Amygdaloid projections to the frontal cortex and the striatum in the rat

Abstract

Projections from the basolateral nucleus of the amygdala (BLA) to the frontal cortex and the striatum were studied by using Phaseolus vulgaris-leucoagglutinin (PHA-L) anterograde tracing technique in the rat. PHA-L injections into the rostral part of the BLA resulted in a dense labeling of fibers with boutons in the dorsal bank of the rhinal fissure and in the lateral and the medial agranular cortex. PHA-L injections into the caudal part of the BLA produced a dense labeling of fibers in the medial surface of the frontal cortex. In most of the cortical regions, labeled fibers were predominantly distributed in two bands: one in the deep part of layers I and II and the other, heavier band, in layers V and VI. PHA-L injections into the rostral BLA resulted in a dense labeling of fibers with boutons in the olfactory tubercle, the rostral and caudolateral portion of the nucleus accumbens, and a large region of the caudate-putamen. The labeled area of the caudate-putamen included the rostroventral area, the central area, and the area caudal to the anterior commissure and dorsal and lateral to the globus pallidus. PHA-L injections into the caudal BLA produced fiber labeling in the most rostromedial area of the caudate-putamen facing the lateral ventricle, the medial portion of the nucleus accumbens, and the lateral septum. In the rostroventral striatum, PHA-L-labeled fibers selectively innervated the matrix compartment that contains abundant somatostatin-immunoreactive fibers. Compartmental segregation was less clear in the caudodorsolateral caudate-putamen and in the nucleus accumbens. Electron microscopy revealed that PHA-L-labeled boutons in the striatum contained abundant, small, round vesicles. These boutons formed asymmetrical synapses with dendritic spines of striatal neurons.

NMDA-dependent facilitation of corticostriatal plasticity by the amygdala

“…Indeed, it was found that muscarinic receptor blockade interferes with the stabilizing and facilitating effects of BLA stimulation on LTP of thalamocortical (24) and perforant path (23) synapses. However, because the cholinergic innervation of the striatum mostly has an intrinsic origin (49) and BLA axons do not target striatal cholinergic interneurons (34), such a mechanism is unlikely to explain our results. Together, these data suggest that BLA axons may influence synaptic plasticity through several parallel mechanisms.…”

“…Only monosynaptic responses were included in the analysis, and the initial half of the rising phase was analyzed for changes in slope. Because BLA and cortical projections are believe to arise from glutamatergic neurons (34,35), it is highly unlikely that the early part of the responses evoked by BLA and cortical stimuli were reversed inhibitory postsynaptic potentials (IPSPs). Moreover, the striatum does not project back to the cortex or amygdala.…”

“…Yet, manipulations that increase NMDA currents (e.g., removal of extracellular Mg 2ϩ or postsynaptic depolarization) can facilitate LTP induction (26). Thus, the present study tested whether amygdalostriatal axons (33,34) can facilitate plasticity at cortical inputs to projection cells of the striatum (35), the medium spiny neurons (MSNs). We show that BLA synapses can facilitate induction of corticostriatal LTP, in part because they have a high NMDA-to-A MPA (␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) ratio.…”

Environmental enrichment increases amphetamine-induced glutamate neurotransmission in the nucleus accumbens: A neurochemical study

“…It is known that the NAcc and related neural pathways are involved in the psychostimulant effects of amphetamine (Wolf, 1998;Rockhold et al, 1998;Wolf et al, 2004;Kalivas and Volkow, 2005). Neuroanatomical studies have indicated that DA neurons in the NAcc receive significant glutamatergic input directly from the limbic cortex and sub-cortical structures (Groenewegen et al 1980;Kelley and Domesick 1982;Kita and Kitai 1990;Parent and Hazrati, 1995;Sesack et al, 1989;Tzschentke and Schmidt, 2000). Since activation of direct and indirect glutamate pathways increases glutamate release in NAcc following acute amphetamine injection (Robinson and Beart, 1988;Parent and Hazrati, 1995;McGinty, 1999;Vanderschuren and Kalivas, 2000), a potential role for glutamate-mediated mechanisms is implicated in the environment-dependent alteration in amphetamine-induced effects in NAcc.…”

Differential involvement of the basolateral amygdala, orbitofrontal cortex, and nucleus accumbens core in the acquisition and use of reward expectancies.

“…The area of interest encompassed the dorsal edge of the rhinal sulcus, which connects to the BLA (Kita & Kitai, 1990). The majority of lesions in the cortex (73%) included complete tissue loss (neurons, fibers, and neuropil) and resulted in glial cells sealing off the damaged region.…”