Dissociation of μ and δ opioid receptor-mediated reductions in evoked and spontaneous synaptic inhibition in the rat hippocampus in vitro

Lupica, Carl R.; Proctor, William R.; Dunwiddie, Thomas V.

doi:10.1016/0006-8993(92)91312-3

Cited by 53 publications

(41 citation statements)

References 37 publications

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“…MORs were most frequently found on interneurons that innervate pyramidal cell bodies and less on interneurons that innervate the distal apical dendrites of CA1 pyramidal cells (Drake and Milner 2002). Consistent with the anatomical studies, activation of MORs was shown to hyperpolarize CA1 inhibitory interneurons (Madison and Nicoll 1988;Svoboda and Lupica 1998;Svoboda et al 1999;Wimpey and Chavkin 1991) and presynaptically inhibit GABAergic inhibitory postsynaptic potentials (IPSPs) onto CA1 pyramidal neurons (Capogna et al 1993;Cohen et al 1992;Lupica 1995;Lupica et al 1992;Masukawa and Prince 1982;Nicoll et al 1980;Rekling 1993;Swearengen and Chavkin 1989;Wimpey et al 1990). Moreover, interneurons in stratum oriens (SO) that project to perisomatic regions of pyramidal cells were almost all sensitive to MOR activation, whereas less than half of interneurons innervating the various dendritic regions were sensitive to the activation of MOR (Svoboda et al 1999).…”

Section: Introductionmentioning

confidence: 63%

“…However, these studies examined only a pair of excitatory synaptic events (50-ms interval) and measured signals only 250 ms after the first synaptic event. The present studies measured Յ1,700 ms after the first synaptic event and used a train of five stimuli (50-ms intervals) to examine a potential inhibition of GABA B synaptic function (Lupica et al 1992). Although MOR activation had little to no effect on the first two excitatory events (McQuiston and Saggau 2003), there was a significant increase in the excitatory events at the end of the stimulus train.…”

Section: Discussionmentioning

confidence: 89%

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Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1

McQuiston

2007

Journal of Neurophysiology

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McQuiston AR. Effects of -opioid receptor modulation on GABA B receptor synaptic function in hippocampal CA1. J Neurophysiol 97: 2301-2311, 2007. First published January 10, 2007 doi:10.1152/jn.01179.2006. Activation of -opioid receptors (MORs) alters information coding, synaptic plasticity, and spatial memory in hippocampal CA1. In CA1, MORs act by inhibiting GABA release onto both GABA A and GABA B receptors exclusively. MOR activation can facilitate excitatory inputs in CA1 dendritic layers by inhibiting synaptic activation of GABA A receptors. In this study, we use voltage-sensitive dye imaging to show that MOR activation by the MOR agonist DAMGO suppressed GABA B inhibitory postsynaptic potentials in all layers of CA1. When stimulating excitatory input in stratum oriens (SO), stratum radiatum (SR), or stratum lacunosummoleculare (SLM) with five pulses at 20 Hz in the presence of bicuculline (50 M), DAMGO (1 M) was most effective at increasing the amplitude of the last excitatory event. This effect was reversed by the MOR antagonist CTOP (1 M) and occluded by the GABA B receptor agonist CGP 55845 (10 M). DAMGO was less effective at increasing the amplitude of later excitatory events compared with the effect of CGP 55845. DAMGO was relatively ineffective at increasing the amplitude of excitatory inputs in SLM but had significantly greater effects on excitatory events as they propagated to stratum pyramidale (SP). When stimulating in SR, DAMGO was least effective at increasing excitatory amplitudes in SLM and most effective in SP and SO. Finally, DAMGO was equally effective at increasing excitatory activity amplitudes in all layers of CA1 after stimulating in SO. Therefore MOR suppresses GABA B synaptic hyperpolarizations in all layers of CA1 and most effectively facilitates excitatory activity in CA1 output layers.

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Section: Introductionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 89%

Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1

McQuiston

2007

Journal of Neurophysiology

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“…Both DPDPE and deltorphin II in contrast to ft opioids failed to induce epileptiform bursting in the rat hippocampus model. The inability of the selective 6 agonists to induce spontaneous or evoked epileptiform burstings, which was also shown in the dentate gyrus, is probably dependent on the inability of 6 agonists to affect hippocampal recurrent inhibition (Lupica et al, 1992). However, g and 6 agonists also affected hippocampal non-recurrent synaptic inhibition, an effect revealed in extracellular studies by an increase of the CAl PS amplitude.…”

Section: Discussionmentioning

confidence: 80%

Dexamethasone‐induced selective inhibition of the central μ opioid receptor: functional in vivo and in vitro evidence in rodents

Pieretti

Giannuario

Domenici

et al. 1994

British J Pharmacology

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U50,488. 3 In experiments performed in an in vitro model of cerebral excitability in the rat hippocampal slice, dexamethasone strongly prevented both the increase of the duration of the field potential recorded in CAl, and the appearance and number of additional population spikes induced by A receptor agonists. 4 In both models pretreatment with cycloheximide, a protein synthesis inhibitor, prevented the antagonism by dexamethasone of responses to the 1i opioid agonists. 5 Our data indicate that in the rodent brain there is an important functional interaction between the corticosteroid and the opioid systems at least at the receptor level, while 6 and K receptors are modulated in different ways.

