Dopamine (DA) effects on prefrontal cortex (PFC) neurons are essential for the cognitive functions mediated by this cortical area. However, the cellular mechanisms of DA neuromodulation in neocortex are not well understood. We characterized the effects of D1-type DA receptor (D1R) activation on the amplification (increase in duration and area) of excitatory postsynaptic potentials (EPSPs) at depolarized potentials, in layer 5 pyramidal neurons from rat PFC. Simulated EPSPs (sEPSPs) were elicited by current injection, to determine the effects of D1R activation independent of modulation of transmitter release or glutamate receptor currents. Application of the D1R agonist SKF81297 attenuated sEPSP amplification at depolarized potentials in a concentration-dependent manner. The SKF81297 effects were inhibited by the D1R antagonist SCH23390. The voltage-gated Na+ channel blocker tetrodotoxin (TTX) abolished the effects of SKF81297 on sEPSP amplification, suggesting that Na+ currents are necessary for the D1R effect. Furthermore, blockade of 4-AP- and TEA-sensitive K+ channels in the presence of TTX significantly increased EPSP amplification, arguing against the possibility that SKF81297 up-regulates currents that attenuate sEPSP amplification. SKF81297 application attenuated the subthreshold response to injection of depolarizing current ramps, in a manner consistent with a decrease in the persistent Na+ current. In addition, D1R activation decreased the effectiveness of temporal EPSP summation during 20 Hz sEPSP trains, selectively at depolarized membrane potentials. Therefore, the effects of D1R activation on Na+ channel-dependent EPSP amplification may regulate the impact of coincidence detection versus temporal integration mechanisms in PFC pyramidal neurons.
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http://dx.doi.org/10.1113/jphysiol.2007.130864 | DOI Listing |
Brain Sci
November 2024
Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.
Background/objectives: Dopamine replacement therapy for Parkinson's disease (PD) may lead to disabling incontrollable movements known as L-DOPA-induced dyskinesias. Transcranial magnetic stimulation (TMS) has been applied as non-invasive therapy to ameliorate motor symptoms and dyskinesias in PD treatment. Recent studies have shown that TMS-induced motor effects might be related to dopaminergic system modulation.
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December 2024
Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas (LaftamBio Pampa), Universidade Federal do Pampa, Itaqui, RS, Brazil. Electronic address:
Amphetamine (AMPH) abuse represents a major global public health issue, highlighting the urgent need for effective therapeutic interventions to manage addiction caused by this psychostimulant. This study aimed to assess the potential of m-trifluoromethyl-diphenyldiselenide [(m-CF-PhSe)] in preventing the addictive effects induced by AMPH through targeting dopamine metabolism proteins. (m-CF-PhSe) is of interest due to its demonstrated efficacy in mitigating opioid abuse, establishing it as a promising candidate for addiction treatment research.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
October 2024
School of Pharmacy, Shandong University of Traditional Chinese Medicine Ji'nan 250300, China Key Laboratory for Applied Technology of Sophisticated Analytical Instruments of Shandong Province, Shandong Analysis and Test Center, Qilu University of Technology (Shandong Academy of Sciences) Ji'nan 250014, China Shandong Provincial Key Laboratory of Natural Active Pharmaceutical Constituents Research in Universities, School of Pharmaceutical Sciences, Qilu University of Technology (Shandong Academy of Sciences) Ji'nan 250014, China.
Sargentodoxae Caulis was extracted with 80% ethanol and separated by macroporous resin, MCI, and ODS column chromatography and semi-preparative high performance liquid chromatography. The structures of the compounds were identified based on the NMR and MS data. A total of 19 compounds were identified as parabaroside D(1),(R)-2-(3,4-dihydroxyphenyl)-2-hydroxyethyl-O-β-D-glucopyranoside(2),(S)-2-(3,4-dihydroxyphenyl)-2-hydroxyethyl-O-β-D-glucopyranoside(3), protocatechin-3-O-β-D-glucoside(4), p-hydroxybenzoate-β-D-glucopyranoside(5), gentisic-5-O-β-D-glucopyranoside(6), vanillic acid 4-O-β-D-glucoside(7), syringic acid glucoside(8), uracil(9), uridine(10), neochlorogenic acid(11), chlorogenic acid(12), cryptochlorogenic acid(13), 3,4-dihydroxyphenylethanol glucoside(14), cuneataside A(15), cuneataside C(16), 4-hydroxy-3-methoxyacetophenone-4-O-β-D-apiose-(1→6)-β-D-glucopyranoside(17), proanthocyanidin B2(18), and baimantuoluoamide B(19).
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Department of Anesthesiology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, Jiangsu Province, PR China; Jiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, Jiangsu, PR China. Electronic address:
Neurobiol Learn Mem
December 2024
Department of Psychology and Collaborative Neuroscience Program, University of Guelph, 50 Stone Road E, Guelph, ON N1G 2W1, Canada.
Consolidated long-term memories can undergo strength or content modification via protein synthesis-dependent reconsolidation. This is the process by which a reminder cue initiates reactivation of the memory trace, triggering destabilization. Older and more strongly encoded spatial memories can resist destabilization due to biological boundary conditions.
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