Intrahippocampal injection of pertussis toxin blocks adenosine suppression of synaptic responses

Stratton, Kathleen R.; Cole, Andrew J.; Pritchett, J.F.; Eccles, Christine U.; Worley, Paul F.; Baraban, Jay M.

doi:10.1016/0006-8993(89)90604-5

Cited by 36 publications

(20 citation statements)

References 25 publications

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“…Because PTx can take several days to be fully effective in the hippocampus in vivo (Goh and Pennefather 1989;Stratton et al 1989), PTx was infused into the DH 1 d before fear conditioning to minimize potential effects on acquisition and consolidation. Mice were then tested 2 d after conditioning.…”

Section: Pertussis Toxin Blocks the Impairing Effects Of Xamoterol Onmentioning

confidence: 99%

“…Infusions were 1 mL/side at 0.4 mL/ min, and the injection cannula was left in place for 30 sec before the mouse was returned to its home cage. Because studies indicate that the effects of PTx are best evaluated 3 d after infusion (Goh and Pennefather 1989;Stratton et al 1989), PTx was infused 3 d before testing. To minimize potential effects of PTx on conditioning, training was administered the day after PTx infusion, and testing was performed 2 d after training.…”

Section: Dorsal Hippocampus Infusionmentioning

confidence: 99%

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Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Schutsky¹,

Ouyang²,

Thomas³

2011

Learn. Mem.

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Xamoterol, a partial b 1 -adrenergic receptor agonist, has been reported to impair the retrieval of hippocampus-dependent spatial reference memory in rats. In contrast, xamoterol restores memory retrieval in gene-targeted mice lacking norepinephrine (NE) and in a transgenic mouse model of Down syndrome in which NE levels are reduced. Restoration of retrieval by xamoterol in these two models complements the observation that NE and b 1 signaling are required for hippocampusdependent retrieval of contextual and spatial reference memory in wild-type mice and rats. Additional evidence indicates that cAMP-mediated PKA and Epac signaling are required for the retrieval of hippocampus-dependent memory. As a result, we hypothesized that xamoterol has effects in addition to the stimulation of b 1 receptors that, at higher doses, act to counter the effects of b 1 signaling. Here we report that xamoterol-induced disruption of memory retrieval depends on b 2 -adrenergic receptor signaling. Interestingly, the impairment of memory retrieval by xamoterol is blocked by pretreatment with pertussis toxin, an uncoupling agent for G i/o signaling, suggesting that b 2 signaling opposes b 1 signaling during memory retrieval at the level of G protein and cAMP signaling. Finally, similar to the time-dependent roles for NE, b 1 , and cAMP signaling in hippocampus-dependent memory retrieval, xamoterol only impairs retrieval for several days after training, indicating that its effects are also limited by the age of the memory. We conclude that the disruption of memory retrieval by xamoterol is mediated by G i/o -coupled b 2 signaling, which opposes the G s -coupled b 1 signaling that is transiently required for hippocampus-dependent emotional memory retrieval.

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Section: Pertussis Toxin Blocks the Impairing Effects Of Xamoterol Onmentioning

confidence: 99%

Section: Dorsal Hippocampus Infusionmentioning

confidence: 99%

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Schutsky¹,

Ouyang²,

Thomas³

2011

Learn. Mem.

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“…Conflicting data exist, however, with regard to the effect of pertussis toxin on the presynaptic action of adenosine in the hippocampus (compare Fredholm et al 1989with Stratton, Cole, Pritchett, Eccles, Worley & Baraban, 1989Scholz & Miller, 1991).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the actions of adenosine at pre‐ and postsynaptic receptors in the rat hippocampus in vitro.

