Research reportDifferential involvement of the shell and core subterritories of the nucleus accumbens in latent inhibition and amphetamine-induced activity
References (80)
- et al.
Neurons in the ventral subiculum, amygdala and entorhinal cortex which project to the nucleus accumbens: their input from somatostatin-immunoreactive boutons
J. Chem. Neuroanat.
(1993) - et al.
Haloperidol enhancement of latent inhibition: relation to therapeutic action?
Biol. Psychiatry
(1988) - et al.
The pharmacological and anatomical substrates of the amphetamine response in the rat
Brain Res.
(1975) - et al.
Pharmacological characterization of dopamine systems in the nucleus accumbens core and shell
Neuroscience
(1992) - et al.
The latent inhibition model of schizophrenic attention disorder: haloperidol and sulpiride enhance rats' ability to ignore irrelevant stimuli
Biol. Psychiatry
(1991) - et al.
Organization of the projections from the subiculum to the ventral striatum in the rat. A study using antero grade transport of Phaseolus vulgaris leucoagglutinin
Neuroscience
(1987) - et al.
Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis
Life Sci.
(1988) - et al.
Input from the amygdala to the rat nucleus accumbens: its relationship with tyrosine hydroxylase immunoreactivity and identified neurons
Neuroscience
(1994) - et al.
The amygdalostriatal projection in the rat — an anatomical study by anterograde and retrograde tracing methods
Neuroscience
(1982) - et al.
The distribution of the projection from the hippocampal formation to the nucleus accumbens in the rat. An anterograde- and retrograde-horseradish peroxidase study
Neuroscience
(1982)
Effects of amphetamine and apomorphine on locomotor activity after 6-OHDA and electrolytic lesions of the nucleus accumbens septi
Pharmacol. Biochem. Behav.
Amphetamine and apomorphine responses in the rat following 6-OHDA lesions of the nucleus accumbens septi and corpus striatum
Brain Res.
Conditioned attention theory
Topographical organization of amygdaloid projections to the caudatoputamen, nucleus accumbens, and related striatal-like areas of the rat brain
Neuroscience
The role of noradrenaline in tuning and dopamine in switching between signals in the CNS
Neurosci. Biobehav. Rev.
Functional studies of the central catecholamines
Int. Rev. Neurobiol.
A direct comparison of amphetamine-induced behaviours and regional brain dopamine release in the rat using intracerebral dialysis
Brain Res.
Both electrolytic and excitotoxic lesions of nucleus accumbens disrupt latent inhibition of learning in rats
Neurobiol. Learn. Memory
The involvement of the nucleus accumbens in the ability of rats to switch to cue-directed behaviors
Life Sci.
Schizophrenia and the frontal lobe
Trends Neurosci.
Facilitation of the expression but not the acquisition of latent inhibition by haloperidol in rats
Pharmacol. Biochem. Behav.
Disruption of latent inhibition by acute administration of low doses of amphetamine
Pharmacol. Biochem. Behav.
Nucleus accumbens lesions reduce amphetamine hyperthermia but not hyperactivity
Eur. J. Pharmacol.
Latent inhibition of conditioned dopamine release in rat nucleus accumbens
Neuroscience
On the significance of subterritories in the ‘accumbens’ part of the rat ventral striatum
Neuroscience
Effects of CS preexposure on avoidance learning in rats with hippocampal lesions
J. Comp. Physiol. Psychol.
The disorder of consciousness in schizophrenia
Schiz. Bull.
The nucleus accumbens as a site of interaction between limbic somatostatin and cholecystokinin, and mesolimbic dopamine
Behav. Pharmacol.
Differential performance of acute and chronic schizophrenics in a latent inhibition task
J. Nerv. Ment. Dis.
Basal ganglia and limbic system pathology in schizophrenia
Arch. Gen. Psychiatry
On the preferential release of mesolimbic dopamine by amphetamine
Neuropsychopharmacology
Effects of antipsychotic drugs on latent inhibition — sensitivity and specificity of an animal behavioral model of clinical drug action
Psychopharmacology
Long-term attentional deficit in nonhandled males: possible involvement of the dopaminergic system
Psychopharmacology
The neuropsychology of schizophrenia
Behav. Brain Sci.
Abolition of latent inhibition in acute, but not chronic, schizophrenics
Neurol. Psychiat. Brain Res.
Abolition of latent inhibition by a single 5 mg dose of d-amphetamine in Man
Psychopharmacology
Functional anatomy of the ventral, limbic system-innervated striatum
Perceptual and Associative Learning
Hippocampal lesions attenuate latent inhibition and the decline of the orienting response in rats
Q. J. Exp. Psychol.
Cited by (136)
Neurocomputational correlates of learned irrelevance in humans
2020, NeuroImageCitation Excerpt :At the neuronal level, the switching model postulates that ‘CS-no event’ associations are encoded by the entorhinal cortex (EC), causing it to inhibit the nucleus accumbens core (NAcc) which is responsible for initiating the expression of the ‘CS-US’ association. This model is supported by animal studies showing that lesions to the EC disrupt both latent inhibition and learned irrelevance (Allen et al., 2002a; Coutureau et al., 1999; Jeanblanc et al., 2004; Shohamy et al., 2000), while lesions to the NAcc core cause latent inhibition to be abnormally persistent, i.e. the inhibition of CRs is prolonged in lesioned animals as compared to control animals (Gal et al., 2005b; Schiller et al., 2006; Weiner, 2003; Weiner et al., 1996). One limitation of the switching model is that it does not account for how exactly ‘CS-no event’ and ‘CS-US’ associations are acquired and regulated.
Deep brain stimulation improves behavior and modulates neural circuits in a rodent model of schizophrenia
2016, Experimental NeurologyConsideration of species differences in developing novel molecules as cognition enhancers
2013, Neuroscience and Biobehavioral ReviewsEffect of blonanserin on methamphetamine-induced disruption of latent inhibition and c-Fos expression in rats
2013, Neuroscience LettersCitation Excerpt :The nucleus accumbens (NAc) and its connections with the prefrontal cortex, hippocampus, basolateral amygdala area, and entorhinal cortex are thought to play principal roles in the regulation of LI [23]. Especially in the NAc, there are two functionally different sub regions, AcbSh and AcbC, and the lesion of AcbSh disrupts LI while the same treatment of AcbC does not LI [16,18,24]. “Switching models” in LI has been suggested to explain this functional differentiation, in which AcbC facilitates CS-reinforcement contingencies during conditioning while AcbSh suppresses them [23].
Catecholaminergic depletion in nucleus accumbens enhances trace conditioning
2011, Advances in Medical Sciences