Anticonflict-like effect of a prefrontal dopaminergic lesion in rats

Involvement of catecholamine neurotransmission in the rat anterior cingulate in effort-related decision making.

“…Furthermore, the ACC is projected on by noradrenaline (NA) fibers from the locus coeruleus; however, the density of NA axon terminals is low relative to that of other neocortical areas (Morrison, Molliver, Grzanna, & Coyle, 1979). Prefrontal 6-OHDA infusions destroy DA and NA terminals (Jonsson & Sachs, 1975); the latter are destroyed even with NA reuptake inhibition (e.g., Hauber, Bubser, & Schmidt, 1994; Ravard, Herve, Thiebot, Soubrie, & Tassin, 1989), as was used in the present study. Thus, our findings imply that changes in choice behavior are brought about by an impaired catecholamine transmission in the ACC.…”

Depletion of brain norepinephrine: differential influence on anxiolyic treatment effects

“…This finding is consistent with the report by Koob et al (1980) that 6-OHDA lesions of the ascending DNB pathway did not affect the anticonflict actions of chlordiazepoxide in a modified Geller-Seifter conflict test. In addition, Ravard, Thiebot and colleagues (Ravard et al 1990;Thiebot et al 1984) reported that the anticonflict actions of diazepam were not modified by prefrontal catecholamine lesions. This lack of effect of NE depletion on the actions of benzodiazepines does not appear to be specific to shockbased conflict tests of anxiety.…”

Desipramine attenuates working memory impairments induced by partial loss of catecholamines in the rat medial prefrontal cortex

“…Differences in the relative loss of NE and DA may be critical in determining the effects of 6-OHDA lesions of the PFC on delayed-response behavior. In fact, lesions of the cortical NE innervation have been shown to alter other behavioral effects of PFC DA depletions (Ravard et al 1990;Taghzouti et al 1988). As with lesion studies, results of studies using acute pharmacological manipulations generally support a role for mPFC DA neurons in working memory that is much more complex than the originally hypothesized direct relationship between PFC D 1 receptor activation and working memory (Arnsten 1997;Romanides et al 1999;Sawaguchi and Goldman-Rakic 1991;Sawaguchi and Goldman-Rakic 1994;Seamans et al 1998;Williams and Goldman-Rakic 1995;Zahrt et al 1997).…”