Possible clinical application of resting-state fMRI in neuropsychiatric disorders

Functional brain imagings studies have shown brain regions having greater neural activity during an experimental task than during rest or sensory-motor task with reduced cognitive demand. Based upon this hypothesis that supports the idea of [default mode of brain function] recent studies have focused on brain regions in which neuronal activity is greater during resting-state than during an experimental task with cognitive demand. Recent Studies have showed that resting-state connectivity is crucial for cognitive performance. To detect dysfunctional connectivity and activity in various resting-state networks in brain that has been suggested to be underlying pathophysiology of some neuropsychiatric disorders, resting-state fMRI could be considered as a relatively novel and beneficial tool for diagnosis of these disorders. In this article, brain resting-state networks are briefly introduced for better understanding of possible clinical applications of resting-state fMRI in diagnosis and early detection of some neuropsychiatric diseases that have been studied in recent years

Regional neurochemical profile following development of apomorphine-induced reinforcement

Dopamine is primary neurotransmitter which mediates the reinforcing effects of abused drugs, serotonin [5- Hydroxytryptamine; 5-HT] also has a crucial role in the pathophysiology of addiction. The binding sites of various drugs of abuse are different from each other, their final rewarding effects are mediated by an increase in the dopamine level in the Nucleus Accumbens. The present study used conditioned place preference [CPP] test to monitor apomorphine's reinforcing effects. Associated alterations in 5-HT and dopamine metabolism were also monitored in various brain regions by HPLC-EC. Withdrawal from apomorphine administration [at a dose of 1.0 mg/kg on six alternate days] induced reinforcement as monitored in the conditioned place preference [CPP] paradigm. Serotonin and dopamine metabolism was also changed particularly in the ventral and dorsal striatum. Results therefore suggest desensitization of dopamine receptors in the presynaptic site is involved in apomorphine-induced reinforcement. Desensitization of somatodendritic 5-HT[1A] receptors resulting in increased availability of 5-HT at 5-HT[2C] receptors could attenuate apomorphine-induced reinforcement. Therefore, further investigations in this area should focus on attempts to attenuate apomorphine-induced reinforcement by desensitizing somatodendritic 5-HT[1A] receptors