Cholecystokinin-8 increases K+-evoked [3H]γ-aminobutyric acid release in slices from various brain areas

Mora, Miguel Pérez de la; Hernández-Gómez, Ana María; Méndez-Franco, J; Fuxé, Kjell

doi:10.1016/0014-2999(93)90029-h

Cited by 41 publications

(20 citation statements)

References 21 publications

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“…This is consistent with the CCK receptor identified in the modulation of [ 3 H]GABA release in the hippocampus (Perez de la Mora et al, 1993), and with autoradiographic studies demonstrating that the CCK B receptor subtype is predominant in the hippocampal formation (Woodruff et al, 1991;Bohme et al, 1988). In addition, previous reports of CCK actions in the hippocampus suggest that they occur through activation of the CCK B receptor (Bohme et al, 1988(Bohme et al, , 1989Migaud et al, 1994;Miller and Lupica, 1994), and this receptor has been implicated in most studies of excitatory effects of CCK throughout the CNS (Boden and Hill, 1988;Bohme et al, 1988;Branchereau et al, 1993).…”

Section: Pharmacology Of Cck-8s Actions On Interneuronssupporting

confidence: 73%

“…However, other studies have shown that CCK-8S could either inhibit population spikes (MacVicar et al, 1987) or have no effect on these responses (Miller and Lupica, 1994). Given these inconsistencies and the observation that CCK-8S can increase GABA release in both the cerebral cortex and hippocampus (Sheehan and De Belleroche, 1985;Perez de la Mora et al, 1993), we hypothesized that at least some of its effects may be on local circuit inhibitory cells. This study was limited to interneurons in the stratum radiatum, because high levels of CCK are found there (Greenwood et al, 1981;Somogyi et al, 1984;Kosaka et al, 1985), and because these cells are easily distinguished from pyramidal neurons residing in stratum pyramidale.…”

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confidence: 99%

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Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Miller¹,

Hoffer²,

Svoboda³

et al. 1997

J. Neurosci.

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Cholecystokinin (CCK) is found co-localized with the inhibitory neurotransmitter GABA in interneurons of the hippocampus. Also, CCK receptors are found in abundance in this brain region. The possibility that CCK alters interneuron activity was examined using whole-cell current-and voltage-clamp recordings from visualized interneurons in the stratum radiatum of area CA1 in rat hippocampal slices. The effect of CCK on GABA-mediated IPSCs was also determined in pyramidal neurons. The sulfated octapeptide CCK-8S increased action potential frequency or generated inward currents in the majority of interneurons. These effects of CCK persisted in the presence of tetrodotoxin and cadmium, suggesting that they were direct. Current-voltage plots revealed that CCK-8S inhibited a conductance that was linear across command potentials and reversed near the equilibrium potential for K ϩ ions. The K ϩ channel blocker tetraethylammonium (10 mM) generated inward currents similar to those initiated by CCK, and it occluded the effect of the peptide. BaCl 2 (1 mM) and 4-aminopyridine (2 mM) did not alter the effect of CCK. The CCK B receptor antagonist PD-135,158 completely blocked the inward currents generated by CCK-8S. CCK also resulted in an increase in spontaneous action potential-dependent IPSC frequency, but no changes in action potential-independent miniature IPSCs or evoked IPSCs in pyramidal neurons. These results provide evidence that CCK can depolarize hippocampal interneurons through the inhibition of a resting K ϩ conductance, leading to increased tonic inhibition of pyramidal neurons. This action of CCK may contribute to its anticonvulsant properties, as observed in limbic seizure models.

