Glutamate and dynorphin release from a subcellular fraction enriched in hippocampal mossy fiber synaptosomes

Terrian, David M.; Johnston, Dean; Claiborne, Brenda J.; Ansah-Yiadom, R.; Strittmatter, Warren J.; Rea, Michael A.

doi:10.1016/0361-9230(88)90146-3

Cited by 93 publications

(61 citation statements)

References 32 publications

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“…1c,d). In addition, we homogenized hippocampal tissue from ephrin-B3 lacZ/lacZ mice and isolated the synaptosome fractions (P3), which have been demonstrated previously to be enriched in mossy fiber boutons (Terrian et al, 1988). Immunoblot analysis of the P3 fraction confirmed that ephrin-B3 is localized to mossy fiber terminals along with the presynaptic protein synaptoporin, whereas no anti-␤-galactosidase signal was evident in the P2 fraction in which we localized the postsynaptic marker PSD95 (Fig.…”

Section: Ephrin-b3 Is Expressed At High Levels In Mossy Fiber Axons Amentioning

confidence: 59%

B-Ephrin Reverse Signaling Is Required for NMDA-Independent Long-Term Potentiation of Mossy Fibers in the Hippocampus

Armstrong¹,

Saganich²,

Xu³

et al. 2006

J. Neurosci.

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The mossy fiber to CA3 pyramidal neuron synapse in the hippocampus displays an atypical form of NMDA receptor-independent long-term potentiation (LTP). Plasticity at this synapse is expressed in the presynaptic terminal as an elevated probability of neurotransmitter release. However, evidence indicates that postsynaptic mechanisms and trans-synaptic signaling through an association between postsynaptic EphB receptors and presynaptic B-ephrins are necessary for the induction of LTP. Here we show that ephrin-B3 protein is highly expressed in mossy fiber axons and terminals. There are specific deficits in mossy fiber LTP in mice in which the cytoplasmic C-terminal signaling domain of the ephrin-B3 protein is replaced with ␤-galactosidase. These deficits are not observed in ephrin-B3 null mutant mice because of functional redundancy by virtue of other B-ephrins. These results indicate that B-ephrin reverse signaling into the presynaptic mossy fiber bouton is required for the induction of NMDA receptor-independent LTP at this synapse.

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Section: Ephrin-b3 Is Expressed At High Levels In Mossy Fiber Axons Amentioning

confidence: 59%

B-Ephrin Reverse Signaling Is Required for NMDA-Independent Long-Term Potentiation of Mossy Fibers in the Hippocampus

Armstrong¹,

Saganich²,

Xu³

et al. 2006

J. Neurosci.

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“…Moreover, a noncompetitive NMDA antagonist was found to inhibit morphine tolerance and dependence (Trujillo and Akil, 1991). Glutamate and dynorphins can each be released from hippocampal mossy fiber synaptosomes (Terrian et al, 1988), with both dynorphin-immunoreactive fibers and glutamate-binding sites found in the same hippocampal regions (Watson et al, 1982;Greenamyre et al, 1984). In contrast to the results of the present study and some of the reports mentioned above, in other model systems the effects of endogenous opioids on EAA release appear to be mediated, at least in part, by opioid receptors.…”

Section: Discussionmentioning

confidence: 99%

Dynorphin increases extracellular levels of excitatory amino acids in the brain through a non-opioid mechanism

1992

J. Neurosci.

103

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Administration of dynorphin A-(1–17) (Dyn 1–17), through a microdialysis probe stereotaxically placed into rat hippocampus, caused marked increases in the extracellular levels of glutamate and aspartate. The degree and duration of elevation of these excitatory amino acids (EAA) induced by Dyn 1–17 were dose dependent but were not modified by the centrally active opioid receptor antagonist nalmefene. At comparable doses, Dyn 2–17, which is inactive at the opioid receptor, produced similar alterations in EAA as Dyn 1–17, whereas Dyn 1–8 caused significantly smaller changes of glutamate. Dynorphin and EAAs have each been implicated as pathophysiological factors in brain or spinal cord injuries, with dynorphin's actions shown to involve both opioid and non-opioid components. The present observations indicate a direct potential linkage between dynorphin and excitotoxin mechanisms of CNS injury and provide further support for the concept that dynorphin's pathophysiologic effects may include non-opioid actions of this peptide.

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“…Dynorphins or enkephalins released from mossy fibers (Gall et al, 198 1;Chavkin et al, 1983aChavkin et al, , 1985bMcGinty et al, 1983;Terrian et al, 1988) could act on distinct K or 6 receptors to either up-or downregulate this form of synaptic plasticity, perhaps via bimodal modulation of I,, or via the pronounced low-and high-threshold Ca'+ currents seen in CA3 pyramidal neurons (Gahwiler and Brown, 1987). Based on their potent hippocampal actions, it is reasonable to suggest that systemic opiates also could alter memory function.…”

Section: Hyperpolarizingmentioning

confidence: 99%

“…Subsequent biochemical and cytochemical findings suggested that this pathway contained mainly dynorphin peptides as well as some proenkephalin-derived fragments (Chavkin et al, 1983b(Chavkin et al, , 1985bMcGinty et al, 1983). Stimulation of the hippocampal CA3 region releases several dynorphins and enkephalins (Chavkin et al, 1983a;Terrian et al, 1988) as well as the excitatory amino acid glutamate (Terrian et al, 1988).…”

mentioning

confidence: 99%

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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Glutamate and dynorphin release from a subcellular fraction enriched in hippocampal mossy fiber synaptosomes

Cited by 93 publications

References 32 publications

B-Ephrin Reverse Signaling Is Required for NMDA-Independent Long-Term Potentiation of Mossy Fibers in the Hippocampus

B-Ephrin Reverse Signaling Is Required for NMDA-Independent Long-Term Potentiation of Mossy Fibers in the Hippocampus

Dynorphin increases extracellular levels of excitatory amino acids in the brain through a non-opioid mechanism

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

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