The origin of the dopamine nerve terminals in limbic and frontal cortex. Evidence for meso-cortico dopamine neurons

Fuxé, Kjell; Hökfelt, Tomas; Johansson, Ӧlle; Jönsson, G; Lidbrink, Peter; Ljundahl, Å.

doi:10.1016/0006-8993(74)90618-0

Cited by 268 publications

(41 citation statements)

References 12 publications

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“…Third, many types of brain damage producing aphagia and adipsia typically also destroy cells, fibers, or terminals of dopamine systems (Marshall, Richardson, & Teitelbaum, 1974;Ungerstedt, 1971). Since there are dopamine terminals within orbital frontal cortex (Fuxe, Hokfelt, Johansson, Jonsson, Lidbrink, & Ljungdahl, 1974), it seems possible that stimulation of them can produce feeding such as that observed in this study, or aphagia consequent to lesions. However, the demonstration that orbital frontal cortex stimulation produces eating also raises three rather specific questions: (1) Is the eating similar to that which follows lateral hypothalamic stimulation?…”

Section: Discussionmentioning

confidence: 85%

Eating and electroencephalographic activity following orbital frontal stimulation in rats

Cioe

Kolb

Whishaw

1980

Bull. Psychon. Soc.

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Periodic electrical stimulation of the sulcal frontal cortex produced a pronounced increase in food consumed in a I-h session as compared with both a control non stimulation period and stimulation of the medial frontal cortex. which did not elicit feeding. Stimulation of the sulcal cortex at slightly higher currents produced behavioral and electrographic seizure activity followed by eating during the postictal period_ These results support the suggested role for the sulcal (orbital) frontal cortex in feeding and complement those obtained from a number of other lines of inquiry.A number of studies have shown that orbital frontal cortex lesions disrupt feeding behavior (Brandes & Johnson, 1978;Braun, 1975;Kolb & Nonneman, 1975; Whishaw, Schallert, & Kolb, in press). Although there are important differences between the effects of lesions to the orbital frontal cortex and the lateral hypothalamic nucleus on feeding and drinking (see Whishaw et al., in press, for details), there are sufficient similarities to suggest that each makes an important contribution to the organization of feeding behavior (Kolb, Nonneman, & Whishaw, 1978;Kolb, Whishaw, & Schallert, 1977; Whishaw, Schallert, & Kolb, in press). Although it is well known that stimulation of the lateral hypothalamus induces eating and drinking in rats (e.g_ Hoebel & Teitelbaum, 1962;Margules & Olds, 1962), there have been no reports of these behaviors with electrical stimulation of the orbital frontal cortex. If the orbital frontal cortex and the hypothalamus do indeed form an interrelated circuit involved in feeding, one might expect feeding to be elicited from stimulation of the orbital frontal cortex but not from stimulation of adjacent cortical regions (such as the medial frontal cortex), which have not been implicated in feeding behavior (Kolb, 1974)_ On the other hand, stimulation of the orbital frontal cortex has been shown to suppress locomotor activity in rats (Wilcott, 1979), so that one could also predict suppression of eating as part of a lowering of general activation following orbital frontal stimulation. Accordingly, this report describes the feeding behavior of rats with orbital frontal or medial frontal stimulation. In view of the report by Wishart, Bland, Vanderwolf, and Altman (1973) bound eating can result from stimulus-induced electrographic (EEG) seizures, EEG recordings were taken during stimulation tests in some of the rats in order to determine if the stimulation induced electrographic as well as behavioral seizures. METHOD SubjectsSubjects were six adult male hooded rats weighing approximately 350 g at the time of surgery. The animals were implanted either with stimulating electrodes bilaterally in the sulcal cortex (n = 3) or with one electrode in the medial cortex and one in the sulcal cortex on the contralateral side (n = 3). The latter three rats were also implanted with recording electrodes bilaterally in the hippocampus. SurgeryThe animals were anesthetized with sodium pentobarbital (50 mg/kg) and were given 1 mg/kg atropin...

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Section: Discussionmentioning

confidence: 85%

Eating and electroencephalographic activity following orbital frontal stimulation in rats

Cioe

Kolb

Whishaw

1980

Bull. Psychon. Soc.

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“…To perform such a function, the PL/IL should integrate afferent activity from these systems with reward information. The PL/IL is innervated by dopaminergic (DA) fibers from the ventral tegmental area (Fuxe et al, 1974;Lindvall et al, 1974;Berger et al, 1976;Descarries et al, 1987), and blockade of certain DA receptors in the PL/IL has the same effect as inactivation on task switching (Ragozzino, 2002;Floresco et al, 2006). DA release can reflect both unexpected reward and the absence of expected reward (Schultz, 1997(Schultz, , 2006, and could thereby "gate" (O'Reilly et al, 2002) PL/IL responses to other afferents.…”

Section: Repeated Task Switching Alters Behavioral Tacticsmentioning

confidence: 99%

Prelimbic/Infralimbic Inactivation Impairs Memory for Multiple Task Switches, But Not Flexible Selection of Familiar Tasks

