kn-93 and adenosine-3--5--cyclic-phosphorothioate

kn-93 has been researched along with adenosine-3--5--cyclic-phosphorothioate* in 2 studies

Other Studies

2 other study(ies) available for kn-93 and adenosine-3--5--cyclic-phosphorothioate

Article	Year
Molecular mechanisms in hippocampus and basolateral amygdala but not in parietal or cingulate cortex are involved in extinction of one-trial avoidance learning. Neurobiology of learning and memory, 2010, Volume: 94, Issue:2 The establishment of extinction of one-trial avoidance involves the dorsal hippocampus (DH) and basolateral amygdala (BLA), two areas that participate in its original consolidation. The posterior parietal (PARIE) and posterior cingulate (CING) cortices also participate in consolidation of this task but their role in extinction has not been explored. Here we study the effect on the extinction of one-trial avoidance in rats of three different drugs infused bilaterally into DH, BLA, PARIE or CING 5min before the first of four daily unreinforced test sessions: The glutamate NMDA receptor antagonist, AP5 (5.0microg/side),and the inhibitors of calcium-calmodulin dependent kinase II (CaMKII), KN-93 (0.3microg/side), or of the cAMP-dependent protein kinase (PKA), Rp-cAMPs (0.5microg/side) hindered extinction when given into DH or BLA. Levels of pPKA and pCaMKII increased in DH after the first extinction trial; in BLA only the CaMKII increase was seen. Thus, this pathway appears to participate in extinction in BLA at the "basal" levels, and at enhanced levels in DH. None of the treatments affected extinction when given into PARIE or CING. The present findings indicate that: (1) the DH and BLA are important for the initiation of extinction at the time of the first unreinforced retrieval session; (2) both the CaMKII and the PKA signaling pathway are necessary for the development of extinction in the two regions; (3) PARIE and CING are probably unrelated to extinction. Topics: 2-Amino-5-phosphonovalerate; Amygdala; Animals; Avoidance Learning; Benzylamines; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Excitatory Amino Acid Antagonists; Extinction, Psychological; Gyrus Cinguli; Hippocampus; Male; Microinjections; Parietal Lobe; Protein Kinase Inhibitors; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Second Messenger Systems; Signal Transduction; Sulfonamides; Thionucleotides	2010
Calcium-dependent, D2 receptor-independent induction of c-fos by haloperidol in dopamine neurons. Naunyn-Schmiedeberg's archives of pharmacology, 2003, Volume: 367, Issue:5 Antipsychotic drugs such as haloperidol act as dopamine D2 receptor antagonists to produce a number of cellular effects including the induction of immediate-early genes such as c-fos. It has been hypothesized that blockade of D2 receptors by antipsychotics is responsible for the induction of c-fos, but the mechanism has not been determined. Using cultured ventral tegmental area (VTA) dopaminergic neurons as a model, we report that nanomolar concentrations of haloperidol cause a time-dependent increase in Fos expression in dopaminergic neurons.Surprisingly, this induction was not mimicked by sulpiride, a selective D2 receptor antagonist, and was not blocked by Rp-cAMPS, an antagonist of protein kinase A (PKA), thus suggesting that D2 receptors and the cAMP cascade are not required. The induction of Fos expression was blocked by tetrodotoxin, BAPTA and KN-93, thus showing that it is activity- and calcium-dependent and requires the activation of a calmodulin-dependent kinase (CaMK). Together, these results suggest that haloperidol induces Fos expression in dopaminergic neurons through a D2 receptor-independent increase in intracellular calcium, leading to CaMK activation. Topics: Animals; Benzylamines; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; Cells, Cultured; Colforsin; Cyclic AMP; Dopamine; Gene Expression; Genes, fos; Haloperidol; Neurons; Rats; Rats, Sprague-Dawley; Receptors, Dopamine D2; Receptors, sigma; RNA, Messenger; Second Messenger Systems; Signal Transduction; Sulfonamides; Tetrodotoxin; Thionucleotides; Ventral Tegmental Area	2003

Article

Year

Molecular mechanisms in hippocampus and basolateral amygdala but not in parietal or cingulate cortex are involved in extinction of one-trial avoidance learning.

