Anesthetic influences on the basal acticity and pharmacological responsiveness of nigrostriatal dopamine neurons

Kelland, Mark D.; Chiodo, Louis A.; Freeman, Arthur

doi:10.1002/syn.890060213

Cited by 138 publications

(131 citation statements)

References 11 publications

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“…Rats that performed more lever-press sign-tracking CRs showed more novelty stress-induced corticosterone release, higher DA levels in NAC, lower DOPAC/DA turnover ratios in caudate putamen, lower 5-HIAA/5-HT turnover in the VTA, but no evidence of elevated dopamine activity in PFC. Similarly, rats that more readily self-administer amphetamine showed more novelty stress-induced corticosterone release (Piazza et al, 1989;Rouge-Pont et al, 1993;Piazza and Le Moal, 1996;Lucas et al, 1998), higher indices of DA functioning in NAC (Piazza et al, 1989;Rouge-Pont et al, 1993;Piazza and Le Moal, 1996;Lucas et al, 1998), but not in PFC (Simon et al, 1988;Piazza et al, 1991) and lower indices of 5-HT functioning in VTA (Piazza et al, 1991; see also Kelland et al, 1990). These results add to the growing body of evidence suggesting that sign-tracking and drug abuse may be related phenomena (Tomie, 1995a(Tomie, , 1996Tomie et al, 2000;Everitt et al, 2001;Uslaner et al, 2006;Flagel et al, 2007a, b).…”

Section: Vulnerability Markerssupporting

confidence: 58%

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

Tomie

Grimes

Pohorecky

2008

Brain Research Reviews

150

134

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Drug abuse researchers have noted striking similarities between behaviors elicited by Pavlovian signtracking procedures and prominent symptoms of drug abuse. In Pavlovian sign-tracking procedures, repeated paired presentations of a small object (conditioned stimulus, CS) with a reward (unconditioned stimulus, US) elicits a conditioned response (CR) that typically consists of approaching the CS, contacting the CS, and expressing consummatory responses at the CS. Signtracking CR performance is poorly controlled and exhibits spontaneous recovery and long-term retention, effects that resemble relapse. Sign-tracking resembles psychomotor activation, a syndrome of behavioral responses evoked by addictive drugs, and the effects of sign-tracking on corticosterone levels and activation of dopamine pathways resemble the neurobiological effects of abused drugs. Finally, the neurobiological profile of individuals susceptible to sign-tracking resembles the pathophysiological profile of vulnerability to drug abuse, and vulnerability to sign-tracking predicts vulnerability to impulsive responding and alcohol self-administration. Implications of sign-tracking for models of drug addiction are considered.

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Section: Vulnerability Markerssupporting

confidence: 58%

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

Tomie

Grimes

Pohorecky

2008

Brain Research Reviews

150

134

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“…Curiously, 2-methyl-5-HT, a 5-HT3 receptor agonist, induced release of dopamine in rat striatal slices apparently independent of the impulse flow (Blandina et al, 1988). Likewise, it has recently been observed that systemic administration of the 5-HT receptor agonist increases extracellular dopamine (Galloway et al, 1993) with little effect on dopamine neuronal firing rate (Kelland et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

5‐HT₃ receptor agonist induced carrier‐mediated release of dopamine in rat striatum in vivo

Santiago

Machado

Cano

1995

British J Pharmacology

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1 In vivo microdialysis was used to study the effect of phenylbiguanide (PBG), a 5-hydroxytryptamine3 receptor agonist, on the extracellular output of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the corpus striatum.2 PBG produced a dose-related (10-500 gM) increase in the release of dopamine (280-2000%).DOPAC and HVA output decreased with the perfusion of PBG. This decrease was similar with 50-500 Mm PBG. 5-HIAA output was not affected by any PBG concentration used.3 When nomifensine (5 gM) was included in the Ringer solution, the effect of PBG on the release of dopamine was ameliorated or inhibited. However, the effect of PBG (50-500 gM) on the extracellular output of DOPAC and HVA was similar in the absence and in the presence of nomifensine (5 gM). 6 These results suggest that the effect of PBG on the release of dopamine is mainly carrier-mediated.

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“…However, evidence indicates that this effect is indirect and reflects a decrease in serotonergic function mediated by 5-HT1A autoreceptorinduced decreases in 5-HT release. In support of this explanation, depletion of 5-HT by the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) blocked the augmentation of firing rate induced by 8-OHDPAT administration (Kelland et al, 1990). Thus, 5-HT may normally inhibit SN DA cell firing and removal of this inhibition (disinhibition) by activation of 5-HT1A autoreceptors may increase DA cell firing rate.…”

Section: Nigrostriatal Pathwaymentioning

confidence: 96%

“…Intravenous administration of the agonist 8-OHDPAT increased the firing rate of a subpopulation of nigrostriatal neurons, those that were slowly firing (Kelland et al, 1990). However, evidence indicates that this effect is indirect and reflects a decrease in serotonergic function mediated by 5-HT1A autoreceptorinduced decreases in 5-HT release.…”

Section: Nigrostriatal Pathwaymentioning

confidence: 99%

Pharmacologic mechanisms of serotonergic regulation of dopamine neurotransmission

Alex

Pehek

2007

Pharmacology & Therapeutics

526

311

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The neurotransmitter dopamine (DA) has a long association with normal functions such as motor control, cognition, and reward, as well as a number of syndromes including drug abuse, schizophrenia, and Parkinson's disease. Studies show that serotonin (5-HT) acts through several 5-HT receptors in the brain to modulate DA neurons in all three major dopaminergic pathways. There are at least 14 5-HT receptor subtypes, many of which have been shown to play some role in mediating 5-HT/DA interactions. Several subtypes, including the 5-HT1A, 5-HT1B, 5-HT2A, 5-HT3 and 5-HT4 receptors, act to facilitate DA release, while the 5-HT2C receptor mediates an inhibitory effect of 5-HT on DA release. Most 5-HT receptor subtypes only modulate DA release when 5-HT and/or DA neurons are stimulated, but the 5-HT2C receptor, characterized by high levels of constitutive activity, inhibits tonic as well as evoked DA release. This review summarizes the anatomical evidence for the presence of each 5-HT receptor subtype in dopaminergic regions of the brain and the neuropharmacological evidence demonstrating regulation of each DA pathway. The relevance of 5-HT receptor modulation of DA systems to the development of therapeutics used to treat schizophrenia, depression, and drug abuse is discussed. Lastly, areas are highlighted in which future research would be maximally beneficial to the treatment of these disorders.

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Anesthetic influences on the basal acticity and pharmacological responsiveness of nigrostriatal dopamine neurons

Cited by 138 publications

References 11 publications

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

5‐HT₃ receptor agonist induced carrier‐mediated release of dopamine in rat striatum in vivo

Pharmacologic mechanisms of serotonergic regulation of dopamine neurotransmission

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Anesthetic influences on the basal acticity and pharmacological responsiveness of nigrostriatal dopamine neurons

Cited by 138 publications

References 11 publications

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

5‐HT3 receptor agonist induced carrier‐mediated release of dopamine in rat striatum in vivo

Pharmacologic mechanisms of serotonergic regulation of dopamine neurotransmission

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5‐HT₃ receptor agonist induced carrier‐mediated release of dopamine in rat striatum in vivo