Inhibition of Phosphodiesterase 10A Increases the Responsiveness of Striatal Projection Neurons to Cortical Stimulation
The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons (MSNs), apparently playing a critical role in the regulation of both cGMP and cAMP signaling cascades. Genetic disruption or pharmacological inhibition of PDE10A reverses behavi...
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Published in | The Journal of pharmacology and experimental therapeutics Vol. 328; no. 3; pp. 785 - 795 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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American Society for Pharmacology and Experimental Therapeutics
01.03.2009
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Abstract | The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons
(MSNs), apparently playing a critical role in the regulation of both cGMP and cAMP signaling cascades. Genetic disruption
or pharmacological inhibition of PDE10A reverses behavioral abnormalities associated with subcortical hyperdopaminergia. Here,
we investigate the effect of PDE10A inhibition on the activity of MSNs using single-unit extracellular recordings performed
in the dorsal striatum of anesthetized rats. Antidromic stimulation of the substantia nigra pars reticulata was used to identify
striatonigral (SNr+) MSNs. Intrastriatal infusion of the selective PDE10A inhibitors papaverine or TP-10 [2-{4-[-pyridin-4-yl-1-(2,2,2-trifluoroethyl)-1 H -pyrazol-3-yl]-phenoxymethyl}-quinoline succinic acid] by reverse microdialysis did not affect spontaneous firing but robustly
increased measures of cortically evoked spike activity in a stimulus intensity-dependent manner. Systemic administration of
TP-10 also increased cortically evoked spike activity in a stimulus intensity- and dose-dependent manner. A robust increase
in cortically evoked activity was apparent in SNr- MSNs (primarily striatopallidal). It is interesting that TP-10 administration
did not affect cortically evoked activity in SNr+ MSNs. However, TP-10 administration increased the incidence of antidromically
activated (i.e., SNr+) MSNs. These findings indicate that inhibition of striatal PDE10A activity increases the responsiveness
of MSNs to depolarizing stimuli. Furthermore, given the lack of effect of TP-10 on SNr+ MSNs, we speculate that PDE10A inhibition
may have a greater facilitatory effect on corticostriatal synaptic activity in striatopallidal MSNs. These data support further
investigation of selective targeting of PDE signaling pathways in MSN subpopulations because this may represent a promising
novel approach for treating brain disorders involving dysfunctional glutamatergic and dopaminergic neurotransmission. |
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AbstractList | The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in
striatal medium-sized spiny projection neurons (MSNs), apparently playing a
critical role in the regulation of both cGMP and cAMP signaling cascades.
Genetic disruption or pharmacological inhibition of PDE10A reverses behavioral
abnormalities associated with subcortical hyperdopaminergia. Here, we
investigate the effect of PDE10A inhibition on the activity of MSNs using
single-unit extracellular recordings performed in the dorsal striatum of
anesthetized rats. Antidromic stimulation of the substantia nigra pars
reticulata was used to identify striatonigral (SNr+) MSNs. Intrastriatal
infusion of the selective PDE10A inhibitors papaverine or TP-10
[2-{4-[-pyridin-4-yl-1-(2,2,2-trifluoroethyl)-1
H
-pyrazol-3-yl]-phenoxymethyl}-quinoline
succinic acid] by reverse microdialysis did not affect spontaneous firing but
robustly increased measures of cortically evoked spike activity in a stimulus
intensity-dependent manner. Systemic administration of TP-10 also increased
cortically evoked spike activity in a stimulus intensity- and dose-dependent
manner. A robust increase in cortically evoked activity was apparent in SNr-
MSNs (primarily striatopallidal). It is interesting that TP-10 administration
did not affect cortically evoked activity in SNr+ MSNs. However, TP-10
administration increased the incidence of antidromically activated (i.e.,
SNr+) MSNs. These findings indicate that inhibition of striatal PDE10A
activity increases the responsiveness of MSNs to depolarizing stimuli.
Furthermore, given the lack of effect of TP-10 on SNr+ MSNs, we speculate that
PDE10A inhibition may have a greater facilitatory effect on corticostriatal
synaptic activity in striatopallidal MSNs. These data support further
investigation of selective targeting of PDE signaling pathways in MSN
subpopulations because this may represent a promising novel approach for
treating brain disorders involving dysfunctional glutamatergic and
dopaminergic neurotransmission. The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons (MSNs), apparently playing a critical role in the regulation of both cGMP and cAMP signaling cascades. Genetic disruption or pharmacological inhibition of PDE10A reverses behavioral abnormalities associated with subcortical hyperdopaminergia. Here, we investigate the effect of PDE10A inhibition on the activity of MSNs using single-unit extracellular recordings performed in the dorsal striatum of anesthetized rats. Antidromic stimulation of the substantia nigra pars reticulata was used to identify striatonigral (SNr+) MSNs. Intrastriatal infusion of the selective PDE10A inhibitors papaverine or TP-10 [2-{4-[-pyridin-4-yl-1-(2,2,2-trifluoroethyl)-1H-pyrazol-3-yl]-phenoxymethyl}-quinoline succinic acid] by reverse microdialysis did not affect spontaneous firing but robustly increased measures of cortically evoked spike activity in a stimulus intensity-dependent manner. Systemic administration of TP-10 also increased cortically evoked spike activity in a stimulus intensity- and dose-dependent manner. A robust increase in cortically evoked activity was apparent in SNr- MSNs (primarily striatopallidal). It is interesting that TP-10 administration did not affect cortically evoked activity in SNr+ MSNs. However, TP-10 administration increased the incidence of antidromically activated (i.e., SNr+) MSNs. These findings indicate that inhibition of striatal PDE10A activity increases the responsiveness of MSNs to depolarizing stimuli. Furthermore, given the lack of effect of TP-10 on SNr+ MSNs, we speculate that PDE10A inhibition may have a greater facilitatory effect on corticostriatal synaptic activity in striatopallidal MSNs. These data support further investigation of selective targeting of PDE signaling pathways in MSN subpopulations because this may represent a promising novel approach for treating brain disorders involving dysfunctional glutamatergic and dopaminergic neurotransmission. The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons (MSNs), apparently playing a critical role in the regulation of both cGMP and cAMP signaling cascades. Genetic disruption or pharmacological inhibition of PDE10A reverses behavioral abnormalities associated with subcortical hyperdopaminergia. Here, we investigate the effect of PDE10A inhibition on the activity of MSNs using single-unit extracellular recordings performed in the dorsal striatum of anesthetized rats. Antidromic stimulation of the substantia nigra pars reticulata was used to identify striatonigral (SNr+) MSNs. Intrastriatal infusion of the selective PDE10A inhibitors papaverine or TP-10 [2-{4-[-pyridin-4-yl-1-(2,2,2-trifluoroethyl)-1 H -pyrazol-3-yl]-phenoxymethyl}-quinoline succinic acid] by reverse microdialysis did not affect spontaneous firing but robustly increased measures of cortically evoked spike activity in a stimulus intensity-dependent manner. Systemic administration of TP-10 also increased cortically evoked spike activity in a stimulus intensity- and dose-dependent manner. A robust increase in cortically evoked activity was apparent in SNr- MSNs (primarily striatopallidal). It is interesting that TP-10 administration did not affect cortically evoked activity in SNr+ MSNs. However, TP-10 administration increased the incidence of antidromically activated (i.e., SNr+) MSNs. These findings indicate that inhibition of striatal PDE10A activity increases the responsiveness of MSNs to depolarizing stimuli. Furthermore, given the lack of effect of TP-10 on SNr+ MSNs, we speculate that PDE10A inhibition may have a greater facilitatory effect on corticostriatal synaptic activity in striatopallidal MSNs. These data support further investigation of selective targeting of PDE signaling pathways in MSN subpopulations because this may represent a promising novel approach for treating brain disorders involving dysfunctional glutamatergic and dopaminergic neurotransmission. |
Author | Christopher J. Schmidt Anthony R. West Sarah Threlfell Stephen Sammut Frank S. Menniti |
AuthorAffiliation | Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois (S.T., S.S., A.R.W.); and Pfizer Global Research and Development, Groton, Connecticut (F.S.M., C.J.S.) |
AuthorAffiliation_xml | – name: Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois (S.T., S.S., A.R.W.); and Pfizer Global Research and Development, Groton, Connecticut (F.S.M., C.J.S.) |
Author_xml | – sequence: 1 givenname: Sarah surname: Threlfell fullname: Threlfell, Sarah email: Anthony.west@rosalindfranklin.edu organization: Department of Neuro-science, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064. Anthony.west@rosalindfranklin.edu – sequence: 2 givenname: Stephen surname: Sammut fullname: Sammut, Stephen – sequence: 3 givenname: Frank S surname: Menniti fullname: Menniti, Frank S – sequence: 4 givenname: Christopher J surname: Schmidt fullname: Schmidt, Christopher J – sequence: 5 givenname: Anthony R surname: West fullname: West, Anthony R |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19056933$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 doi:10.1124/jpet.108.146332. This work was supported by the National Institutes of Health National Institute of Neurological Disorders and Stroke [Grant NS 047452]; by the Chicago Medical School; and by the National Alliance for Research on Schizophrenia and Depression, Pfizer Incorporated. Address correspondence to: Dr. Anthony R. West, Department of Neuro-science, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064. E-mail: Anthony.west@rosalindfranklin.edu ABBREVIATIONS: PDE10A, cyclic nucleotide phosphodiesterase 10A; SNr+, striatonigral; MSN, medium-sized spiny projection neuron; SNr, substantia nigra pars reticulata; PDE, cyclic nucleotide phosphodiesterase; TP-10, 2-{4-[-pyridin-4-yl-1-(2,2,2-trifluoroethyl)-1H-pyrazol-3-yl]-phenoxymethyl}-quinoline succinic acid; IT, intratelencephalic; PT, pyramidal tract; aCSF, artificial cerebral spinal fluid; ANOVA, analysis of variance. |
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Snippet | The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons
(MSNs), apparently playing a... The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons (MSNs), apparently playing a... The cyclic nucleotide phosphodiesterase 10A (PDE10A) is highly expressed in striatal medium-sized spiny projection neurons (MSNs), apparently playing a... |
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SubjectTerms | Animals Corpus Striatum - drug effects Corpus Striatum - physiology Electric Stimulation Electrophysiology - methods Evoked Potentials - drug effects Evoked Potentials - physiology Frontal Lobe - drug effects Frontal Lobe - physiology Globus Pallidus - drug effects Globus Pallidus - physiology Male Microdialysis Neurons - drug effects Neurons - physiology Neuropharmacology Papaverine - pharmacology Phosphodiesterase Inhibitors - pharmacology Phosphoric Diester Hydrolases - metabolism Pyramidal Cells - drug effects Pyramidal Cells - physiology Rats Rats, Sprague-Dawley Signal Transduction - drug effects Signal Transduction - physiology Substantia Nigra - drug effects Substantia Nigra - physiology |
Title | Inhibition of Phosphodiesterase 10A Increases the Responsiveness of Striatal Projection Neurons to Cortical Stimulation |
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