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 inThe Journal of pharmacology and experimental therapeutics Vol. 328; no. 3; pp. 785 - 795
Main Authors Threlfell, Sarah, Sammut, Stephen, Menniti, Frank S, Schmidt, Christopher J, West, Anthony R
Format Journal Article
LanguageEnglish
Published United States 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.
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.)
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  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
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  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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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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StartPage 785
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
URI http://jpet.aspetjournals.org/content/328/3/785.abstract
https://www.ncbi.nlm.nih.gov/pubmed/19056933
https://search.proquest.com/docview/66946231
https://pubmed.ncbi.nlm.nih.gov/PMC2646805
Volume 328
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