1 The sensitivity of single neurones to microelectrophoretically applied dopamine, noradrenaline (NA), 5-hydroxytryptamine (5-HT) and acetylcholing (ACh) was investigated in the caudate nucleus of the rat, anaesthetized with halothane. Both excitatory and depressant responses could be observed to each of the agonists. There was a high correlation between the direction of responses to dopamine and noradrenaline, whereas there was no significant correlation between the direction of responses to dopamine and ACh. 2 The effect of desipramine was studied on both excitatory and depressant responses to dopamine, NA and 5-HT, and on excitatory responses to ACh. Both potentiation and antagonism of neuronal responses to monoamines and ACh could be observed after a brief application of desipramine. 3 Excitatory responses to glutamate were not affected by desipramine. 4 The observation that responses to dopamine and NA can be potentiated by desipramine in the caudate nucleus suggests that uptake blockade is not a prerequisite for potentiation. 5 It is suggested that the potentiation of neuronal responses to dopamine by desipramine may be responsible for the therapeutic efficacy of desipramine in Parkinson's disease.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666469 | PMC |
| http://dx.doi.org/10.1111/j.1476-5381.1975.tb07567.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Modulation of Autophagy and Nitric Oxide Signaling via Glycyrrhizic Acid and 7-Nitroindazole in MPTP-induced Parkinson's Disease Model.
Ann Neurosci
October 2024
Department of Pathology, King George's Medical University, Lucknow, Uttar Pradesh, India.
Background: Parkinson's disease (PD) is characterized by dopaminergic (DA) neuron loss, Lewy body build-up, and motor dysfunction. One of the primary pathogenic mechanisms of PD development is autophagy dysfunction and nitric oxide-mediated neurotoxicity.
Purpose: The current study focuses on autophagy and nitric oxide (NO) signaling roles in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated PD mice and their protection by their modulators.
Hinokinin Decreases Methamphetamine-Induced Hyperlocomotion via the Regulatory Effects on Dopamine Levels.
ACS Chem Neurosci
January 2025
College of Pharmacy, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do 28160, Republic of Korea.
The global abuse of stimulant methamphetamine (METH) imposes a significant social burden. Despite this, effective therapeutic interventions for mitigating the harmful effects associated with METH-induced central nervous system (CNS) stimulation remain elusive. (hinoki), containing hinokinin as its active constituent, has been identified to exhibit CNS depressant properties.
View Article and Find Full Text PDFMitigation of Neuroinflammation and Oxidative Stress in Rotenone-Induced Parkinson Mouse Model through Liposomal Coenzyme-Q10 Intervention: A Comprehensive In-vivo Study.
Inflammation
January 2025
Department of Chemistry, University of Agriculture Faisalabad, Faisalabad, Pakistan.
Parkinson's disease (PD) stands as the sec most prevalent incapacitating neurodegenerative disorder characterized by deterioration of dopamine-producing neurons in the substantia nigra. Coenzyme Q10 (CoQ10) has garnered attention as a potential antioxidant, anti-inflammatory agent and enhancer of mitochondrial complex-I activity. This study aimed to examine and compare the effectiveness of liposomal and non-encapsulated CoQ10 in rotenone induced-PD mouse model over a 21-day treatment duration.
View Article and Find Full Text PDFMu opioid receptors expressed in striatal D2 medium spiny neurons have divergent contributions to cocaine and morphine reward.
Neuroscience
January 2025
Institute for Neuroscience, The University of Texas at Austin, Austin, TX, USA; Waggoner Center for Alcohol & Addiction Research, The University of Texas at Austin, Austin, TX, USA; Department of Neuroscience, The University of Texas at Austin, Austin, TX, USA; Department of Neurology, Dell Medical School, The University of Texas at Austin, Austin, TX, USA. Electronic address:
While our understanding of the neurobiological mechanisms underlying cocaine and opiate reward has historically been dopamine-focused, evidence from genetic and pharmacological approaches indicates that µ-opioid receptors (MORs) in the striatum are important contributors. Within the striatum, MORs are expressed in both dopamine D1-receptor and D2-receptor expressing GABAergic medium spiny neurons (MSNs), as well as in interneurons and various afferents. Thus, it remains unclear how these distinct MOR populations regulate drug reward.
View Article and Find Full Text PDFD dopamine / mu opioid receptor interactions in operant conditioning assays of pain-depressed responding and drug-induced rate suppression, and a conditioned place preference procedure: assessment of therapeutic index in male Sprague Dawley rats.
Psychopharmacology (Berl)
January 2025
Department of Psychology, University of New England, Biddeford, ME, USA.
Rationale And Objectives: In vivo receptor interactions vary as a function of behavioral endpoint, with key differences between reflexive and non-reflexive measures that assess the motivational aspects of pain and pain relief. There have been no assessments of D dopamine agonist / mu opioid receptor (MOR) agonist interactions in non-reflexive behavioral measures of pain. We examined the hypothesis that D/MOR mixtures show enhanced effectiveness in blocking pain depressed behaviors while showing decreased side effects such as sedation and drug reward.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!