ArticleThe Journal of pharmacology and experimental therapeutics2008
Neurotensin in the ventral pallidum increases extracellular gamma-aminobutyric acid and differentially affects cue- and cocaine-primed reinstatement.
Article in The Journal of pharmacology and experimental therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Changes in dorsomedial striatum activity during expression of goal-directed vs. habit-like cue-induced cocaine seeking.Addiction neuroscience · 2024Article
- Differential Modulation of GABAergic and Glutamatergic Neurons in the Ventral Pallidum by GABA and Neuropeptides.eNeuro · 2023Article
- Intermittent cocaine self-administration has sex-specific effects on addiction-like behaviors in rats.Neuropharmacology · 2023Article
- Ventral pallidal regulation of motivated behaviors and reinforcement.Frontiers in neural circuits · 2023Review
- Effect of D1- and D2-like Dopamine Receptor Antagonists on the Rewarding and Anxiolytic Effects of Neurotensin in the Ventral Pallidum.Biomedicines · 2022Article
- BEHAVIORAL AND NEUROBIOLOGICAL MECHANISMS OF PAVLOVIAN AND INSTRUMENTAL EXTINCTION LEARNING.Physiological reviews · 2021Review
- Dorsolateral striatum dopamine-dependent cocaine seeking is resistant to pavlovian cue extinction in male and female rats.Neuropharmacology · 2021Article
- Phosphoproteomic analysis of cocaine memory extinction and reconsolidation in the nucleus accumbens.Psychopharmacology · 2019Article
- Antagonism of Neurotensin Receptors in the Ventral Tegmental Area Decreases Methamphetamine Self-Administration and Methamphetamine Seeking in Mice.The international journal of neuropsychopharmacology · 2018Article
- Ventral pallidal encoding of reward-seeking behavior depends on the underlying associative structure.eLife · 2018Article
- Neurotensin speeds inhibition of dopamine neurons through temporal modulation of GABANeuropharmacology · 2018Article
- Effects of Adolescent Cannabinoid Self-Administration in Rats on Addiction-Related Behaviors and Working Memory.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Ventral Pallidum Output Pathways in Context-Induced Reinstatement of Alcohol Seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Phosphoproteomic Analysis Reveals a Novel Mechanism of CaMKIIα Regulation Inversely Induced by Cocaine Memory Extinction versus Reconsolidation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Motivational Processes Underlying Substance Abuse Disorder.Current topics in behavioral neurosciences · 2016Review
- Metabotropic Glutamate Receptor 7 (mGluR7) as a Target for the Treatment of Psychostimulant Dependence.CNS & neurological disorders drug targets · 2015Review
- Role of cues and contexts on drug-seeking behaviour.British journal of pharmacology · 2014Review
- Elucidating the role of neurotensin in the pathophysiology and management of major mental disorders.Behavioral sciences (Basel, Switzerland) · 2014Review
- Neurotensin agonist attenuates nicotine potentiation to cocaine sensitization.Behavioral sciences (Basel, Switzerland) · 2014Article
- Cocaine dysregulates opioid gating of GABA neurotransmission in the ventral pallidum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cocaine-primed reinstatement is an animal model of drug relapse. The neurocircuitry underlying cocaine-primed reinstatement includes a decrease in GABA in the ventral pallidum (VP) that is inhibited by a mu opioid receptor antagonist, suggesting that opioid peptides colocalized with GABA in the projection from the nucleus accumbens to the VP may mediate this effect. Neurotensin is also colocalized with GABA and has been shown to increase GABA release in several brain regions. Therefore, the present study determined whether neurotensin increases GABA release in the VP, antagonizes cocaine-induced decreases in GABA, and prevents reinstatement of cocaine seeking. In vivo microdialysis revealed that the neurotensin agonist neurotensin peptide fragment 8-13 [NT(8-13)] increased GABA in the VP in a neurotensin receptor and tetrodotoxin-dependent manner and blocked the cocaine-induced decrease in GABA. NT(8-13) (3 nmol) microinjected into the VP prevented cue-induced reinstatement without affecting cocaine self-administration. In contrast, 3 nmol NT(8-13) potentiated cocaine-primed reinstatement. The neurotensin antagonist SR142948 (2-[[[5-(2,6-dimethoxyphenyl)-1-[4-[[[3-(dimethylamino)propyl]methylamino]carbonyl]-2-(1-methylethyl)phenyl]-1H -pyrazol-3-yl]carbonyl]amino]-tricyclo-[3.3.1.13,7]decane-2-carboxylic acid) had no effect on any behavioral measure when infused in the VP at the dose tested but attenuated cocaine-primed reinstatement when administered systemically. In contrast to reinstatement, NT(8-13) did not alter the motor response to acute cocaine or the development of motor sensitization by chronic cocaine. Three conclusions can be drawn from these data: 1) neurotensin promotes GABA release in the VP and correspondingly inhibits cue-induced reinstatement, 2) neurotensin and cocaine interact in a manner that countermands the neurotensin-induced increase in GABA and promotes reinstatement, and 3) endogenous release of neurotensin in the VP is not necessary for reinstatement.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.