Convergence and Segregation of Ventral Striatal Inputs and Outputs

Abstract

The ventral striatum, which prominently includes the nucleus accumbens (Acb), is a heterogeneous area. Within the Acb of rats, a peripherally located shell and a centrally situated core can be recognized that have different connectional, neurochemical, and functional identities. Although the Acb core resembles in many respects the dorsally adjacent caudate-putamen complex in its striatal character, the Acb shell has, in addition to striatal features, a more diverse array of neurochemical characteristics, and afferent and efferent connections. Inputs and outputs of the Acb, in particular of the shell, are inhomogeneously distributed, resulting in a mosaical arrangement of concentrations of afferent fibers and terminals and clusters of output neurons. To determine the precise relationships between the distributional patterns of various afferents (e.g., from the prefrontal cortex, the basal amygdaloid complex, the hippocampal formation, and the midline/intralaminar thalamic nuclei) and efferents to the ventral pallidum and mesencephalon, neuroanatomical anterograde and retrograde tracing experiments were carried out. The results of the double anterograde, double retrograde, and anterograde/retrograde tracing experiments indicate that various parts of the shell (dorsomedial, ventromedial, ventral, and lateral) and the core (medial and lateral) have different input-output characteristics. Furthermore, within these Acb regions, various populations of neurons can be identified, arranged in a cluster-like fashion, onto which specific sets of afferents converge and that project to particular output stations, distinct from the input-output relationships of neighboring, cluster-like neuronal populations. These results support the idea that the nucleus accumbens may consist of a collection of neuronal ensembles with different input-output relationships and, presumably, different functional characteristics.

Latent Inhibition-Related Dopaminergic Responses in the Nucleus Accumbens are Disrupted Following Neonatal Transient Inactivation of the Ventral Subiculum

“…The establishment of neural networks depends in part on electrical activity involved in neuronal survival (Farber and Olney, 2003), synaptic proliferation (Marty et al, 2000), axons' myelination (Barres and Raff, 1993;Demerens et al, 1996;Zalc and Fields, 2000), the rearrangement of synaptic connections in the target structures (Stryker and Harris, 1986;Katz and Shatz, 1996;Hutchins and Kalil, 2008), and the maturation of dendritic spines (Drakew et al, 1999;Frotscher et al, 2000). The transient functional disconnection of the SUB in the critical 2-week period after birth (Clancy et al, 2001) may thus, by a combination of the afore mentioned mechanisms, permanently affect communication with structures directly connected to the SUB, in particular the nucleus accumbens (Brog et al, 1993;Groenewegen et al, 1987Groenewegen et al, , 1999Mulder et al, 1998). Indeed, the dopaminergic changes in preexposed TTX-conditioned animals in both the core and dorsomedial shell parts of the nucleus accumbens after SUB inactivation at PND8 are different from those observed after SUB blockade in adult animals before the pre-exposure session in previous experiments in our laboratory (Peterschmitt et al, 2008).…”

Impairment of acquisition of intravenous cocaine self-administration by RNA-interference of dopamine D1-receptors in the nucleus accumbens shell

“…Thus, a medioventral part, the shell, and a dorso-lateral part, the core, have been distinguished (Groenewegen et al, 1999;Heimer et al, 1997). These two subdivisions, in turn, have been assigned different functions in behavior motivated by food and drugs of abuse (Corbit et al, 2001, Corbit andBalleine, 2011;Di Chiara, 2002;Di Chiara et al, 2004;Parkinson et al, 2002).…”

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

“…mGluR 2 and mGluR 3 are expressed in the NAc (Ohishi et al, 1993a, b;Tamaru et al, 2001;Richards et al, 2005), and this brain area receives glutamatergic projections from the prefrontal cortex, thalamus, basolateral amygdala, and hippocampus (Brog et al, 1993;Heimer et al, 1997;Groenewegen et al, 1999b). Infusions of an mGluR 2/3 agonist into the NAc decrease glutamate release .…”