Intrahippocampal infusion of a cyclooxygenase-2 inhibitor attenuates memory acquisition in rats

Rall, Jason M.; Mach, Sara A.; Dash, Pramod K.

doi:10.1016/s0006-8993(03)02248-0

Cited by 80 publications

(53 citation statements)

References 12 publications

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“…(D) In slices in which NS-398 blocked the induction of LTP, paired-pulse facilitation recorded 60 min after tetanic stimulation did not differ from that recorded before washing in NS-398. (Teather et al 2002;Rall et al 2003). Moreover, COX-2 transgenic mice have been shown to develop deficits in spatial memory (Andreasson et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7)-induced plasticity changes in the lateral amygdala are mediated by COX-2 and NO

Albrecht¹

2007

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It is known from studies outside the brain that upon binding to its receptor, angiotensin-(1-7) elicits the release of prostanoids and nitric oxide (NO). Cyclooxygenase (COX) is a key enzyme that converts arachidonic acid to prostaglandins. Since there are no data available so far on the role of COX-2 in the amygdala, in a first step we demonstrated that the selective COX-2 inhibitor NS-398 significantly reduced the probability of long-term potentiation (LTP) induction in the lateral nucleus of the amygdala. Similarly, in COX-2 −/− mice, LTP induced by external capsule (EC) stimulation was impaired. Second, we evaluated the action of angiotensin-(1-7) in the amygdala. In wild-type mice, angiotensin-(1-7) increased LTP. This LTP-enhancing effect of Ang-(1-7) was not observed in COX-2 +/− mice. However, in COX-2 −/− mice, Ang-(1-7) caused an enhancement of LTP similar to that in wild-type mice. The NO synthetase inhibitor L-NAME blocked this angiotensin-(1-7)-induced increase in LTP in COX-2 −/− mice. Low-frequency stimulation of external capsule fibers did not cause long-term depression (LTD) in drug-free and angiotensin-(1-7)-treated brain slices in wild-type mice. In contrast, in COX-2 −/− mice, angiotensin-(1-7) caused stable LTD. Increasing NO concentration by the NO-donor SNAP also caused LTD in wild-type mice. Our study shows for the first time that LTP in the amygdala is dependent on COX-2 activity. Moreover, COX-2 is involved in the mediation of angiotensin-(1-7) effects on LTP. Finally, it is recognized that there is a molecular cross-talk between COX-2 and NO that may regulate synaptic plasticity.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7)-induced plasticity changes in the lateral amygdala are mediated by COX-2 and NO

Albrecht¹

2007

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“…The participation of COX-2 in synaptic transmission and plasticity is supported by the evidence that COX-2 is localized in neuronal dendritic spines, specialized structures where synaptic signaling occurs [4,26,27]. In addition, the involvement of COX-2 in long-term synaptic plasticity and cognition has been supported from the behavioral tests where administration of COX-2 inhibitors impairs passive avoidance task [28,29], memory acquisition, memory retention [30,31], and spatial memory consolidation [32,33]. Since COX-2 plays a key role in neuroinflammation, which is closely associated with brain injury and certain neurologic disorders such as multiple sclerosis, epilepsy, Parkinson's and Alzheimer's diseases [2,15,[34][35][36][37][38][39][40][41][42][43], an elucidation of COX-2 in excitatory glutamatergic synaptic transmission and plasticity has greatly advanced our understanding of mechanisms responsible for the occurrence of these neurological disorders.…”

Section: Cox-2 In Neural Plasticitymentioning

confidence: 94%

Cyclooxygenase-2 in Synaptic Signaling

Yang

Chen²

2008

CPD

166

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Cyclooxygenase-2 (COX-2), a rate-limiting enzyme converting arachidonic acid to prostaglandins and a key player in neuroinflammation, has been implicated in the pathogenesis of neurodegenerative diseases such as multiple sclerosis, Parkinson's and Alzheimer's diseases, and in traumatic brain injury-and ischemia-induced neuronal damage, and epileptogenesis. Accumulated information suggests that the contribution of COX-2 to neuropathology is associated with its involvement in synaptic modification. Inhibition or elevation of COX-2 has been shown to suppress or enhance excitatory glutamatergic neurotransmission and long-term potentiation (LTP). These events are mainly mediated via PGE 2 , the predominant reaction product of COX-2, and the PGE 2 subtype 2 receptor (EP 2 )-protein kinase A pathway. Recent evidence shows that endogenous cannabinoids are substrates for COX-2 and can be oxygenated by COX-2 to form new classes of prostaglandins (prostaglandin glycerol esters and prostaglandin ethanolamides). These COX-2 oxidative metabolites of endocannabinoids, as novel signaling mediators, modulate synaptic transmission and plasticity and cause neurodegeneration. The actions of these COX-2 metabolites are likely mediated by mitogen-activated protein kinase (MAPK) and inositol 1,4,5-trisphosphate (IP 3 ) signal transduction pathways. These discoveries suggest that the contributions of COX-2 to neurotransmission and brain malfunction result not only from its conversion of arachidonic acid to classic prostaglandins but also from its oxidative metabolism of endocannabinoids to novel prostaglandins. Thus, elucidation of COX-2 in synaptic signaling may provide a mechanistic basis for designing new drugs aimed at preventing, treating or alleviating neuroinflammation-associated neurological disorders.

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“…Additionally, intraperitoneal injection of a nonspecific COX inhibitor or a specific COX-2 inhibitor impaired memory formation of a passive avoidance task in mice (Sato et al 2007) and spatial memory retention in the Morris water maze in rats (Teather et al 2002). Moreover, infusion of a selective COX-2 inhibitor into rat hippocampal CA1 field impaired both acquisition (Rall et al 2003) and retention (Sharifzadeh et al 2005) of spatial memory in the Morris water maze. Finally, the concentration of prostaglandins (COX products of AA metabolism) was enhanced in the chick intermediate medial hyperstriatum ventrale after passive avoidance training, and intracerebral infusions of specific COX-1 or COX-2 inhibitors prevented the training-related increase of prostaglandins release (Hölscher 1995b).…”

Section: Reduced Pla 2 Activity and Memory Impairment In Research Animentioning

confidence: 98%

Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease

2008

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Intrahippocampal infusion of a cyclooxygenase-2 inhibitor attenuates memory acquisition in rats

Cited by 80 publications

References 12 publications

Angiotensin-(1-7)-induced plasticity changes in the lateral amygdala are mediated by COX-2 and NO

Angiotensin-(1-7)-induced plasticity changes in the lateral amygdala are mediated by COX-2 and NO

Cyclooxygenase-2 in Synaptic Signaling

Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease

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