A time course analysis of cyclooxygenase-2 suggests a role in spatial memory retrieval in rats

Sharifzadeh, Mohammad; Tavasoli, Mahtab; Soodi, Maliheh; Mohammadi-Eraghi, S; Ghahremani, Mohammad H.; Roghani, Ali

doi:10.1016/j.neures.2005.11.004

Cited by 30 publications

(21 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1 ). These results are similar to those obtained in our previous studies [22,[25][26][27] . Posttraining bilateral infusions of H-89 (2.5 and 5 mol/l) into the CA1 region of the hippocampus caused significant increase in escape latency ( * * * p !…”

Section: Comparison Of Effects Of H-89 Dmso and Saline On Time And Dsupporting

confidence: 93%

Protective Effects of Chronic Lithium Treatment against Spatial Memory Retention Deficits Induced by the Protein Kinase AII Inhibitor H-89 in Rats

Sharifzadeh¹,

Aghsami²,

Gholizadeh³

et al. 2007

Pharmacology

Self Cite

View full text Add to dashboard Cite

We have previously shown that infusion of the PKAII inhibitor H-89 in the CA1 area of the hippocampus impaired spatial memory retention. There is some evidence suggesting the neuroprotective effects of chronic lithium administration including its ability to attenuate a deleterious effect of chronic stress on spatial memory in rats. In the present study, we investigated whether chronic administration of lithium can improve memory as well as influence the inhibitory effect of H-89 on spatial memory retention. Male albino rats were treated systemically with lithium (600 mg/l) for 4 weeks and then trained for 4 days in the Morris water maze. Testing the animals 48 h later showed a significant reduction in escape latency (p < 0.05) and travel distance (p < 0.05) compared to the controls. In separate experiments, the rats were similarly treated with lithium for 4 weeks, followed by similar training for 4 days and then immediately infused bilaterally with vehicle or 5 µmol/l H-89 into the CA1 region of the hippocampus. Animals were then tested 48 h after H-89 infusion in order to assess their spatial memory retention. The lithium treatment caused a significant reduction in escape latency (p < 0.001) and travel distance (p < 0.001) compared to H-89-treated animals. The data suggest that lithium treatment for 4 weeks improved spatial memory retention and that lithium pretreatment prevented or reversed the H-89-induced spatial memory deficits.

show abstract

Section: Comparison Of Effects Of H-89 Dmso and Saline On Time And Dsupporting

confidence: 93%

Protective Effects of Chronic Lithium Treatment against Spatial Memory Retention Deficits Induced by the Protein Kinase AII Inhibitor H-89 in Rats

Sharifzadeh¹,

Aghsami²,

Gholizadeh³

et al. 2007

Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

“…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

169

116

View full text Add to dashboard Cite

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.

show abstract

“…In contrast, using a between-days analysis, retention and retrieval is disrupted following CA1, but not following CA3 or DG lesions (Lee and Kesner, 2004a;Lee and Kesner, 2004b;Jerman et al, 2006). Impairments have also been demonstrated in delay-dependent retrieval without impairing immediate recall or encoding of spatial information after infusing glutamatergic antagonists (Lee and Kesner, 2002), or cyclooxygenase-2 inhibitors (Sharifzadeh et al, 2006) into the CA1 subregion, but not when infused into the CA3 subregion. Similar retrieval deficits are apparent with selective lesions to the stratum lacuno-sum moleculare (s.l-m) dendritic layer, where the axons of the direct perforant path (pp) terminate (Remondes and Schuman, 2004).…”

Section: Introductionmentioning

confidence: 89%

“…There is strong evidence suggesting the CA1 subregion plays a significant role in intermediate/long-term spatial memory and consolidation, but not short-term acquisition or encoding processes (O'Reilly and McClelland, 1994;Treves and Rolls, 1994;Maren et al, 1997;Bertaina-Anglade et al, 2000;Kesner et al, 2004;Lee and Kesner, 2004a;Remondes and Schuman, 2004;Daumas et al, 2005;Hasselmo, 2005;Sharifzadeh et al, 2006). Encoding of information acquired in a Hebb-Williams maze or in contextual fear conditioning, using a within-days analysis, is impaired by targeted lesions to the CA3 and dentate gyrus (DG) subregions, but not from targeted lesions to the CA1 subregion.…”

Section: Introductionmentioning

confidence: 99%

The role of the direct perforant path input to the CA1 subregion of the dorsal hippocampus in memory retention and retrieval

2007

View full text Add to dashboard Cite

Subregional analyses of the hippocampus have suggested a selective role for the CA1 subregion in intermediate/long-term spatial memory and consolidation, but not short-term acquisition or encoding processes. It remains unclear how the direct cortical projection to CA1 via the perforant path (pp) contributes to these CA1-dependent processes. It has been suggested that dopamine selectively modulates the pp projection to CA1 while having little to no effect on the Schaffer collateral (SC) projection to CA1. This series of behavioral and electro-physiological experiments takes advantage of this pharmacological dissociation to demonstrate that the direct pp inputs to CA1 are critical in CA1-dependent intermediate-term retention and retrieval function. Here we demonstrate that local infusion of the nonselective dopamine agonist, apomorphine (10, 15 μg), into the CA1 subregion of awake animals produces impairments in between-day retention and retrieval, sparing within-day encoding of a modified Hebb-Williams maze and contextual conditioning of fear. In contrast, apomorphine produces no deficits when infused into the CA3 subregion. To complement the behavioral analyses, electrophysiological data was collected. In anesthetized animals, local infusion of the same doses of apomorphine significantly modifies evoked responses in the distal dendrites of CA1 following angular bundle stimulation, but produces no significant effects in the more proximal dendritic layer following stimulation of the SC. These results support a modulatory role for dopamine in the EC-CA1, but not CA3-CA1 circuitry, and suggest the possibility of a more fundamental role for EC-CA1 synaptic transmission in terms of intermediate-term, but not short-term spatial memory.

show abstract

A time course analysis of cyclooxygenase-2 suggests a role in spatial memory retrieval in rats

Cited by 30 publications

References 73 publications

Protective Effects of Chronic Lithium Treatment against Spatial Memory Retention Deficits Induced by the Protein Kinase AII Inhibitor H-89 in Rats

Protective Effects of Chronic Lithium Treatment against Spatial Memory Retention Deficits Induced by the Protein Kinase AII Inhibitor H-89 in Rats

Cyclooxygenase-2 in Synaptic Signaling

The role of the direct perforant path input to the CA1 subregion of the dorsal hippocampus in memory retention and retrieval

Contact Info

Product

Resources

About