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“…A similar disinhibitory mechanism may be exerted by enkephalins in CA3 and dentate gyrus (Gruol et al, 1983;. In all hippocampal regions, this effect appears to derive from activation of either the k or 6 subtype of opioid receptor (Chavkin et al, 1985b;Wimpey et al, 1989;Lupica et al, 1992;Watson and Lanthorn, 1993).…”

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confidence: 93%

Voltage-dependent effects of opioid peptides on hippocampal CA3 pyramidal neurons in vitro

et al. 1994

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Opioid peptides, and especially the dynorphins, have been localized to several circuits in the CA3 hippocampal region, yet electrophysiological studies often find mixed effects of opiates on the excitability of CA3 neurons. Reasoning that these mixed effects might involve voltage-dependent actions, we tested the effect of several opiates on CA3 pyramidal neurons using single-electrode voltage-clamp recording in a slice preparation of rat hippocampus. In most CA3 neurons, the voltage-dependent K+ current known as the M-current (IM) was uniquely sensitive to the opioid peptides, with the direction of response dependent upon the opiate type and concentration. Thus, an opiate selective for kappa receptors, U-50,488H, significantly augmented IM. The kappa-selective agonists dynorphin A and dynorphin B, which exist in mossy fiber afferents to CA3 pyramidal neurons, also markedly augmented IM at low concentrations (20–100 nM). By contrast, dynorphin A at higher concentrations (1–1.5 microM) often reduced IM. Similarly, several opiates [e.g., D-Ala2,D-Leu5-enkephalin: (DADL), [D- Pen2,5]-enkephalin (DPDPE)] known to act on the delta receptor subtypes reduced the M-current, with partial reversal of this effect by naloxone. Neither the selective mu-receptor agonist [D-Ala2, NMe-Phe4, Gly-ol]-enkephalin (DAMGO) nor the nonopioid fragment of dynorphin, des- Tyr-dynorphin, consistently altered IM. These opiate effects on IM were accompanied by changes in conductance and holding current consistent with their respective effects on IM. Dynorphin A did not measurably affect the Q-current, a conductance known to contribute to inward rectification in hippocampal pyramidal neurons. The opiate effects on IM were not altered by pretreatment with Cs+ (which blocks IQ) or Ca2+ channel blockers. The opposing effects of the dynorphins (both A and B) and DADL on IM were antagonized by naloxone (1–3 microM), and the dynorphin-induced augmentations of IM were usually reversed by the kappa receptor antagonist norbinaltorphimine. These results suggest that the opiates can have opposing effects on the same voltage- dependent K+ channel type (the M channel) in the rat CA3 pyramidal neuron, with the direction of the response depending on which receptor subtype is activated. These data not only help explain the mixed effects of opiates seen in other studies, but also suggest a potential postsynaptic function for the endogenous opiates contained in the CA3 mossy fibers.

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Dissociation of μ and δ opioid receptor-mediated reductions in evoked and spontaneous synaptic inhibition in the rat hippocampus in vitro

Cited by 53 publications

References 37 publications

Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1

Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1

Dexamethasone‐induced selective inhibition of the central μ opioid receptor: functional in vivo and in vitro evidence in rodents

Voltage-dependent effects of opioid peptides on hippocampal CA3 pyramidal neurons in vitro

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Dissociation of μ and δ opioid receptor-mediated reductions in evoked and spontaneous synaptic inhibition in the rat hippocampus in vitro

Cited by 53 publications

References 37 publications

Effects of μ-Opioid Receptor Modulation on GABAB Receptor Synaptic Function in Hippocampal CA1

Effects of μ-Opioid Receptor Modulation on GABAB Receptor Synaptic Function in Hippocampal CA1

Dexamethasone‐induced selective inhibition of the central μ opioid receptor: functional in vivo and in vitro evidence in rodents

Voltage-dependent effects of opioid peptides on hippocampal CA3 pyramidal neurons in vitro

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Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1

Effects of μ-Opioid Receptor Modulation on GABA_B Receptor Synaptic Function in Hippocampal CA1