L-type Ca2+ channel blockers promote Ca2+ accumulation when dopamine receptors are activated in striatal neurons

Eaton, Molly; Macı́as, Wendy; Youngs, Rachael M.; Rajadhyaksha, Anjali M.; Dudman, Joshua T.; Konradi, Christine

doi:10.1016/j.molbrainres.2004.08.007

Cited by 13 publications

(9 citation statements)

References 38 publications

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“…Similar to PKA, CaMKII can stimulate MEK/ERK, via β-Raf, and phosphorylate CREB directly (Waltereit and Weller 2003; Lee and Messing 2008). Conversely, PKA can activate CaMKII by phosphorylating NR1 NMDA receptor subunits (Raman et al 1996; Tingley et al 1997) and possibly by activating L-type voltage gated calcium channels (Eaton et al 2004). Thus, PKA may be able to compensate for CaMKII inhibition via one or a combination of these mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Involvement of amygdalar protein kinase A, but not calcium/calmodulin-dependent protein kinase II, in the reconsolidation of cocaine-related contextual memories in rats

et al. 2013

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Rationale Contextual control over drug relapse depends on the successful reconsolidation and retention of context-response-cocaine associations in long-term memory stores. The basolateral amygdala (BLA) plays a critical role in cocaine memory reconsolidation and subsequent drug context-induced cocaine-seeking behavior; however, less is known about the cellular mechanisms of this phenomenon. Objectives The present study evaluated the hypothesis that protein kinase A (PKA) and calcium/calmodulin-dependent protein kinase II (CaMKII) activation in the BLA is necessary for the reconsolidation of context-response-cocaine memories that promote subsequent drug context-induced cocaine-seeking behavior. Methods Rats were trained to lever-press for cocaine infusions in a distinct context, followed by extinction training in a different context. Rats were then briefly re-exposed to the previously cocaine-paired context or an unpaired context in order to reactivate cocaine-related contextual memories and initiate their reconsolidation or to provide a similar behavioral experience without explicit cocaine-related memory reactivation, respectively. Immediately after this session, rats received bilateral microinfusions of vehicle, the PKA inhibitor, Rp-Adenosine 3′,5′-cyclic monophosphorothioate triethylammonium salt (Rp-cAMPS), or the CaMKII inhibitor, KN-93, into the BLA or the posterior caudate putamen (anatomical control region). Rats were then tested for cocaine-seeking behavior (responses on the previously cocaine-paired lever) in the cocaine-paired context and the extinction context. Results Intra-BLA infusion of Rp-cAMPS, but not KN-93, following cocaine memory reconsolidation impaired subsequent cocaine-seeking behavior in a dose-dependent, site-specific, and memory reactivation-dependent fashion. Conclusions PKA, but not CaMKII, activation in the BLA is critical for cocaine memory re-stabilization processes that facilitate subsequent drug context-induced instrumental cocaine-seeking behavior.

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Section: Discussionmentioning

confidence: 99%

Involvement of amygdalar protein kinase A, but not calcium/calmodulin-dependent protein kinase II, in the reconsolidation of cocaine-related contextual memories in rats

et al. 2013

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“…D 1 -like agonists can convert L-type Ca 2+ inhibitors into Ca 2+ influx facilitators in cultured striatal neurons (Eaton et al, 2004). Some of these responses can be mimicked by introduction of cyclic AMP analogs (Liu et al, 1992; Surmeier et al, 1995) and blocked by inhibitors of PKA (Surmeier et al, 1995), suggesting that phosphorylation of calcium channels probably contributes to such responses.…”

