Differential effects of inescapable footshocks and of stimuli previously paired with inescapable footshocks on dopamine turnover in cortical and limbic areas of the rat

Herman, J.P.; Guillonneau, D; Dantzer, Robert; Scatton, B.; Semerdjian-Rouquier, L.; Moal, Michel Le

doi:10.1016/0024-3205(82)90295-8

Cited by 414 publications

(99 citation statements)

References 13 publications

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“…Moreover, whereas mild stressors fail to increase DA levels in the NAc and dorsal striatum, they can evoke significant increases in prefrontal cortical DA levels (Abercrombie et al 1989). Similar results have been shown with respect to measures of the DA metabolite DOPAC in the frontal cortex and NAc (Herman et al 1982;cf. Horger and Roth 1996;Tissari et al 1979).…”

supporting

confidence: 85%

“…For example, multiple studies have shown that rodents exposed acutely to a stressor such as tail shock, foot shock or restraint exhibit marked increases in extracellular DA levels in the mPFC and moderate increases in the NAc and/or striatum (Abercrombie et al 1989;Roth et al 1988;Thierry et al 1976; for review, see Finlay and Zigmond 1997). Moreover, whereas mild stressors fail to increase DA levels in the NAc and dorsal striatum, they can evoke significant increases in prefrontal cortical DA (Herman et al 1982; cf. Horger and Roth 1996;Tissari et al 1979).…”

mentioning

confidence: 99%

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Chronic Cold Stress Reduces the Spontaneous Activity of Ventral Tegmental Dopamine Neurons

Moore

Rose

Grace

2001

Neuropsychopharmacology

112

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The dopamine (DA) Stress-induced changes in forebrain dopamine (DA) transmission have been implicated in the symptomatology of a number of psychiatric disorders including schizophrenia (Grace 1991; Seeman et al. 1976), major depression (Anisman and Zacharko 1990;Willner 1995), and behavioral disorders related to drug abuse (Quick et al. 1986). The mesoaccumbens and mesocortical DA systems, comprised of cells in the ventral tegmental area (VTA) and medial substantia nigra pars compacta (mSN) projecting to the medial prefrontal cortex (mPFC) or nucleus accumbens (NAc; Fallon and Loughlin 1995), have been shown to be sensitive to a number of stressors (Horger and Roth 1996). For example, multiple studies have shown that rodents exposed acutely to a stressor such as tail shock, foot shock or restraint exhibit marked increases in extracellular DA levels in the mPFC and moderate increases in the NAc and/or striatum (Abercrombie et al. 1989;Roth et al. 1988;Thierry et al. 1976; for review, see Finlay and Zigmond 1997). Moreover, whereas mild stressors fail to increase DA levels in the NAc and dorsal striatum, they can evoke significant increases in prefrontal cortical DA (Herman et al. 1982; cf. Horger and Roth 1996;Tissari et al. 1979).Thus, it appears that the DA projections from the VTA and substantia nigra are systematically activated during acute stress, with the sensitivity to stress being highest in the mesocortical DA system. Although the changes in mesoaccumbens and mesocortical DA transmission following acute exposure to a stressor have been well characterized, less is known about the response of these systems to chronic stress or exposure to highly traumatic conditions. However, there is evidence that DA release in the NAc and PFC may show some adaptation to the stressor after repeated (Cabib and Puglisi-Allegra 1996;Imperato et al. 1992Imperato et al. , 1993 or chronic (Gresch et al. 1994;Mizoguchi et al. 2000) exposure. Finlay et al. (1995) have shown that following chronic exposure to inescapable cold, considered a chronic stressor, extracellular DA levels in the NAc and PFC are unchanged or slightly lower than in controls (Gresch et al. 1994). Moreover, examined across studies, DA efflux evoked by a novel stressor appears to be similar in cold-stressed and control rats (Finlay et al. 1995;Gresch et al. 1994). Thus, it appears that in contrast to their responses to acute stress, the mesocortical and mesolimbic DA systems may show adaptation in response to chronic stress (see also Ortiz et al. 1996). The DAergic response contrasts with the sensitization of the sympathetic innervation to the adrenals and heightened response of the NE-containing neurons of the locus coeruleus in cold-stressed rats (Finlay et al. 1995;Fluharty et al. 1985;Gresch et al. 1994;Jedema et al. 1999Jedema et al. , 2001Mana and Grace 1997). This potentially distinct response of midbrain DA neurons to chronic stress may be relevant to the anhedonia and psychomotor slowing associated with post-traumatic stress disorder (Yehuda and A...

