Novelty-induced increase in dopamine release in the rat prefrontal cortex in vivo: inhibition by diazepam

Feenstra, Matthijs G.P.; Botterblom, M.H.A.; Uum, J.F.M. Van

doi:10.1016/0304-3940(95)11456-7

Cited by 149 publications

(68 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…27 Dopamine might be a likely candidate, as it is well established that dopamine projections to the PFC are activated by stressful stimuli. 59 Previous studies have shown that, despite the fact that stress-induced locomotor activity is increased in VH lesioned rats, 44 these animals display reduced dopamine release. 60 Accordingly the lack of BDNF up-regulation in PFC after restraint stress may be related to a reduced dopaminergic response.…”

Section: Discussionmentioning

confidence: 97%

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

Molteni

Lipska²,

Weinberger³

et al. 2001

Mol Psychiatry

View full text Add to dashboard Cite

The neonatal (PND 7) lesion of the ventral hippocampus (VH) with ibotenic acid represents a well-established experimental paradigm that recapitulates many schizophrenia-like phenomena. In order to investigate molecular changes that could contribute to long lasting consequences on brain function, we have investigated the effects of the VH lesion on the expression for the trophic factors FGF-2 and BDNF. We used RNase protection assay to measure their mRNA levels in cortical regions of prepubertal (PND 35) and young adult (PND 56) animals, both under basal condition as well as in response to an acute restraint stress. The expression of BDNF was not altered by the VH lesion in prefrontal (PFC) and frontal cortex (FC) of PND 35 or PND 56 rats. An acute restraint stress at PND 35 produced a significant increase of the neurotrophin expression in PFC of sham as well as lesioned animals. However in young adult animals a significant elevation of BDNF expression was observed only in sham rats. We also found that the VH lesion produced a significant reduction of basal BDNF mRNA levels in the cingulate cortex of young adult, but not prepubertal rats. This effect was not accompanied by changes in the acute modulation of the neurotrophin, which was up-regulated by stress in both experimental groups. Conversely the expression of FGF-2 at PND 35 and PND 56 was not altered by early postnatal VH lesion, and there were no major differences between sham and lesioned animals in response to the acute stress. The changes in trophic factor expression may be relevant for the long-term effects of VH lesion on synaptic plasticity and may determine an increased vulnerability of the brain under challenging situations. Molecular Psychiatry (2001) 6, 285-292.

show abstract

Section: Discussionmentioning

confidence: 97%

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

Molteni

Lipska²,

Weinberger³

et al. 2001

Mol Psychiatry

View full text Add to dashboard Cite

show abstract

“…Additionally, findings by Doherty and Gratton (1999) indicate that infusion of a GABA A agonist (muscimol) directly into the PFC inhibits stress-induced release of DA in the mPFC, while a GABA B antagonist (phaclofen) enhances this same release. On the contrary, under similar conditions Feenstra et al (Feenstra et al 1998) found no influence of the locally applied GABA B agonist baclofen or glutamate receptor agonists and antagonists (ACPD, dixocilpine) in the mPFC, although in an earlier study (Feenstra et al 1995) this group reported a benzodiazepine (diazepam) to inhibit the stress-induced release of DA in the mPFC. Taken together, these studies indicate that GABA B antagonism and GABA A agonism could play a possible role in the enhanced DAergic response to MP challenge in the mPFC induced by stress, although additional investigations would be required to support this hypothesis.…”

Section: Brief Stress Enhances the Da Response To Mp When Administerementioning

confidence: 92%

“…This augmented response might be due to cross innervation of the mPFC from several brain stem projections, such as the A10 pathway from the ventral tegmental area (VTA) and/or noradrenergic connections from the locus coeruleus (LC). More specifically, systemic stressors such as handling, restraint, or immobilization increase mPFC levels of DA by 150-300% (Enrico et al 1998;Feenstra et al 1995), and NE levels by 160-250% Kawahara et al 2000;Shimizu et al 1994). These responses can be modulated by infusion of pharmacologic agents directly into the LC and the VTA, indicating the influence of these regions on mPFC function.…”

mentioning

confidence: 99%

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Marsteller

Gerasimov

Schiffer

et al. 2002

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…As to this latter aspect, the DH has been considered to be part of the socalled behavioral inhibition system and it exerts a key role in the control of anxiety (4). All of these structures are part of the mesocorticolimbic system, in which biogenic amine levels are highly sensitive to exposure to a wide variety of acute stressors (10,11,18).…”

Section: Introductionmentioning

confidence: 99%

Changes in the biogenic amine content of the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens of rats submitted to single and repeated sessions of the elevated plus-maze test

Carvalho

Albrechet‐Souza

Masson

et al. 2005

Braz J Med Biol Res

View full text Add to dashboard Cite

It has been demonstrated that exposure to a variety of stressful experiences enhances fearful reactions when behavior is tested in current animal models of anxiety. Until now, no study has examined the neurochemical changes during the test and retest sessions of rats submitted to the elevated plus maze (EPM). The present study uses a new approach (HPLC) by looking at the changes in dopamine and serotonin levels in the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens in animals upon single or double exposure to the EPM (one-trial tolerance). The study involved two experiments: i) saline or midazolam (0.5 mg/kg) before the first trial, and ii) saline or midazolam before the second trial. For the biochemical analysis a control group injected with saline and not tested in the EPM was included. Stressful stimuli in the EPM were able to elicit one-trial tolerance to midazolam on re-exposure (61.01%). Significant decreases in serotonin contents occurred in the prefrontal cortex (38.74%), amygdala (78.96%), dorsal hippocampus (70.33%), and nucleus accumbens (73.58%) of the animals tested in the EPM (P < 0.05 in all cases in relation to controls not exposed to the EPM). A significant decrease in dopamine content was also observed in the amygdala (54.74%, P < 0.05). These changes were maintained across trials. There was no change in the turnover rates of these monoamines. We suggest that exposure to the EPM causes reduced monoaminergic neurotransmission activity in limbic structures, which appears to underlie the "one-trial tolerance" phenomenon.

show abstract

Novelty-induced increase in dopamine release in the rat prefrontal cortex in vivo: inhibition by diazepam

Cited by 149 publications

References 23 publications

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Changes in the biogenic amine content of the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens of rats submitted to single and repeated sessions of the elevated plus-maze test

Contact Info

Product

Resources

About