Effect of ibotenic acid lesions of the medial prefrontal cortex on amphetamine-induced locomotion and regional brain catecholamine concentrations in the rat

Jaskiw, George E.; Karoum, Farouk; Freed, William J.; Phillips, I. D. J.; Kleinman, Joel E.; Weinberger, Daniel R.

doi:10.1016/0006-8993(90)90138-2

Cited by 124 publications

(56 citation statements)

References 73 publications

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“…Congruent with a prior report from our laboratory (Jaskiw et al 1990), we observed that lesioned rats exhibited a greater degree of hyperlocomotion in response to amphetamine than sham rats two weeks following surgery; however, also similar to the results reported by Jaskiw et al (1990) at 28 days postoperatively, we saw no difference between groups when animals were retested at eight weeks. The persistence of NAA alterations in both the mPFC and striatum at eight weeks despite the normalization of amphetamineinduced locomotion suggests that compensation occurs at another level and may be independent of the gross integrity of the prefrontal-striatal circuit.…”

Section: Our Findings Confirm Thatsupporting

confidence: 83%

“…Glutamate injections into the prefrontal cortex or direct electrical stimulation of the mPFC increases firing of VTA neurons and enhances release of dopamine in the nucleus accumbens (Murase et al 1993;; moreover, excitatory amino acid antagonists infused into the VTA block prefrontal-mediated striatal dopamine release, suggesting that the PFC exerts a tonic excitatory control of striatal dopamine via the substantia nigra/VTA Karreman and Moghaddam 1996). However, lesions or pharmacologic manipulations of mPFC inputs to these downstream targets result in abnormal locomotor behaviors and changes in firing characteristics of VTA dopaminergic neurons in response to stimuli (Jaskiw et al 1990;Murase et al 1993). …”

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confidence: 99%

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Local and Downstream Effects of Excitotoxic Lesions in the Rat Medial Prefrontal Cortex on In Vivo 1H-MRS Signals

Roffman

2000

Neuropsychopharmacology

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Section: Our Findings Confirm Thatsupporting

confidence: 83%

mentioning

confidence: 99%

Local and Downstream Effects of Excitotoxic Lesions in the Rat Medial Prefrontal Cortex on In Vivo 1H-MRS Signals

Roffman

2000

Neuropsychopharmacology

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“…The reasons for these differences may be two-fold. First, the neonatal lesion in this study may be more confined to the ventral portions of the mPFC (infralimbic/prelimbic IL/PL[Cg3] regions) as compared to the more widespread lesion in the previous studies in adults, which comprised the PL (Cg3), the entire anterior cingulate area (Cg1 and ACd), and portions of the precentral medial area (FR2 or PrCm) (Jaskiw et al 1990. Lipska et al 1995b).…”

Section: Discussionmentioning

confidence: 97%

Excitotoxic Lesions of the Rat Medial Prefrontal Cortex Effects on Abnormal Behaviors Associated with Neonatal Hippocampal Damage

Lipska

Al-Amin

Weinberger

1998

Neuropsychopharmacology

108

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excitotoxic damage of the ventral hippocampus (VH) is a heuristic model of schizophrenia. We investigated whether: (1) neonatal damage of the medial prefrontal cortex (mPFC) has effects similar to the neonatal VH lesion; and (2) intrinsic mPFC neurons contribute to the abnormal behaviors associated with VH lesions. Neonatal rats were lesioned in the mPFC. In adulthood, they showed attenuated locomotion in response to novelty, amphetamine, and Structural neurodevelopmental abnormalities in the temporolimbic cortex, dysfunction of the prefrontal cortex (PFC), and dysregulation of dopamine and glutamate systems are implicated in the pathophysiology of schizophrenia (Weinberger 1987;Robbins 1990;Grace 1991;Mittleman et al. 1993;Weinberger and Lipska 1995). In an attempt to recreate these neuropathological features in an animal, we previously investigated the consequences of neonatal excitotoxic damage of the ventral hippocampal formation in the rat on behaviors related to dopamine and glutamate function (Lipska et al. , 1995a Weinberger 1993, 1994; AlAmin et al. 1997). The results of these studies indicate that the neonatally lesioned rats display a constellation of behavioral abnormalities indicative of hyperdopaminergic subcortical activity and hyperresponsivity to glutamate antagonists and that the appearance of these behaviors is delayed until early adult life. Our results and subsequent reports from other laboratories (Flores et al. 1996a;Black et al. 1996;Wan et al. 1996;Wan and Corbett 1997) suggest that this lesion reproduces a constellation of core phenomena associated with schizophrenia, and may thus be used as an animal model of this disorder. Such neonatally lesioned rats also express Received January 5, 1998; revised April 16, 1998; accepted April 30, 1998. 452 B.K. Lipska et al. N EUROPSYCHOPHARMACOLOGY 1998 -VOL . 19 , NO . 6 behaviors that implicate dysfunction of the PFC (Chambers et al. 1996;Sams-Dodd et al. 1997), possibly because neonatal damage of the ventral hippocampus disrupts neuronal development of the PFC, with which the hippocampus is closely interconnected (Swanson 1981;Ferino et al. 1987;Jay et al. 1989;Laroche et al. 1990;Jay et al. 1992;Carr and Sesack 1996). Because PFC dysfunction has been shown in rodents (Adler 1961;Lynch et al. 1969;Iversen 1971;Pycock et al. 1980;Kolb 1984;Reibaud et al. 1984;Louilot et al. 1989;Jaskiw et al. 1991;Vezina et al. 1991;Deutch 1992;Jaskiw and Weinberger 1992;King and Finlay 1995;Taber et al. 1995;Karreman and Moghaddam 1996) and in primates (Kolachana et al. 1995;Roberts et al. 1994) to affect subcortical dopamine activity, the effect of the VH lesion on dopamine function might be indirectly mediated by an alteration at the level of the mPFC.The current study addresses the question of whether direct excitotoxic damage of the prefrontal cortex induced in neonatal rats affects glutamatergic and subcortical dopaminergic function in a manner similar to that observed in animals with the neonatal ventral hippocampal lesion. The lesion was inten...

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“…The cannulae remained in place for 8 min after the end of the injection. The lesion was verified in parallel experiments by staining cryostat sections with cresyl violet (23). Four weeks later, the two groups were subdivided further into four groups of 12 animals receiving saline or cocaine (10 mg/kg) i.p.…”

Section: Methodsmentioning

confidence: 99%

“…The nucleus accumbens was dissected from a slice extending from AP +0.7 to +2.7 mm relative to bregma. Cingulate cortex and medial and lateral caudate nucleus were dissected from a slice extending from AP +0.7 to +1.3 mm (23).…”

Section: Methodsmentioning

confidence: 99%

Cocaine-induced reduction of brain neuropeptide Y synthesis dependent on medial prefrontal cortex.

Wahlestedt

Karoum

Jaskiw

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Repeated admiration of cocaine elicits substantial, long-lasting, but reversible reductions in neuropeptide Y (NPY) and NPY mRNA in the rat cerebral cortex and nucleus accumbens. The NPY reduction appears to be mediated through a decrease in NPY biosynthesis, occurring transneuronaly, perhaps in response to changes in synaptic dopamine asiated with mesoimbic and mesocortical dopamine neurons. The medial prefrontal cortex appears necessary for maintenance of cocaine's action on this neuronal network since excitotoxic lesions of this area prevented (lesion before cocaine) and reversed (lesion after cocaine) the reductions in NPY elicited by the cocaine. NPY may be a sensitive marker for chronic cocaine use. Its decrease may relate to the anxiety and depression associated with cocaine withdrawal in humans.Many of the acute euphoric effects of cocaine are thought to be a consequence of the augmented concentration of dopamine (DA) in regions of the limbic forebrain (1)(2)(3)(4)(5)(6). The enhanced accumulation of DA presumably results from cocaine blocking presynaptic DA uptake (7,8). Although DA may initiate self-reinforcing behaviors, the biochemical consequences of repeated cocaine administration and its termination are less well understood. Behaviorally, the end of a cocaine binge is often associated with intense anxiety (9-11) and an episode of major depression (12, 13). The dysphoria resulting from cocaine withdrawal can be lengthy and of importance for cocaine craving and recidivism (12,13). Conceivably, the behavioral changes associated with prolonged use and withdrawal from cocaine may reflect the unmasking of long-lasting central adaptive processes that act to oppose the immediate excitant actions of the drug (13). These long-term aftereffects may thereby share common anatomical and neurochemical features with those that are activated by acute administration of the drug. One candidate neurotransmitter that may relate to long-term cocaine use and withdrawal is neuropeptide Y (NPY), a 36-amino acid peptide that is widely distributed in the central and peripheral nervous systems (14, 15). NPY has been implicated in the expression of anxiety (16) and depression (17,18) and its biosynthesis appears to be regulated by . We therefore sought to determine whether chronic cocaine administration and its withdrawal are associated with changes in the content and regulation of this neuropeptide in brain and, if so, whether such changes depend upon the integrity of the medial prefrontal cortex, a region thought to be critical for the expression of some of the reinforcing properties of the drug (5, 6). MATERIALS AND METHODSAnimals. Study 1. Sixty-four male Sprague-Dawley rats (200-275 g; Zivic-Miller) were housed in groups of four with free access to food and water and a constant light/dark schedule (8 a.m. to 6:00 p.m.). The rats were treated with either cocaine (10 mg/kg; Sigma) or saline i.p. twice daily for 1 week and sacrificed 1 hr, 2 weeks, 6 weeks, or 12 weeks after the last injection. The brains were disse...

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Effect of ibotenic acid lesions of the medial prefrontal cortex on amphetamine-induced locomotion and regional brain catecholamine concentrations in the rat

Cited by 124 publications

References 73 publications

Local and Downstream Effects of Excitotoxic Lesions in the Rat Medial Prefrontal Cortex on In Vivo 1H-MRS Signals

Local and Downstream Effects of Excitotoxic Lesions in the Rat Medial Prefrontal Cortex on In Vivo 1H-MRS Signals

Excitotoxic Lesions of the Rat Medial Prefrontal Cortex Effects on Abnormal Behaviors Associated with Neonatal Hippocampal Damage

Cocaine-induced reduction of brain neuropeptide Y synthesis dependent on medial prefrontal cortex.

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