"Instead of acting at the classical sleep–wake-regulatory neurons , such as the cholinergic BF neurons and the sleep-promoting preoptic neurons, caffeine appears to induce arousal by activating , at least initially, many neuronal pathways that have traditionally been associated with locomotion and motivational behaviors. The NAc shell has long been thought to activate, mainly through indirect pathways via the ventral pallidum and substantia innominata, midbrain–pontine areas that are involved in exploratory locomotion (Mogenson et al., 1983; Groenewegen and Trimble, 2007). In addition, reciprocal connections between the NAc shell and the ventral tegmental area (Zahm and Heimer, 1993), a site of dopamine neurons involved in motivation, reward , and motor control, promote arousal driven by motivation (Sesack and Grace, 2010). "
"The amygdala is part of the neural network that underlies normal social behavior and is a crucial component sustaining context-appropriate social behaviors [Adolphs, 2010]. Existing data indeed suggest that the basolateral complex of the amygdala regulates complex behaviors in tandem with the prefrontal cortex and the ventral striatum [Groenewegen and Trimble, 2007; Mogenson et al., 1980] and that species-specific basic survival behaviors are mediated by the emotional motor subcortical system, which includes the central nucleus of the amygdala and the periaqueductal gray [Holstege, 1991]. Here, we revealed that the amygdala also accesses descending corticospinal tracts via the premotor and primary motor cortex [Dum and Strick, 2005] and is, therefore, in a good anatomical position to exert significant influence over purposive motor functions. "
"Destroying dopaminergic neurons in the nucleus accumbens does not block caffeine-induced hyperlocomotion, which means that the neuronal networks involved in the action of caffeine or dopaminergic agents do not overlap (Swerdlow and Koob, 1985). Caffeine also activates midbrain–pontine areas involved in exploratory locomotion (Groenewegen and Trimble, 2007). It stimulates the locus coeruleus and its noradrenergic influence on neocortical neurons, therefore enhancing vigilance (Aston-Jones and Cohen, 2005) and, subsequently, locomotion (Svenningsson et al., 1997; Bennett and Semba, 1998; Nehlig et al., 1998; Nehlig and Boyet, 2000). "
[Show abstract][Hide abstract] ABSTRACT: Rats with a neonatal ventral hippocampal lesion (NVHL) are used to model schizophrenia. They show enhanced locomotion and difficulties in learning after puberty. Such behavioral modifications are strengthened by dopaminergic psychostimulant drugs, which is also relevant for schizophrenia because illustrating its dopaminergic facet. But it remains questionable that only dopaminergic drugs elicit such effects. The behavioral effects could simply represent a non specific arousal, in which case NVHL rats should also be hyper-responsive to other vigilance enhancing drugs. We administered an adenosine (caffeine) or an adrenaline receptor antagonist, (RX821002) at doses documented to modify alertness of rats, respectively 5 mg/kg and 1 mg/kg. Rats were selected prior to the experiments using magnetic resonance imaging (MRI). Each group contained typical and similar NVHL lesions. They were compared to sham lesioned rats. We evaluated locomotion in a new environment and the capacity to remember a visual or acoustic cue that announced the occurrence of food. Both caffeine and RX82100 enhanced locomotion in the novel environment, particularly in NVHL rats. But, RX82100 had a biphasic effect on locomotion, consisting of an initial reduction preceding the enhancement. It was independent of the lesion. Caffeine did not modify the learning performance of NVHL rats. But, RX821002 was found to facilitate learning. Patients tend to intake much more caffeine than healthy people, which has been interpreted as a means to counter some cognitive deficits. This idea was not validated with the present results. But adrenergic drugs could be helpful for attenuating some of their cognitive deficits.
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