The cortical projections of the mediodorsal nucleus and adjacent thalamic nuclei in the rat

Krettek, J. E.; Price, Joseph L.

doi:10.1002/cne.901710204

Cited by 1,224 publications

(597 citation statements)

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“…However, the BLA and mPFC also receive common sources of afferent input from thalamus (Krettek and Price, 1977;Ray and Price, 1992), hippocampus (Ishikawa and Nakamura, in press) and monoamine cell bodies (Fallon et al, 1978;Oades and Halliday, 1987;Room et al, 1981). Therefore these regions are also likely to contribute to the pattern of correlated activity between neurons in mPFC and BLA observed in this report.…”

Section: Discussionmentioning

confidence: 60%

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

Stevenson

Halliday

Marsden

et al. 2007

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The medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) coordinate various stress responses. Although the effects of stressors on mPFC and BLA activity have been previously examined, it remains unclear to what extent stressors affect functional interactions between these regions. In vivo electrophysiology in the anesthetized rat was used to examine mPFC and BLA activity simultaneously in response to FG-7142, a benzodiazepine receptor partial inverse agonist that mimics various stress responses, in an attempt to model the effects of stressors on corticolimbic functional connectivity. Extracellular unit and local field potential (LFP) recordings, using multielectrode arrays positioned in mPFC and BLA, were conducted under basal conditions and in response to systemic FG-7142 administration. This drug increased mPFC and BLA unit firing at the lowest dose tested, whereas higher doses of FG-7142 decreased various burst firing parameters in both regions. Moreover, LFP power was attenuated at lower (<1 Hz) and potentiated at higher frequencies in mPFC (1-12 Hz) and BLA (4-8 Hz). Interestingly, FG-7142 diminished synchronized unit firing, both within and between mPFC and BLA. Finally, FG-7142 decreased LFP synchronization between these regions. In a separate group of animals, pretreatment with the selective benzodiazepine receptor antagonist flumazenil blocked the changes in burst firing, LFP power and synchronized activity induced by FG-7142, confirming direct benzodiazepine receptor-mediated effects. These results indicate that FG-7142 disrupts corticolimbic network interactions via benzodiazepine receptor partial inverse agonism. Perturbation of mPFC-BLA functional connectivity induced by FG-7142 may provide a useful model of corticolimbic dysfunction induced by stressors.

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Section: Discussionmentioning

confidence: 60%

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

Stevenson

Halliday

Marsden

et al. 2007

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“…Verification of neonatal and adult mPFC lesions using thionin stained sections revealed cell loss and gliosis restricted to the cingulate areas Cg1 (ventral portion), Cg3, and parts of the infralimbic area IL of the mPFC (Zilles and Wree 1995;Paxinos and Watson 1986) (or a ventral portion of the anterior cingulate area Acd and prelimbic PL, and IL areas, respectively, according to Krettek and Price, 1977) in the anterior-posterior coordinates approximately 3.7 to 2.7 mm from bregma, according to the atlas of Paxinos and Watson. Other areas of the frontal cortex adjacent to Cg1, Cg3, and IL were spared, including the frontal area Fr2 (or medial precentral area PrCm) (Figures 1-3).…”

Section: Resultsmentioning

confidence: 99%

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 mediodorsal thalamic nuclei also acts as a critical link between basal forebrain and the prefrontal cortex (Krettek and Price, 1977). Whereas this cortex is relevant to novelty detection (Dias et al, 2002), exposure of rats to unfamiliar environments results in metabolic activation of mediodorsal thalamic nuclei (Sarter et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

The CCK-system underpins novelty-seeking behavior in the rat: Gene expression and pharmacological analyses

2008

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Cholecystokinin (CCK) and its receptor CCK-2R have been shown to promote emotional responsivity and behavioral sensitization to psychostimulants in the rat. An animal model has been developed based on locomotor response to a novel inescapable environment. Animals exhibiting consistent differences in locomotor response to novelty have been termed as High and Low Responder rats (HR and LR respectively). This paradigm is deemed to model sensation-seeking, a personality trait closely associated with substance abuse. The present study provides genetic and pharmacological evidence that the CCK-ergic system modulates this behavior. Distinctive patterns of CCK-related gene expression in HR and LR animals occurred beyond the mesolimbic pathways. CCK gene expression was higher in hippocampus, amygdala, and prefrontal cortex, but lower in the ventral tegmental area of HR relative to LR rats. Levels of CCK-2R mRNA were more elevated in LR animals in some areas of the forebrain such as the prefrontal cortex, nucleus accumbens, and hippocampus. Additionally, CCK-2R blockade with the antagonist LY225.910 (0.5 mg/Kg) removed phenotype differences in sustained exploration of novel stimuli (i.e., a novel-object) in HR and LR rats exposed to an enriched open-field test series. Finally, CCK-2R blockade also altered M 2 and 5-HT 7 receptor gene expression in the mediodorsal thalamus (a strategic structure for corticothalamic trafficking) in a phenotype-dependent manner. Taken together, the findings reported here suggest that distinct CCK-ergic function may contribute to promoting individual differences in noveltyseeking behavior.

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The cortical projections of the mediodorsal nucleus and adjacent thalamic nuclei in the rat

Cited by 1,224 publications

References 39 publications

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

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

The CCK-system underpins novelty-seeking behavior in the rat: Gene expression and pharmacological analyses

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