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![Increase of neurotransmission produced by pharmacological modulation of neural Ca 2+ /cAMP signaling interaction (A) Records showing that contractile responses mediated by neurotransmitter released from sympathetic nerves by means Electrical Field Stimulation (EFS) in rat vas deferens (neurogenic contractions) were significantly reduced by L-type CCB (verapamil) in high concentrations (> 10-6 M), but paradoxically increased in concentrations below 10-6 M, characterizing CCB-induced sympathetic hyperactivity. This increase of neurogenic contractions by verapamil (< 10-6 M) was potentiated by pre-treatment of isolated tissue with cAMP-enhancer compounds, such as rolipram 10-7 M; (B) IBMX 10-6 M; (C) and forskolin 10-7 M; (D) Each point below the record represents molar concentration of verapamil (interval of 0.5 log unity). Each line below the record represents incubation time with cAMP-enhancer compounds. Representative records extracted from Bergantin, et al. [5].](profile/Leandro-Bergantin/publication/325497996/figure/fig1/AS:632699479916544@1527858719375/Increase-of-neurotransmission-produced-by-pharmacological-modulation-of-neural-Ca-2.png)
Increase of neurotransmission produced by pharmacological modulation of neural Ca 2+ /cAMP signaling interaction (A) Records showing that contractile responses mediated by neurotransmitter released from sympathetic nerves by means Electrical Field Stimulation (EFS) in rat vas deferens (neurogenic contractions) were significantly reduced by L-type CCB (verapamil) in high concentrations (> 10-6 M), but paradoxically increased in concentrations below 10-6 M, characterizing CCB-induced sympathetic hyperactivity. This increase of neurogenic contractions by verapamil (< 10-6 M) was potentiated by pre-treatment of isolated tissue with cAMP-enhancer compounds, such as rolipram 10-7 M; (B) IBMX 10-6 M; (C) and forskolin 10-7 M; (D) Each point below the record represents molar concentration of verapamil (interval of 0.5 log unity). Each line below the record represents incubation time with cAMP-enhancer compounds. Representative records extracted from Bergantin, et al. [5].
Source publication
Due to the involvement of the imbalance of neuronal Ca2+ homeostasis in the pathogenesis of several neurodegener-ative diseases, the use of drugs to prevent or attenuate this imbalance emerged as a new therapeutic strategy for treating these diseases. Thus, our discovery of the involvement of the interaction between intracellular signaling pathways...
Contexts in source publication
Context 1
... is a progressive neurodegenerative disorder re- lated to ageing characterized by cognitive and memory deterioration. Neuritic plaques represent the patho- duced by L-type CCB (verapamil) in high concentrations (> 1 μmol/L), but paradoxically increased in concentra- tions below 1 μmol/L, characterizing CCB-induced sym- pathetic hyperactivity ( Figure 1A). These paradoxical CCB-effects were significantly potentiated by pre-treat- ment of vas deferens with cAMP-enhancer compounds, such as AC activators (forskolin) and Phosphodiesterase (PDE) inhibitors (rolipram and Isobutyl Methyl Xanthine (IBMX)) ( Figure 1B, Figure 1C and Figure 1D). ...
Context 2
... plaques represent the patho- duced by L-type CCB (verapamil) in high concentrations (> 1 μmol/L), but paradoxically increased in concentra- tions below 1 μmol/L, characterizing CCB-induced sym- pathetic hyperactivity ( Figure 1A). These paradoxical CCB-effects were significantly potentiated by pre-treat- ment of vas deferens with cAMP-enhancer compounds, such as AC activators (forskolin) and Phosphodiesterase (PDE) inhibitors (rolipram and Isobutyl Methyl Xanthine (IBMX)) ( Figure 1B, Figure 1C and Figure 1D). This poten- tiation by cAMP-enhancer compounds was prevented by inhibition of AC with SQ 22536. ...
Context 3
... plaques represent the patho- duced by L-type CCB (verapamil) in high concentrations (> 1 μmol/L), but paradoxically increased in concentra- tions below 1 μmol/L, characterizing CCB-induced sym- pathetic hyperactivity ( Figure 1A). These paradoxical CCB-effects were significantly potentiated by pre-treat- ment of vas deferens with cAMP-enhancer compounds, such as AC activators (forskolin) and Phosphodiesterase (PDE) inhibitors (rolipram and Isobutyl Methyl Xanthine (IBMX)) ( Figure 1B, Figure 1C and Figure 1D). This poten- tiation by cAMP-enhancer compounds was prevented by inhibition of AC with SQ 22536. ...
Context 4
... plaques represent the patho- duced by L-type CCB (verapamil) in high concentrations (> 1 μmol/L), but paradoxically increased in concentra- tions below 1 μmol/L, characterizing CCB-induced sym- pathetic hyperactivity ( Figure 1A). These paradoxical CCB-effects were significantly potentiated by pre-treat- ment of vas deferens with cAMP-enhancer compounds, such as AC activators (forskolin) and Phosphodiesterase (PDE) inhibitors (rolipram and Isobutyl Methyl Xanthine (IBMX)) ( Figure 1B, Figure 1C and Figure 1D). This poten- tiation by cAMP-enhancer compounds was prevented by inhibition of AC with SQ 22536. ...
