Orbitofrontal cortex

Both amphetamine and cocaine have also been reported to support intracranial self-administration in the mesolimbic/mesocortical dopaminergic system. Rats will self-administer cocaine into the medial prefrontal cortex (Goeders and Smith 1983). while amphetamine is self-administered into the orbitofrontal cortex of rhesus monkeys (Phillips and Rolls 1981) and the nucleus accumbens of rats (Hoebel et al. 1983 Monaco et al. 1981). These data indicate that the mesolimbic/mesocortical dopaminergic system is involved in the initiation of stimulant reinforcement processes, and this work suggests that the region of the nucleus accumbens, more specifically the mesolimbic dopamine system, may be an important substrate for reinforcing properties of several psychomotor stimulant drugs. 

The average increase in rCMR after THC administration was less in marijuana users than in controls, and users had lower cerebellar metabolism than the controls at baseline [8]. Thus the cerebellum shows the greatest metabolic increase in response to acute THC and responds to chronic marijuana exposure with a decrease in baseline CMR. Habitual users but not controls responded to THC administration with increased rCMR in prefrontal cortex, orbitofrontal cortex, and basal ganglia. In contrast to the robust effects of THC on relative rCMR, changes in global CMR in response to THC were quite variable, with increases, decreases, and no changes seen in equal numbers of subjects. There was also variability in subjective effects, which were pleasurable for most subjects but either minimal or unpleasant (anxiety or paranoia) for others. 

Functional imaging studies (Ch. 58) in human addicts have found that cue-elicited craving is associated with activation of the amygdala, the anterior cingulate cortex, the orbitofrontal cortex, and the dorsolateral prefrontal cortex [18]. Activation of other regions has been reported less consistently. The amygdala is critical for associative... 

Schoenbaum, G., Chiba, A.A. and Gallagher, M. (1999) Neural encoding in orbitofrontal cortex and basolateral amygdala during olfactory discrimination learning. J. Neurosci. 19,1876-1884. 

FTND Fagerstrom test for nicotine dependence, M mean NR not reported NA not applicable ACC anterior cingulate cortex PCC posterior cingulate cortex OFC orbitofrontal cortex SFG superior frontal gyrus DLPFC dorsal lateral prefrontal cortex DRD4L dopamine receptor 4 variable number tandem repeat Data shown for FTND and pack-years are means for the smokers Pack-years = packs of cigarettes smoked per day x number of years smoked... 

Hopefully the combination of TMS with fMRI will enable the more precise location of the regional dysfunction in depression to be located and thereby enable the neuronal pathways concerned to be identified. To date, the early studies of TMS with fMRI have shown that the effects of TMS occur in brain regions distant from the site of stimulation, including the caudate, orbitofrontal cortex and the cerebellum. 

Table 1. Dopaminergic activities in orbitofrontal cortex in dementia with Lewy bodies...

Rolls, E. (1996) The orbitofrontal cortex. Phil Trans R Soc Land B 351 1433-1444. 

Functional neuroimaging studies provide strong evidence for dysfunction of the cortical-striatal-thalamocortical (CSTC) circuitry. Symptoms of OCD are associated with increased activity in orbitofrontal cortex in neutral state (Swedo et ah, 1989b Baxter, 1994 Saxena et ah, 1998). Increased activity was also noted in some of these studies in anterior cingulate gyrus, caudate nucleus, and thalamus. Horwitz et al. (1991) found that the pattern of intercorrelations between various brain regions in patients with OCD differed from that of controls. 

The enhanced 5-HT release would probably act via the activation of postsynaptic 5-HT2 receptors that remain normosensitive after the 8-week SSRI treatment (el Mansari and Blier, 1997). Indeed, the response of orbitofrontal cortex neurons to 5-HT and 5-HT2 agonists is unaltered, whereas that to a 5-HTia agonist is decreased after such treatment. It has not been conclusively shown that these 5-HT2 receptors are located directly on the glutamatergic pyramidal neurons or on inhibitory GABA interneurons. Wherever their precise localization, the effect of 5-HT on these neurons, which send an excitatory output to the caudate nucleus, is inhibitory in nature, which could account for the dampening of the hyperactivity observed following successful SSRI treatment. These results clearly identify the terminal 5-HTib autoreceptor and the postsynaptic 5-HT2 receptors as potential novel targets for the treatment of OCD. 

Pyramidal neurons in the orbitofrontal cortex are glutamatergic in nature and release their excitatory neurotransmitter glutamate in the head of the caudate. The beneficial action of internal capsulotomy (which inter-... 

Structures implicated in the production or maintenance of sleep include the nucleus of the solitary tract, dorsal medullary reticular formation, raphe nuclei, thalamus, anterior hypothalamus, preoptic area, basal forebrain, orbitofrontal cortex, caudate nucleus, basal ganglia, and cerebral cortex. None of these structures are individually necessary for sleep. No lesion has produced a long lasting total insomnia. After some sleep-reducing lesions, sleep returns toward normal if sufficient time is allowed for recovery. 

El Mansari, M. Blier, P. (2005). Responsiveness of 5-HT(lA) and 5-HT2 receptors in the rat orbitofrontal cortex after long-term serotonin reuptake inhibition. J. Psychiatry... 

Role of the Orbitofrontal Cortex in Reinforcement Processing and Inhibitory Control Evidence from Functional Magnetic Resonance Imaging Studies in Healthy Human Subjects Rebecca Elliott and Bill Deakin... 

Beer, J., John, O., Scabini, D., 8c Knight, R. (2006). Orbitofrontal cortex and social behavior Integrating self-monitoring and emotion-cognition interactions. Journal of Cognitive Neuroscience, 18, 871-879. 

Elliott R, Dolan RJ, Frith CD. 2000. Dissociable functions in the medial and lateral orbitofrontal cortex Evidence from human neuroimaging studies. Cereb Cortex 10 308-317. 

Hoptman MJ, Volavka J, Weiss EM, Czobor P, Szeszko PR, et al. 2005. Quantitative MRI measures of orbitofrontal cortex in patients with chronic schizophrenia or schizoaffective disorder. Psychiatry Res Neuroimaging 140 133-145. 

O Doherty J, Kringelbach ML, Rolls ET, Hornak J, Andrews C. 2001. Abstract reward and punishment representations in the human orbitofrontal cortex. Nat Neurosci 4 95-102. 

Wallis JD. 2007. Orbitofrontal cortex and its contribution to decision-making. Annu Rev Neurosci 30 31-56. 

Garey LJ, Von Bussmann KA, Hirsch SR. 2006. Decreased numerical density of kainate receptor-positive neurons in the orbitofrontal cortex of chronic schizophrenics.Exp Brain Res. 173(2) 234-42. 

Meador-Woodruff JH, Haroutunian V, Powchik P, Davidson M, Davis KL, et al. 1997. Dopamine receptor transcript expression in striatum and prefrontal and occipital cortex. Focal abnormalities in orbitofrontal cortex in schizophrenia. Arch Gen Psychiatry 54 1089-1095. 

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