Thompson

Haas

Gähwiler

1992

The Journal of Physiology

349

162

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SUMMARY1. Intracellular microelectrode recordings were used to study the cellular location, the receptor pharmacology, and the mechanism of action of adenosine on pyramidal cells and presynaptic axonal endings in area CA3 of organotypic hippocampal slice cultures.2. Adenosine (bath applied at 50 /iM) caused a 10-15 mV hyperpolarization of CA3 cells, as well as a 75-100 % decrease in the amplitude of excitatory and polysynaptic inhibitory postsynaptic potentials (EPSPs and IPSPs). Adenosine had no effect on the amplitude of monosynaptic IPSPs elicited in the presence of excitatory amino acid receptor antagonists, but did reduce the amplitude of isolated EPSPs, elicited after blocking GABAA receptors and reducing subsequent epileptic bursts with excitatory amino acid receptor antagonists. These data indicate that adenosine receptors are located on excitatory, but not inhibitory, presynaptic elements.3. The A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, bath applied at 200 nM) blocked the pre-and postsynaptic actions of adenosine. DPCPX had no effect on the amplitude of control synaptic responses, suggesting that there is no tonic activation of adenosine receptors in hippocampal slice cultures under control conditions. The Al receptor agonists R-N6-phenylisopropyladenosine (R-PIA) mimicked all pre-and postsynaptic actions of adenosine.4. Pertussis toxin pretreatment (500 ng/ml for 48 h) prevented adenosine from activating postsynaptic K+ conductance, but not frori inhibiting EPSPs. In contrast, stimulation of protein kinase C with phorbol ester (phorbol 12, 13-dibutyrate, 1 ,tM for 10 min) reduced the presynaptic, but nbt the postsynaptic, actions of adenosine. 5. Barium (bath applied at 1 mM) blocked the adenosiAe=aotivated K+ conductance, but not the inhibition of isolated EPSPs by adenosine.6. Adenosine at 0-03-1 JtM reduced the frequency of, or blocked, spontaneous epileptiform bursting produced by bicuculline. DPCPX (200 nM) increased the rate of spontaneous bursting, consistent with a tonic activation of adenosine receptors during hyperactivity, and led to the development of prolonged ictal-like bursts,

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“…Pertussis toxin (PTx) inactivates G i/o proteins through ADP ribosylation, uncoupling them from their receptors. Because it takes several days to observe optimal efficacy when PTx is administered in vivo, PTx was infused into the BLA 3 d before conditioning (Goh and Pennefather, 1989;Stratton et al, 1989). BLA pretreatment with PTx had no effect on consolidation when saline was infused immediately after training, suggesting that G i/o signaling is not essential for consolidation (Fig.…”

Section: Figurementioning

confidence: 99%

“…Infusion was 0.2 l/side at 0.08 l/min, with the injection cannulae being left in place for 30 s before the mouse was returned to its home cage. Because studies indicate that the effects of PTx are best evaluated 3 d after infusion, PTx was infused into the BLA 3 d before training (Goh and Pennefather, 1989;Stratton et al, 1989). For sites adjacent to the BLA, infusions were displaced 0.75 mm from the BLA coordinates in the direction indicated.…”

Section: Animalsmentioning

confidence: 99%

Catecholamines in Post-Traumatic Stress Disorder

Thomas¹

2012

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThe purpose of these studies is to test the hypothesis that adrenergic and dopaminergic signaling contribute to consolidation (and possibly reconsolidation) of fear memory in a redundant manner by stimulation of β2-adrenergic and the D1-class of dopaminergic receptors in the basolateral amygdala. Combined pharmacologic and genetic studies in mice have examined the above hypothesis for the consolidation of fear memory. The results are in agreement with the hypothesis. Roles for these signaling pathways in reconsolidation are not as clear, as combined treatment does not appear to influence reconsolidation. Current results indicate that treatment with β-adrenergic receptor antagonists (β blockers) alone shortly after trauma is unlikely to prevent the development of PTSD. However, combination therapy of β blockers and D1 receptor antagonists shortly after trauma may reduce the incidence of PTSD.15.

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Intrahippocampal injection of pertussis toxin blocks adenosine suppression of synaptic responses

Cited by 36 publications

References 25 publications

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Comparison of the actions of adenosine at pre‐ and postsynaptic receptors in the rat hippocampus in vitro.

Catecholamines in Post-Traumatic Stress Disorder

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Intrahippocampal injection of pertussis toxin blocks adenosine suppression of synaptic responses

Cited by 36 publications

References 25 publications

Xamoterol impairs hippocampus-dependent emotional memory retrieval via Gi/o-coupled β2-adrenergic signaling

Xamoterol impairs hippocampus-dependent emotional memory retrieval via Gi/o-coupled β2-adrenergic signaling

Comparison of the actions of adenosine at pre‐ and postsynaptic receptors in the rat hippocampus in vitro.

Catecholamines in Post-Traumatic Stress Disorder

Contact Info

Product

Resources

About

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling