Behavioural brain research
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Role of interleukin-1 beta in impairment of contextual fear conditioning caused by social isolation.
Isolating rats immediately after conditioning impairs contextual but not auditory-cue fear conditioning. The reported experiments examine the involvement of brain interleukin-1beta (IL-1beta) in the impairment in contextual fear conditioning caused by social isolation. As measured by the conditioned freezing response, 5 h of social isolation after conditioning, impaired contextual but not auditory-cue fear conditioning in adult male Sprague-Dawley rats. ⋯ Like isolation, ICV IL-1beta (10 or 20 ng) after conditioning also impaired contextual but not auditory-cue fear conditioning. These results suggest that increased levels of brain IL-1beta play a role in producing the impairment in contextual fear conditioning produced by social isolation. These findings also add to the generality of the idea that stressors induce IL-1beta activity in the brain and that IL-1beta may play physiological roles in the uninjured brain.
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Clinical Trial Controlled Clinical Trial
Cortical potentials during imagined movements in individuals with chronic spinal cord injuries.
A closed-loop model of motor control predicts that central deafferentation should disrupt cortical motor processes when imagining movements of paralyzed limbs. To test this prediction, event-related potentials (ERP) were recorded from the supplementary motor area and the primary sensorimotor area in individuals with paraplegia or quadriplegia as well as able-bodied controls during executed/attempted and imagined movements of the hand and foot. The cross-correlation of ERPs generated during hand movement and imagery was slightly negative for controls, moderate and positive for paraplegics, and high and positive for quadriplegics. ⋯ First, cortical motor processes are altered by the absence of kinesthetic feedback during attempted movement of a deafferented limb as well as during imagery. Second, inhibitory processes, present during imagined movements of an intact limb, may be weakened by a spinal cord injury (SCI) so that movement and imagery processes appear isomorphic. While the absence of kinesthetic feedback from deafferented limbs likely contributes to some variability in motor processing, the influence of an SCI on movement inhibition requires further testing.
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We have previously reported that at the initiation of cocaine self-administration sessions, neurons in the nucleus accumbens (NA) exhibit a spontaneous transition in firing rate from activity unrelated to the reinforced response, to one of four types of patterned discharges (Carelli RM, King VC, Hampson RE, Deadwyler SA. Firing patterns of nucleus accumbens neurons during cocaine self-administration in rats. Brain Res 1993;626:14-22; Carelli RM, Deadwyler SA. ⋯ Eticlopride increased the number of Session responses (5, 10, and 20 microg/kg), but did not alter the number of Load-up responses at any dose tested. The transition in NA cell firing corresponded with the shift in behavioral responding and was delayed within the session following SCH23390 but not eticlopride pretreatment. These findings support the notion that cocaine self-administration sessions in rats consists of two distinct behavioral phases that are mediated by different neurophysiological mechanisms operating in the NA.
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Intracranial self-administration (ICSA) and intracranial place conditioning (ICPC) methodologies have been mainly used to study drug reward mechanisms, but they have also been applied toward examining brain reward mechanisms. ICSA studies in rodents have established that the ventral tegmental area (VTA) is a site supporting morphine and ethanol reinforcement. ICPC studies confirmed that injection of morphine into the VTA produces conditioned place preference (CPP). ⋯ Among these regions, ICPC findings suggest that cocaine and amphetamine are rewarding in the rostral ventral pallidum (VP); ICSA and ICPC studies indicate that morphine is rewarding in the dorsal hippocampus, central gray and lateral hypothalamus. Finally, substance P mediated systems within the caudal VP (nucleus basalis magnocellularis) and serotonin systems of the dorsal and median raphe nuclei may also be important anatomical components involved in brain reward mechanisms. Overall, the ICSA and ICPC studies indicate that there are a number of receptors, neuronal pathways, and discrete CNS sites involved in brain reward mechanisms.
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The amygdala is a critical temporal lobe structure involved in the expression of anxiety and stress responses. The basolateral nucleus (BLA) of the amygdala in particular, may play a key role in anxiety. Furthermore, corticotropin-releasing factor (CRF), a 41 amino acid peptide, has been strongly implicated in the regulation of stress and anxiety responses. ⋯ Furthermore, repetitive administration of subthreshold doses of Ucn and CRF resulted in 'priming'. Once primed, these animals exhibited behavioral and cardiovascular responses to intravenous sodium lactate, a panicogenic agent in susceptible human patients. These results suggest central CRF and Ucn play a role in generating anxiety which may be similar to that seen in pathological conditions such as panic disorder.