate and GABA levels in the rat fronto-parietal cortex was investigated with in vivo microdialysis. The peptide was infused through the microdialysis probe trying to mimic local CCK-8S release. Basal levels of dynorphin B were around 20 pM, aspartate 100 nM, glutamate 600 nM and GABA 30 nM. CCK-8S (10 microM) induced a approximately 3-fold increase in extracellular dynorphin B, aspartate and glutamate levels, while GABA levels were only slightly increased. The effect of CCK-8S was restricted to the stimulated neocortex. Systemic pretreatment with the CCKB antagonist, L-365, 260, but not with the CCKA antagonist, L-364, 718, significantly antagonised the effect of CCK-8S on cortical dynorphin B and aspartate release. However, both CCKA and CCKB antagonists inhibited the increase in cortical glutamate levels. Thus, the present results indicate that cortical CCK release exerts a stimulatory modulation on cortical dynorphin B and aspartate release via the CCKB receptor subtype, and on glutamate release via both CCKA and CCKB receptor subtypes. Considering electrophysiological evidence that CCK increases neuronal firing rates in many brain regions, it may be suggested that CCK represents a stimulatory system modulating the function of the neocortex.

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Section: Discussionsupporting

confidence: 59%

Cholecystokinin-8S increases dynorphin B, aspartate and glutamate release in the fronto-parietal cortex of the rat via different receptor subtypes

You

Godukhin

Goiny

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Furthermore, it has been demonstrated that CCK may increase endogenous glutamate and aspartate levels both in the rat frontoparietal cortex (Godukhin et al 1995) and hippocampus (Migaud et al 1994) through direct interaction with CCK B receptors. Interestingly, it has been recently reported that CCK may regulate dopamine release from anterior accumbal punches through an action on the glutamatergic system (Léna et al 1997); in addition there is in vivo evidence that dopamine release in the nucleus accumbens is under glutamatergic control through non-NMDA receptors (Imperato et al 1990).…”

Section: Discussionmentioning

confidence: 98%

Cholecystokinin (CCK) increases GABA release in the rat anterior nucleus accumbens via CCKB receptors located on glutamatergic interneurons

Lanza¹,

Makovec²

2000

Naunyn-Schmiedeberg's Arch Pharmacol

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The effects of cholecystokinin sulfate octapeptide (CCK-8S) on [3H]gamma-aminobutyric acid (GABA) release have been studied in the anterior side of the rat nucleus accumbens on tissue punches exposed in superfusion to 30 mM KCl. CCK-8S in a concentration dependent manner (10-3000 nM) increased K+-evoked [3H]GABA release (EC50=192 nM). The increase caused by 1 microM CCK-8S ranged from 37% to 42%. CR 2945, (beta-[2-[[2-(8-azaspiro[4.5]dec-8-ylcarbonyl)-4,6-dimethylp henyl]-amino]-2-oxoethyl]-(R)-1-naphthalenepropanoic acid), a potent and selective nonpeptidergic CCK(B) antagonist, concentration-dependently blocked CCK-8S effect (IC50=2.16 nM). CCK-8S-induced increase in [3H]GABA overflow was completely blocked by 1 microM tetrodotoxin. Both the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) and the N-methyl-D-aspartic acid (NMDA) receptor antagonist dizocilpine (MK-801) antagonized the CCK-8S effect. By contrast, (+)-bicuculline, a GABA(A) receptor antagonist, was completely ineffective. Phaclofen, a selective GABA(B) antagonist, increased K+-evoked [3H]GABA release but did not affect the facilitative effect of CCK-8S. Moreover, tetrodotoxin failed to block AMPA-evoked [3H]GABA release but completely prevented the effect of NMDA (Mg2+ free conditions). The data presented suggest that CCK(B) receptors modulating [3H]GABA release from anterior accumbal punches may not be present on GABAergic terminals but could be located on glutamatergic interneurons.

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“…The effects of two transport inhibitors, dihydrokainic acid (DHKA) (Johnston et For ex vivo tissue biochemistry see Tossman et al (1986), and Chen et al (1997). For in vivo microdialysis experiments see Godukhin et al (1995), Herrera-Marschitz et al (1996), You et al (1996a, b). , 1979) and L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) (Bridges et al, 1991) on striatal Glu and Asp levels, measured under basal and K+-depolarising conditions are shown in Table 2.…”

Section: On the Origin Of Extracellular Levels Of Glutamate And Asparmentioning

confidence: 99%

Release of endogenous excitatory amino acids in the neostriatum of the rat under physiological and pharmacologically-induced conditions

et al. 1998

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There is immunohistochemical evidence suggesting that glutamate (Glu) is released from nerve terminals and acts, via several receptor subtypes, as a major excitatory neurotransmitter in the cortico-striatal pathway of the rat. Aspartate (Asp) is also present in cortico-striatal neurons, but its role as a neurotransmitter has been questioned, since, in contrast to Glu, it has not been demonstrated in presynaptic vesicles. Glu and Asp can be found at submicroM concentrations in the extracellular compartment of most areas of the basal ganglia. Their concentrations are largely regulated by transport mechanisms, but also by a synaptotagmin-dependent exocytotic release, and are sufficiently high to occupy junctional and extrajunctional receptors. We have investigated whether Glu and Asp release in the neostriatum can be selectively modulated by different neuronal systems. Dopamine (DA) and cholecystokinin (CCK) selectively stimulate Asp release, via D1 and CCKB receptor subtypes, respectively. Also opioid kappa-agonists increase Asp release. We propose that the selective modulation of Asp release by D1-, CCKB- and kappa-agonists involves striatal neurons containing Asp, but not Glu. In contrast, local perfusion with the mu-opioid antagonist D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) increases both Glu and Asp release. This effect is probably exerted on cortico-striatal terminals, via presynaptic inhibitory mu-receptors. Thus, these results demonstrate that extracellular levels of Glu and Asp are modulated differentially by different neuronal systems, and suggest that in the neostriatum of the rat there are neuronal populations using Glu and/or Asp as messenger(s).

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Effect of local cholecystokinin-8 administration on extracellular levels of amino acids and glycolytic products monitored by in vivo microdialysis in the fronto-parietal cortex of the rat

Cited by 15 publications

References 19 publications

Cholecystokinin-8S increases dynorphin B, aspartate and glutamate release in the fronto-parietal cortex of the rat via different receptor subtypes

Cholecystokinin-8S increases dynorphin B, aspartate and glutamate release in the fronto-parietal cortex of the rat via different receptor subtypes

Cholecystokinin (CCK) increases GABA release in the rat anterior nucleus accumbens via CCKB receptors located on glutamatergic interneurons

Release of endogenous excitatory amino acids in the neostriatum of the rat under physiological and pharmacologically-induced conditions

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