Neurobiology of learning and memory, 2010, Volume: 94, Issue:2

The establishment of extinction of one-trial avoidance involves the dorsal hippocampus (DH) and basolateral amygdala (BLA), two areas that participate in its original consolidation. The posterior parietal (PARIE) and posterior cingulate (CING) cortices also participate in consolidation of this task but their role in extinction has not been explored. Here we study the effect on the extinction of one-trial avoidance in rats of three different drugs infused bilaterally into DH, BLA, PARIE or CING 5min before the first of four daily unreinforced test sessions: The glutamate NMDA receptor antagonist, AP5 (5.0microg/side),and the inhibitors of calcium-calmodulin dependent kinase II (CaMKII), KN-93 (0.3microg/side), or of the cAMP-dependent protein kinase (PKA), Rp-cAMPs (0.5microg/side) hindered extinction when given into DH or BLA. Levels of pPKA and pCaMKII increased in DH after the first extinction trial; in BLA only the CaMKII increase was seen. Thus, this pathway appears to participate in extinction in BLA at the "basal" levels, and at enhanced levels in DH. None of the treatments affected extinction when given into PARIE or CING. The present findings indicate that: (1) the DH and BLA are important for the initiation of extinction at the time of the first unreinforced retrieval session; (2) both the CaMKII and the PKA signaling pathway are necessary for the development of extinction in the two regions; (3) PARIE and CING are probably unrelated to extinction.

Topics: 2-Amino-5-phosphonovalerate; Amygdala; Animals; Avoidance Learning; Benzylamines; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Excitatory Amino Acid Antagonists; Extinction, Psychological; Gyrus Cinguli; Hippocampus; Male; Microinjections; Parietal Lobe; Protein Kinase Inhibitors; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Second Messenger Systems; Signal Transduction; Sulfonamides; Thionucleotides

2010

Calcium-dependent, D2 receptor-independent induction of c-fos by haloperidol in dopamine neurons.

Naunyn-Schmiedeberg's archives of pharmacology, 2003, Volume: 367, Issue:5

Antipsychotic drugs such as haloperidol act as dopamine D2 receptor antagonists to produce a number of cellular effects including the induction of immediate-early genes such as c-fos. It has been hypothesized that blockade of D2 receptors by antipsychotics is responsible for the induction of c-fos, but the mechanism has not been determined. Using cultured ventral tegmental area (VTA) dopaminergic neurons as a model, we report that nanomolar concentrations of haloperidol cause a time-dependent increase in Fos expression in dopaminergic neurons.Surprisingly, this induction was not mimicked by sulpiride, a selective D2 receptor antagonist, and was not blocked by Rp-cAMPS, an antagonist of protein kinase A (PKA), thus suggesting that D2 receptors and the cAMP cascade are not required. The induction of Fos expression was blocked by tetrodotoxin, BAPTA and KN-93, thus showing that it is activity- and calcium-dependent and requires the activation of a calmodulin-dependent kinase (CaMK). Together, these results suggest that haloperidol induces Fos expression in dopaminergic neurons through a D2 receptor-independent increase in intracellular calcium, leading to CaMK activation.

Topics: Animals; Benzylamines; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; Cells, Cultured; Colforsin; Cyclic AMP; Dopamine; Gene Expression; Genes, fos; Haloperidol; Neurons; Rats; Rats, Sprague-Dawley; Receptors, Dopamine D2; Receptors, sigma; RNA, Messenger; Second Messenger Systems; Signal Transduction; Sulfonamides; Tetrodotoxin; Thionucleotides; Ventral Tegmental Area

2003