PubMed · 11130908
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R E Adamec. 2001. Partial kindling and behavioral pathologies.. https://doi.org/10.1016/s0074-7742(01)45021-5
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Although the basolateral nucleus (BL) of the amygdala is known to contain an abundance of gamma-aminobutyric acid (GABA)ergic neurons that regulate the amygdaloid projection neurons and influence storage and consolidation of memory, it remains to be determined what type of neuronal input controls GABAergic neurons in the BL. We examined the synapses that GABAergic neurons form with GABAergic and noradrenergic neurons and terminals with unknown transmitters by double-labeling immunoelectron microscopy using anti-GABA and dopamine-beta-hydroxylase (DBH) antisera. The medium and small dendrites of the GABAergic neurons were shown to receive symmetric, inhibitory-type synapses from GABAergic axon terminals and asymmetric, excitatory-type synapses from noradrenergic axon terminals. Each segment of the GABAergic neurons from perikarya to dendritic spines received both symmetric and asymmetric synapses from unlabeled axon terminals of various forms and sizes. The incidence rates of the two types of synapses were almost identical. Our results suggest that GABAergic neurons in the BL of the rat amygdala might be affected by the excitatory influence of the noradrenergic system and the inhibitory influence of the GABAergic system. Furthermore, these neurons are also strongly influenced by both excitatory and inhibitory-type synapses from neuronal systems other than the GABAergic and noradrenergic systems.
Orphanin FQ/nociceptin (OFQ/N), the endogenous ligand for the orphan receptor-like/kappa(3)-like opioid receptor clone, produces a variety of behavioral responses, including those associated with pronociception and antinociception. The OFQ/N precursor rattus-proOFQ (rppOFQ/N) contains several paired basic amino acids, which raises the possibility that post-translational processing can be responsible for the production of a number of additional biologically active peptide fragments. One of these putative peptides, rppOFQ/N (rppOFQ/N(154-181)), was examined for antinociceptive and pronociceptive processes in four brain sites involved in pain inhibition: the ventrolateral periaqueductal gray (vlPAG), the amygdala, the locus coeruleus (LC), and the rostroventromedial medulla (RVM). Endogenous rppOFQ/N(154-181) was identified in each region. rppOFQ/N(154-181) produced a dose-dependent antinociception in all four sites using the tailflick assay. Injections into misplaced cannula sites failed to exert effects. Antinociception in the four sites differed in their response to the opioid antagonist naloxone. Naloxone pretreatment completely blocked rppOFQ/N(154-181)-induced antinociception in the vlPAG and the amygdala, but not in the LC or RVM. In contrast rppOFQ/N(154-181) was hyperalgesic in the LC and RVM, but not in the vlPAG or amygdala. rppOFQ/N(154-181) also was compared with either its N-terminal 17-amino acid peptide (rppOFQ/N(154-170), also known as OFQ2) or its 8-amino acid C-terminal fragment (rppOFQ/N(174-181)). Although both rppOFQ/N(154-181) and rppOFQ/N(154-170) produced antinociception, the latter was less effective because the C-terminal fragment was inactive. Thus, rppOFQ/N(154-181) has complex antinociceptive and pronociceptive actions within the brain, and the pharmacological specificity of its actions differs among supraspinal sites.
Visual pathways to the amygdala, a brain structure critical for classical fear conditioning, were investigated. Conditioned fear was measured in rats as increased acoustic startle amplitude in the presence versus absence of a light or an odor paired previously with foot shock (fear-potentiated startle). Post-training lesions of both the lateral geniculate body (LG) and lateral posterior nucleus (LP) of the thalamus together, but not lesions of LG or LP alone, completely blocked the expression of fear-potentiated startle to a visual conditioned stimulus (CS) but not to an olfactory CS. These lesions also did not block contextual fear conditioning using startle or freezing as measures. Local infusion of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f] quinoxaline-7-sulfonamide disodium, an AMPA antagonist, into the visual thalamus immediately before testing also blocked fear-potentiated startle to a visual CS, suggesting that the lesion effects were not attributable to damage of fibers of passage. Iontophoretic injections into the LP of the anterograde tracer biotinylated dextran amine resulted in heavy anterograde labeling in two amygdala-fugal cortical areas: area TE2 and dorsal perirhinal cortex (PR), and moderate labeling in the lateral amygdaloid nucleus (L). These results suggest that, during classical fear conditioning, a visual stimulus can be transmitted to the amygdala via either lemniscal (i.e., LG --> V1, V2 --> TE2/PR) or non-lemniscal (i.e., LP --> V2, TE2/PR) thalamo-cortico-amygdala pathways, or direct thalamo-amygdala (i.e., LP --> L) projections.