Section: Signaling Cascades Associated With D1-like Receptor Stimumentioning

confidence: 99%

Pharmacology of signaling induced by dopamine D1-like receptor activation

Undieh

2010

Pharmacology & Therapeutics

110

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Dopamine D1-like receptors consisting of D1 and D5 subtypes are intimately implicated in dopaminergic regulation of fundamental neurophysiologic processes such as mood, motivation, cognitive function, and motor activity. Upon stimulation, D1-like receptors initiate signal transduction cascades that are mediated through adenylyl cyclase or phosphoinositide metabolism, with subsequent enhancement of multiple downstream kinase cascades. The latter actions propagate and further amplify the receptor signals, thus predisposing D1-like receptors to multifaceted interactions with various other mediators and receptor systems. The adenylyl cyclase response to dopamine or selective D1-like receptor agonists is reliably associated with the D1 subtype, while emerging evidence indicates that the phosphoinositide responses in native brain tissues may be preferentially mediated through stimulation of the D5 receptor. Besides classic coupling of each receptor subtype to specific G proteins, additional biophysical models are advanced in attempts to account for differential subcellular distribution, heteromolecular oligomerization, and activity-dependent selectivity of the receptors. It is expected that significant advances in understanding of dopamine neurobiology will emerge from current and anticipated studies directed at uncovering the molecular mechanisms of D5 coupling to phosphoinositide signaling, the structural features that might enhance pharmacological selectivity for D5 versus D1 subtypes, the mechanism by which dopamine may modulate phosphoinositide synthesis, the contributions of the various responsive signal mediators to D1 or D5 interactions with D2-like receptors, and the spectrum of dopaminergic functions that may be attributed to each receptor subtype and signaling pathway.

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“…For example, in lactotrophs activation of the D2S receptor inhibits dihydropyridine-sensitive Ltype channels and thus diminishes extracellular calcium influx [68]. Conversely, when the D1 receptor is activated calcium entry through the L-type calcium channel is increased [73]. In our experiments it appeared that apomorphine decreased or blocked part of the dihydropyridine-sensitive effect.…”

Section: Discussionmentioning

confidence: 45%

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Gui-Hua¹,

Gardner²,

Westfall³

2007

Biochemical Pharmacology

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In rat pheochromocytoma (PC-12) cells the dopamine D 2 receptor agonists apomorphine (APO) and n-propylnorapomorphine (NPA) produced a concentration dependent inhibition of K + -evoked neuropeptide Y release (NPY-ir). The effect of APO was blocked by the dopamine D 2 -receptor antagonist, eticlopride, but not the D 1 /D 3 or the D 4 /D 2 antagonists, SCH23390 or clozapine, respectively. The D 1 /D 5 receptor agonist, SKF38393 or the D 3 agonists PD128907 and 7-OH DPAT had no effect. Selective N and L-type voltage gated Ca 2+ channel blockers, ω-Conotoxin GVIa (CtxGVIa) and nifedipine, respectively, produced a concentration dependent inhibition of NPY-ir release but were not additive with APO. The Ca 2+ /calmodulin-dependent protein kinase (CaM kinase) II inhibitor KN-62 produced a concentration-dependent inhibition of NPY-ir release but the combination of KN-62 and APO produced no further inhibition. PMA-mediated protein kinase C stimulation significantly increased both basal and K + -evoked release of NPY-ir, and in the presence of PMA APO had no inhibitory effect. The PKC antagonist, chelerythrine, inhibited K + -evoked NPYir release but was not additive with APO. Neither forskolin-mediated adenylate cyclase activation and the active cAMP analog Sp-cAMPS, nor the adenylate cyclase inhibitor SQ 22536, and the competitive inhibitor of cAMP-dependent protein kinases Rp-cAMPS, had any significant effect on K + -evoked NPY-ir release. This suggests the inhibitory effect of APO on K + -evoked release of NPYir from PC 12 cells is most likely mediated through activation of dopamine D 2 receptors leading to direct inhibition of N and L-type voltage gated Ca 2+ channels, or indirect inhibition of PKC, both of which would reduce [Ca 2+ ] i and inactivate CaM kinase.

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L-type Ca2+ channel blockers promote Ca2+ accumulation when dopamine receptors are activated in striatal neurons

Cited by 13 publications

References 38 publications

Involvement of amygdalar protein kinase A, but not calcium/calmodulin-dependent protein kinase II, in the reconsolidation of cocaine-related contextual memories in rats

Involvement of amygdalar protein kinase A, but not calcium/calmodulin-dependent protein kinase II, in the reconsolidation of cocaine-related contextual memories in rats

Pharmacology of signaling induced by dopamine D1-like receptor activation

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

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