Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although calcium/calmodulin-dependent protein kinase II (CaMK) has been shown to play a critical role in long-term potentiation (LTP) and emotional learning mediated by the basolateral amygdala, little is known about its cellular localization in this region. We have utilized immunohistochemical methods to study the neuronal localization of CaMK, and its relationship to gamma-aminobutyric acid (GABA)-ergic structures, in the rat basolateral amygdala (ABL). Light microscopic observations revealed dense CaMK staining in the ABL. Although the cell bodies and proximal dendrites of virtually every pyramidal cell appeared to be CaMK(+), the cell bodies of small nonpyramidal neurons were always unstained. Dual localization of CaMK and GABA immunoreactivity with confocal immunofluorescence microscopy revealed that CaMK and GABA were found in different neuronal populations in the ABL. CaMK was contained only in pyramidal neurons; GABA was contained only in nonpyramidal cells. At the ultrastructural level, it was found that CaMK was localized to pyramidal cell bodies, thick proximal dendrites, thin distal dendrites, most dendritic spines, axon initial segments, and axon terminals forming asymmetrical synapses. These findings suggest that all portions of labeled pyramidal cells, with the exception of some dendritic spines, can exhibit CaMK immunoreactivity. By using a dual immunoperoxidase/immunogold-silver procedure at the ultrastructural level, GABA(+) axon terminals were seen to innervate all CaMK(+) postsynaptic domains, including cell bodies (22%), thick (>1 microm) dendrites (34%), thin (<1 microm) dendrites (22%), dendritic spines (17%), and axon initial segments (5%). These findings indicate that CaMK is a useful marker for pyramidal neurons in ultrastructural studies of ABL synaptology and that the activity of pyramidal neurons in the ABL is tightly controlled by a high density of GABAergic terminals that target all postsynaptic domains of pyramidal neurons.
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PMID:GABAergic innervation of alpha type II calcium/calmodulin-dependent protein kinase immunoreactive pyramidal neurons in the rat basolateral amygdala. 1193 37

The generation of emotional responses by the basolateral amygdala is determined largely by the balance of excitatory and inhibitory inputs to its principal neurons, the pyramidal cells. The activity of these neurons is tightly controlled by gamma-aminobutyric acid (GABA)-ergic interneurons, especially a parvalbumin-positive (PV(+)) subpopulation that constitutes almost half of all interneurons in the basolateral amygdala. In the present semiquantitative investigation, we studied the incidence of synaptic inputs of PV(+) axon terminals onto pyramidal neurons in the rat basolateral nucleus (BLa). Pyramidal cells were identified by using calcium/calmodulin-dependent protein kinase II (CaMK) immunoreactivity as a marker. To appreciate the relative abundance of PV(+) inputs compared with excitatory inputs and other non-PV(+) inhibitory inputs, we also analyzed the proportions of asymmetrical (presumed excitatory) synapses and symmetrical (presumed inhibitory) synapses formed by unlabeled axon terminals targeting pyramidal neurons. The results indicate that the perisomatic region of pyramidal cells is innervated almost entirely by symmetrical synapses, whereas the density of asymmetrical synapses increases as one proceeds from thicker proximal dendritic shafts to thinner distal dendritic shafts. The great majority of synapses with dendritic spines are asymmetrical. PV(+) axon terminals form mainly symmetrical synapses. These PV(+) synapses constitute slightly more than half of the symmetrical synapses formed with each postsynaptic compartment of BLa pyramidal cells. These data indicate that the synaptology of basolateral amygdalar pyramidal cells is remarkably similar to that of cortical pyramidal cells and that PV(+) interneurons provide a robust inhibition of both the perisomatic and the distal dendritic domains of these principal neurons.
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PMID:Pyramidal cells of the rat basolateral amygdala: synaptology and innervation by parvalbumin-immunoreactive interneurons. 1637 2

The basolateral amygdala contains several subpopulations of inhibitory interneurons that can be distinguished on the basis of their content of calcium-binding proteins or peptides. Although previous studies have shown that interneuronal subpopulations containing parvalbumin (PV) or vasoactive intestinal peptide (VIP) innervate distinct postsynaptic domains of pyramidal cells as well as other interneurons, very little is known about the synaptic outputs of the interneuronal subpopulation that expresses somatostatin (SOM). The present study utilized dual-labeling immunocytochemical techniques at the light and electron microscopic levels to analyze the innervation of pyramidal cells, PV+ interneurons, and VIP+ interneurons in the anterior basolateral amygdalar nucleus (BLa) by SOM+ axon terminals. Pyramidal cell somata and dendrites were selectively labeled with antibodies to calcium/calmodulin-dependent protein kinase II (CaMK); previous studies have shown that the vast majority of dendritic spines, whether CAMK+ or not, arise from pyramidal cells. Almost all SOM+ axon terminals formed symmetrical synapses. The main postsynaptic targets of SOM+ terminals were small-caliber CaMK+ dendrites and dendritic spines, some of which were CaMK+. These SOM+ synapses with dendrites were often in close proximity to asymmetrical (excitatory) synapses to these same structures formed by unlabeled terminals. Few SOM+ terminals formed synapses with CaMK+ pyramidal cell somata or large-caliber (proximal) dendrites. Likewise, only 15% of SOM+ terminals formed synapses with PV+, VIP+, or SOM+ interneurons. These findings suggest that inhibitory inputs from SOM+ interneurons may interact with excitatory inputs to pyramidal cell distal dendrites in the BLa. These interactions might affect synaptic plasticity related to emotional learning.
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PMID:Postsynaptic targets of somatostatin-containing interneurons in the rat basolateral amygdala. 1712 Feb 89

Dopaminergic (DA) inputs to the basolateral nuclear complex of the amygdala (BLC) are critical for several important functions, including reward-related learning, drug-stimulus learning, and fear conditioning. Despite the importance of the DA projection to the BLC, very little is known about which neuronal subpopulations are innervated. The present study utilized dual-labeling immunohistochemistry at the electron microscopic level to examine DA inputs to pyramidal cells in the anterior basolateral amygdalar nucleus (BLa) in the rat. DA axon terminals and BLa pyramidal cells were labeled using antibodies to tyrosine hydroxylase (TH) and calcium/calmodulin-dependent protein kinase II (CaMK), respectively. Serial section reconstructions of TH-positive (TH+) terminals were performed to determine the extent to which these axon terminals formed synapses versus non-synaptic appositions in the BLa. Our results demonstrate that at least 77% of TH+ terminals form synapses in the BLa, and that 90% of these synapses are with pyramidal cells. The distal dendritic compartment received the great majority of these synaptic contacts, with CaMK+ distal dendrites and spines receiving one-third and one-half, respectively, of all synaptic inputs to pyramidal cells. Many spines receiving innervation from TH+ terminals also received asymmetrical synaptic inputs from putative excitatory terminals. In addition, TH+ terminals often formed non-synaptic appositions with axon terminals, most of which were putatively excitatory in that they were CaMK+ and/or made asymmetrical synapses. Thus, using CaMK as a marker, the present study demonstrates that pyramidal cells, especially their distal dendritic compartments, are the primary targets of dopaminergic inputs to the basolateral amygdala.
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PMID:Dopaminergic innervation of pyramidal cells in the rat basolateral amygdala. 1883 10