Rich

Shapiro²

2007

J. Neurosci.

150

134

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Behavioral flexibility, in the form of strategy switching or set shifting, helps animals cope with changing contingencies in familiar environments. The prelimbic (PL) and infralimbic (IL) regions of the rat prefrontal cortex (PFC) contribute to this ability so that rats trained to use one strategy have difficulty learning a new one if the PL/IL is inactivated. Thus, the PL/IL mediates learning new tasks in place of old ones, but it may also be required to switch between familiar tasks. To test this hypothesis, we trained rats to perform multiple task switches on a plus-shaped maze, alternating between two familiar tasks. Muscimol inactivation of the PL/IL never impaired switch acquisition, but did impair memory for the recently acquired switch 24 h later. Additional experiments determined that control rats continued to perform the new task 24 h after a switch, but rats with PL/IL inactivation had impaired memory and performed the same task that was learned before inactivation. This impairment was observed in multiple switches, demonstrating that PL/IL activity was required to remember which of two familiar tasks was most recently successful. After many switches, however, muscimol no longer impaired performance, and both saline-and muscimol-infused rats appeared to use immediate task contingencies rather than memory to select among familiar tasks. This strategy may account for the decreased effect of PL/IL inactivation observed after extensive training. Thus, although PL/IL activity contributed to memory for multiple task switches, it was not required for flexibly selecting among highly familiar tasks.

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“…Because the PFC is highly innervated by dopaminergic fibers originating from the VTA (Fluxe et al, 1974), we evaluated the number of DA neurons, as identified by a TH immunostaining, in the VTA of chronically stressed rats (Table 3). The numbers of DA neurons in the VTA were not changed between chronically stressed and naive nonstressed rats (F (1,8) ϭ 0.659; p ϭ 0.440).…”

Section: The Number Of Da Neuronsmentioning

confidence: 99%

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

et al. 2000

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Although the mechanism responsible for cognitive deficits in stress-related neuropsychiatric disorders has been obscure, prefrontal cortical (PFC) dopaminergic dysfunction is thought to be involved. In animals, the mesoprefrontal dopaminergic system is particularly vulnerable to stress, and chronic stress induces working memory impairment. However, the relation between the working memory impairment and altered dopaminergic activity in chronically stressed rats is unclear. Furthermore, the change of dopaminergic activity in the PFC induced by stress is thought to express as a stress response, not as a disorder of organic function. We have previously reported that chronic stress administered by water immersion and restraint for 4 weeks induces a organic disorder such as hippocampal neuronal degeneration. We therefore examined whether chronically stressed (4 weeks) and recovered (10 d) rats show a working memory impairment caused by reduced dopamine (DA) transmission in the PFC, as suspected in the neuropsychiatric disorders. The stress impaired the spatial working memory evaluated by T-maze task and induced a marked reduction of DA transmission concomitant with an increase in DA D1 receptor density in the PFC. This memory impairment was sufficiently ameliorated by intra-PFC infusion of 10 ng SKF 81297, a D1 receptor-specific agonist. Pretreatment with intraperitoneal injection of 20 g/kg SCH 23390, a D1 receptor antagonist, reversed the SKF 81297 response. These results indicate that chronic stress induces working memory impairment through a D1 receptor-mediated hypodopaminergic mechanism in the PFC. These findings provide important information for understanding of the mechanisms underlying PFC dysfunction in stress-related neuropsychiatric disorders.Key words: chronic stress; working memory; prefrontal cortex; dopaminergic neuron; D1 receptor; cognitive deficit Exposure to stress is known to precipitate or exacerbate many neuropsychiatric disorders such as depression, Parkinson's disease, schizophrenia, and others (Schwab and Zieper, 1965;Mazure, 1995). All these disorders involve a working memory deficit caused by prefrontal cortical (PFC) dysfunction (Mattes, 1980;Weinberger et al., 1986;Deutch, 1993;Fibiger, 1995). Several antidepressants increase dopamine (DA) levels in the PFC (Tanda et al., 1994), and raising the DA level in patients with Parkinson's disease with L-3,4-dihydroxyphenylalanine improves their working memory deficit (Lange et al., 1992). These findings suggest that a reduced dopaminergic transmission in the PFC is responsible for the working memory deficits in the neuropsychiatric disorders.In animals, reduced PFC dopaminergic function or blockade of DA receptor in the PFC of monkeys and rats impairs working memory function (Brozoski et al., 1979;Simon et al., 1980;Bubser and Schmidt, 1990), which supports the observations in the neuropsychiatric disorders. In addition, an exposure to acute stress in monkeys or rats has been reported to produce working memory impairment, which can be blocked by...

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The origin of the dopamine nerve terminals in limbic and frontal cortex. Evidence for meso-cortico dopamine neurons

Cited by 268 publications

References 12 publications

Eating and electroencephalographic activity following orbital frontal stimulation in rats

Eating and electroencephalographic activity following orbital frontal stimulation in rats

Prelimbic/Infralimbic Inactivation Impairs Memory for Multiple Task Switches, But Not Flexible Selection of Familiar Tasks

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

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