Effects of context‐drug learning on synaptic connectivity in the basolateral nucleus of the amygdala in rats

Abstract

Context-drug learning produces structural and functional synaptic changes in the circuitry of the basolateral nucleus of the amygdala (BLA). However, how the synaptic changes translated to the neuronal targets was not established. Thus, in the present study, immunohistochemistry with a cell specific marker and the stereological quantification of synapses was used to determine if context-drug learning increases the number of excitatory and inhibitory/modulatory synapses contacting the gamma-aminobutyric acid (GABA) interneurons and/or the pyramidal neurons in the BLA circuitry. Amphetamine conditioned place preference (AMPH CPP) increased the number of asymmetric (excitatory) synapses contacting the spines and dendrites of pyramidal neurons and the number of multisynaptic boutons contacting pyramidal neurons and GABA interneurons. Context-drug learning increased asymmetric (excitatory) synapses onto dendrites of GABA interneurons and increased symmetric (inhibitory or modulatory) synapses onto dendrites but not perikarya of these same interneurons. The formation of context-drug associations alters the synaptic connectivity in the BLA circuitry, findings that have important implications for drug-seeking behavior.

LGALS3 (galectin 3) mediates an unconventional secretion of SNCA/α-synuclein in response to lysosomal membrane damage by the autophagic-lysosomal pathway in human midbrain dopamine neurons

“…S8(B, C)). As previously described [ 110 , 111 ] and in accord with well recognized criteria [ 112 ], a synapse was identified by the presence of presynaptic neurotransmitter vesicles and a synaptic cleft with parallel, electron dense, thickened pre- and postsynaptic membranes and the presence of electron dense content in the synaptic cleft. Consistent with the report that greater than 90% of the dopaminergic synapses in the human striatum are symmetric [ 113 ] and are functionally inhibitory or modulatory, all of the synapses observed were symmetric synapses (Fig.…”

Nerve injury alters restraint-induced activation of the basolateral amygdala in male rats

“…Increased BLA activity is a characteristic of some rat models of addiction (Rademacher et al, 2015) and results in insensitivity to reward devaluation (Wassum and Izquierdo, 2015). Insensitivity to reward devaluation is also triggered by stress, however, certain stressors can also result in the enhancement of the motivation for reward (Sharp, 2017).…”

The basolateral amygdala in reward learning and addiction

“…Indeed, the long-lasting effect of chronic cocaine exposure to produce insensitivity to reward devaluation has been suggested to rely on a persistent, off-drug alteration in BLA signaling (Schoenbaum and Setlow, 2005). Using immunohistochemical and stereological analysis, it was recently found that amphetamine conditioned place preference experience alters synaptic connectivity within the BLA network through its GABA interneurons, resulting in long-lasting effects on BLA signaling (Rademacher et al, 2015). After 30 days of withdrawal from cocaine, the proportion of BLA delay-dependent anticipatory neurons is reduced.…”