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Section: Pharmacology Of Cck-8s Actions On Interneuronssupporting

confidence: 73%

mentioning

confidence: 99%

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Miller¹,

Hoffer²,

Svoboda³

et al. 1997

J. Neurosci.

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“…CCK-8S produced a concentration-dependent rise in electrically evoked [ 3 H]GABA overflow, which was counteracted by the CCK 2 receptor antagonist LY225910. This finding is in agreement with results obtained from other brain regions (Pérez de la Mora et al, 1993;Chung and Moore, 2007). Previous work tried to correlate anxiety-like effects of CCK 2 receptor agonists to the enhancement of cortical GABA release.…”

Section: Discussionsupporting

confidence: 93%

Cannabinoid CB₁ and Cholecystokinin CCK₂ Receptors Modulate, in an Opposing Way, Electrically Evoked [³H]GABA Efflux from Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety

Antonelli

Tomasini

Mazza

et al. 2009

J Pharmacol Exp Ther

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“…Mercer et al, 2000). Reports of CCK's physiological actions are inconsistent, with both excitation (Dodd & Kelly, 1979;Boden & Hill, 1988;Bohme et al, 1988;Shinohara & Kawasaki, 1997), and inhibition (MacVicar et al, 1987;Perez de la Mora et al, 1993) of pyramidal cells having been demonstrated. CCK may inhibit pyramidal cells indirectly (Perez de la Mora et al, 1993) by increasing GABA release from interneurons (Miller & Lupica, 1994;Miller et al, 1997;Ferraro et al, 1999;Deng & Lei, 2006).…”

Section: Introductionmentioning

confidence: 99%

Cholecystokinin inhibits endocannabinoid-sensitive hippocampal IPSPs and stimulates others

2008

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Cholecystokinin (CCK) is the most abundant neuropeptide in the central nervous system. In the hippocampal CA1 region, CCK is co-localized with GABA in a subset of interneurons that synapse on pyramidal cell somata and apical dendrites. CCK-containing interneurons also uniquely express a high level of the cannabinoid receptor, CB 1 , and mediate the retrograde signaling process called DSI. Reported effects of CCK on inhibitory post-synaptic potentials (IPSPs) in hippocampus are inconsistent, and include both increases and decreases in activity. Hippocampal interneurons are very heterogeneous, and these results could be reconciled if CCK affected different interneurons in different ways. To test this prediction, we used sharp microelectrode recordings from pyramidal cells with ionotropic glutamate receptors blocked, and investigated the effects of CCK on pharmacologically distinct groups of IPSPs during long-term recordings. We find that CCK, acting via the CCK 2 receptor, increases some IPSPs and decreases others, and most significantly, that the affected IPSPs can be classified into two groups by their pharmacological properties. IPSPs that are increased by carbachol (CCh-sIPSPs), are depressed by CCK, ω-conotoxin GVIA, and endocannabinoids. IPSPs that are enhanced by CCK (CCK-sIPSPs) are blocked by ω-agatoxin IVA, and are unaffected by carbachol or endocannabinoids. Interestingly, a CCK 2 antagonist enhances CCh-sIPSPs, suggesting normally they may be partially suppressed by endogenous CCK. In summary, our data are compatible with the hypothesis that CCK has opposite actions on sIPSPs that originate from functionally distinct interneurons.

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Cholecystokinin-8 increases K+-evoked [3H]γ-aminobutyric acid release in slices from various brain areas

Cited by 41 publications

References 21 publications

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Cannabinoid CB₁ and Cholecystokinin CCK₂ Receptors Modulate, in an Opposing Way, Electrically Evoked [³H]GABA Efflux from Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety

Cholecystokinin inhibits endocannabinoid-sensitive hippocampal IPSPs and stimulates others

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Cholecystokinin-8 increases K+-evoked [3H]γ-aminobutyric acid release in slices from various brain areas

Cited by 41 publications

References 21 publications

Cholecystokinin Increases GABA Release by Inhibiting a Resting K+Conductance in Hippocampal Interneurons

Cholecystokinin Increases GABA Release by Inhibiting a Resting K+Conductance in Hippocampal Interneurons

Cannabinoid CB1 and Cholecystokinin CCK2 Receptors Modulate, in an Opposing Way, Electrically Evoked [3H]GABA Efflux from Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety

Cholecystokinin inhibits endocannabinoid-sensitive hippocampal IPSPs and stimulates others

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Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Cannabinoid CB₁ and Cholecystokinin CCK₂ Receptors Modulate, in an Opposing Way, Electrically Evoked [³H]GABA Efflux from Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety