A1 catecholamine cell group: Fine structure and synaptic input from the nucleus of the solitary tract

Abstract

Preembedding immunoperoxidase staining methods were used to characterize tyrosine hydroxylase-immunoreactive (TH-ir) elements in the caudal ventrolateral medulla, and to determine the extent to which neurons of the A1 cell group are directly innervated by projections of the nucleus of the solitary tract (NTS). TH-ir neurons in the A1 region were medium-sized and multipolar. They possessed rounded nuclei with infrequent invaginations, well-developed Golgi apparati, high cytoplasmic densities of mitochondria, and a low to moderate tendency for rough endoplasmic reticulum (RER) to align in parallel stacks. A1 cell bodies were commonly juxtaposed to TH-positive and TH-negative neurons, myelinated profiles, glia and/or vascular elements, but close membrane appositions were only seen with glial elements. Synaptic input to A1 neurons was predominantly asymmetric, provided virtually exclusively by non-TH-ir terminals, and directed principally to dendritic shafts; A1 somata are relatively sparsely innervated. In a second experiment, silver-intensified immunogold localization of TH-ir was combined with immunoperoxidase labeling for anterogradely transported Phaseolus vulgaris-leucoagglutinin (PHA-L), following tracer injections in the caudal aspect of the medial division of the NTS. These experiments revealed a small proportion of PHA-L-labeled axon terminals that made asymmetric contacts with dendritic shafts of TH-ir neurons. These results suggest that the fine structure and synaptic input of A1 neurons are somewhat distinct from that of rostrally situated C1 catecholamine cells. In addition, while they document a direct NTS-A1 projection that may participate in the interoceptive control of vasopressin secretion, the bulk of ventrolaterally directed projections from the caudomedial NTS contact noncatecholaminergic elements in the A1 region, some of which may correspond to so-called depressor neurons implicated in the baroreflex control of sympathetic outflow and vasopressin secretion.

Dorsal and Ventral Medullary Catecholamine Cell Groups Contribute Differentially to Systemic Interleukin-1β-Induced Hypothalamic Pituitary Adrenal Axis Responses

“…This is perhaps not too surprising given the evidence of reciprocal connections between the VLM and NTS [35, 36, 37], but the issue of which pathway(s) are the most functionally important remains to be determined. Regardless of the precise route, the IL-1β-induced recruitment of both NTS and VLM catecholamine cells appears to largely depend on a prostaglandin-mediated transduction mechanism [19].…”

Selective Losses of Brainstem Catecholamine Neurons After Hypoxia-Ischemia in the Immature Rat Pup

“…For example, the cerebral cortex has direct projections to the NTS and the VLM (37) and in the case of the VLM there are bilateral neural pathways (38). The bilateral loss of VLM neurons may also result from NTS neuron losses because bilateral connections exist between the NTS and VLM (39,40) including direct, excitatory NTS inputs to VLM A1 noradrenergic cells (40). The precise sequence of events and potential brain regions involved in the loss of brainstem neurons are not known and future studies are required to at least clarify the temporal relationships of the observed changes.…”

Central afferent pathways conveying nociceptive input to the hypothalamic paraventricular nucleus as revealed by a combination of retrograde labeling and c-fos activation

“…Tracer studies have shown projections to the caudal VLM from the lateral PB (Chamberlin and Saper, 1992) and from lamina II of the medullary dorsal horn (Sun and Panneton, 1998). Afferents that reach the A1 area more precisely within the caudal VLM have been observed to arise from the NTS (Chan et al, 1995) and the rostral VLM (Aicher et al, 1995), but most labeled terminals did not contact aminergic neurons. However, this happened with BDA-labeled terminal fibers arising from the trigeminal dorsal subnucleus caudalis or the dorsal medullary reticular formation (Esser et al, 1998), which receives abundant nociceptive fibers from the spinal dorsal horn (Almeida et al, 1995).…”