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supporting

confidence: 85%

mentioning

confidence: 99%

Chronic Cold Stress Reduces the Spontaneous Activity of Ventral Tegmental Dopamine Neurons

Moore

Rose

Grace

2001

Neuropsychopharmacology

112

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“…However, the time spent on social interaction was reliably diminished in lesioned rats, a finding that is clearly in contrast with the fact that prefrontal transection enhances social interaction in rats Tucci et al, 2000), suggesting that neurotransmitter systems other than the mPFC dopaminergic one are involved in this effect. The reduction of social interaction is difficult to explain, but it could be accounted for by a low attention level or disrupted cognitive processes, which are known to emerge after prefrontal dopamine loss (Lavielle et al, 1979;Herman et al, 1982), leading to lower interest for exploring a conspecific. However, lesioned rats did not show an attentional deficit as revealed by normal (or augmented) responses in the contextual fear conditioning experiment, pointing to a cognitive deficit altering the normal performance in the social interaction task.…”

Section: Discussionmentioning

confidence: 99%

Prefrontocortical Dopamine Loss in Rats Delays Long-Term Extinction of Contextual Conditioned Fear, and Reduces Social Interaction Without Affecting Short-Term Social Interaction Memory

Fernández-Espejo

2002

Neuropsychopharmacol

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Prefrontal dopamine loss delays extinction of cued fear conditioning responses, but its role in contextual fear conditioning has not been explored. Medial prefrontal lesions also enhance social interaction in rats, but the role of prefrontal dopamine loss on social interaction memory is not known. Besides, a role for subcortical accumbal dopamine on mnesic changes after prefrontal dopamine manipulation has been proposed but not explored. The objective was to study the involvement of dopaminergic neurotransmission in the medial prefrontal cortex (mPFC) and nucleus accumbens in two mnesic tasks: contextual fear conditioning and social interaction memory. For contextual fear conditioning, short-and long-term freezing responses after an electric shock were studied, as well as extinction retention. Regarding social interaction memory, the recognition of a juvenile, a very sensitive short-term memory test, was used. Dopamine loss was carried out by injection of 6-hydroxydopamine, and postmortem catecholamine levels were analyzed by high-performance liquid chromatography. Prefrontocortical dopamine loss (476%) led to a reactive enhancement of accumbal dopamine content (po0.01), supporting the hypothesis that a hyperdopaminergic tone emerges in the nucleus accumbens after prefrontocortical dopamine loss. In lesioned rats, long-term extinction of contextual fear conditioning was significantly delayed and extinction retention was impaired without changes in acquisition and short-term contextual fear conditioning and, on the other hand, acquisition and short-term social interaction memory were not affected, although time spent on social interaction was significantly reduced. Added dopamine loss in the nucleus accumbens (476%) did not alter these behavioral changes. In summary, the results of the present study indicate that the dopaminergic network in the mPFC (but not in the nucleus accumbens) coordinates the normal long-term extinction of contextual fear conditioning responses without affecting their acquisition, and it is involved in time spent on social interaction, but not acquisition and short-term social interaction memory.

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“…This also ensures that ani mals are exposed to footshock on two occasions and per mits comparison to Bourne et al (1992) where they ex posed rats to swim stress following CS exposure on two occasions. The shock parameters employed were select ed because 30 min of intermittent footshock has been shown to increase dopaminergic activity (Herman et al 1982;Abercrombie et al 1989) and because amphetamine-induced CTA has been demonstrated with a 30-min CS-UCS interval (D 'Mello et al 1977). Thus, our shock procedure employed fewer shocks than used in studies reporting shock-induced attenuation of LiCl CTA (Dess et al 1988;Revusky and Reilly 1989) but more shocks than studies reporting shock-induced facilitation of rotation-or apomorphine-induced CTA (Lasiter and Braun 1981).…”

Section: Methodsmentioning

confidence: 99%

Time-dependent exacerbation of amphetamine-induced taste aversions following exposure to footshock

1996

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A bstract Previous studies have shown that stressors at tenuate LiCl-induced conditioned taste aversions (CTA) but not morphine-induced CTA. The current studies ex amined the effects of footshock on the acquisition and extinction of amphetamine-induced CTA. Experiment 1 demonstrated that exposure to 30 footshocks between saccharin consumption and amphetamine injections did not alter either the acquisition or the extinction of amphe tain ine-CTA. Experiment 2 demonstrated that expo sure to the same shock parameters 2 and 4 days before saccharin-amphetamine pairing increased the magnitude of amphetamine-CTA after one saccharin-amphetamine pairing and delayed the recovery from the CTA. Experi ment 2 also demonstrated that footshock increased the initial neophobic response to novel saccharin but did not alter subsequent saccharin consumption among saline-in jected animals. These results indicate that stress-induced facilitation of amphetamine CTA are time-dependent and contrast with reports that stressors attenuate LiCl CTA. They also add support to the contention that CTAs in duced by self-administered drugs like amphetamine are qualitatively different from CTAs induced by toxic sub stances like LiCL.

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Differential effects of inescapable footshocks and of stimuli previously paired with inescapable footshocks on dopamine turnover in cortical and limbic areas of the rat

Cited by 414 publications

References 13 publications

Chronic Cold Stress Reduces the Spontaneous Activity of Ventral Tegmental Dopamine Neurons

Chronic Cold Stress Reduces the Spontaneous Activity of Ventral Tegmental Dopamine Neurons

Prefrontocortical Dopamine Loss in Rats Delays Long-Term Extinction of Contextual Conditioned Fear, and Reduces Social Interaction Without Affecting Short-Term Social Interaction Memory

Time-dependent exacerbation of amphetamine-induced taste aversions following exposure to footshock

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