Organization of adrenergic inputs to the paraventricular and supraoptic nuclei of the hypothalamus in the rat

Abstract

Anterograde transport, retrograde transport, and immunohistochemical techniques were used to characterize the organization of neural inputs to the paraventricular (PVH) and supraoptic (SO) nuclei from the C1, C2, and C3 adrenergic cell groups in the rostral medulla. The results are as follows: 1) Phenylethanolamine-N-methyltransferase-immunoreactive (PNMT-IR) fibers and terminals were distributed to all parts of the parvicellular division of the PVH; the dorsal and dorsal medial subdivisions received the most prominent inputs, the lateral and ventral medial parts the least. Sparse terminal fields were found consistently in the magnocellular division of the PVH and in the SO. 2) A combined retrograde transport-immunohistochemical method was used to estimate the number and proportion of cells in the regions of the C1, C2, and C3 cell groups that contribute to the PNMT-IR innervation of the PVH. On average, 232 +/- 37 retrogradely labeled cells in the C1 cell group, 73 +/- 32 in the C2 cell group, and 96 +/- 26 in the C3 group stained positively for PNMT-IR. These values comprised 70%, 84%, and 89%, respectively, of all retrogradely labeled neurons in these regions. 3) Fibers and terminals arising from the regions of each of the three adrenergic cell groups were labeled by local injections of the anterogradely transported plant lectin PHA-L. Each component projection was found to distribute in a very similar fashion and to mimic the overall distribution of PNMT-IR; differential projection patterns within the PVH or SO were not seen consistently following deposits in any of the individual adrenergic cell groups or at different rostrocaudal levels of any individual cell group. 4) A dual anterograde tracing (PHA-L)-immunohistochemical (PNMT) labeling method revealed an appreciable number of varicosities arising from the regions of C1, C2, and C3 cell groups to contain PNMT-IR. These results suggest that adrenergic inputs to the PVH and SO, while arising from distinct medullary cell groups and presumably relaying different types of sensory information, are in a position to influence similar groups of parvicellular neurosecretory and/or autonomic-related projection neurons.

Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat

“…In aggregate, our findings indicate that CLP leads to the sustained activation of several central pathways that converge in the PVH (Cunningham, et al, 1990;Cunningham and Sawchenko, 1988;Sawchenko and Swanson, 1983). Such activation is now referred to as allostatic overload (Schulkin, 2003) and is implicated in pathologies such as posttraumatic stress syndrome that blunt circadian rhythms (McEwen, 2003).…”

“…The responsive cells in the NTS included a subset of the neurons within the catecholaminergic A2 and C2 cell groups whose sites of projection include the parvocellular PVH (Cunningham et al, 1990;Cunningham and Sawchenko, 1988). Vagal sensory input from the abdomen implicated in the central neural (Wan, et al, 1994), hyperthermic , and hormonal (Fleshner, et al, 1995;Gaykema, et al, 1995;Kapcala, et al, 1996) responses to inflammatory stimuli may have contributed to this response as may the action of circulating mediators on the area postrema (Cunningham et al, 1994).…”

The vagus nerve, food intake and obesity

“…Some of these projections are direct, while others are indirect, via relay stations in the ventrolateral medulla, locus coeruleus, and parabrachial nucleus. There are particularly prominent direct ascending projections from the NTS to the paraventricular nucleus and weaker ones to the lateral hypothalamus and the dorsomedial and arcuate nuclei (Ricardo and Koh, 1978;Ter Horst et al, 1989;Cunningham et al, 1990). Thus, information from vagal afferents can be integrated with other nutritional information, as well as information pertaining to the time of day, reproductive cycle and state of arousal, all represented in the hypothalamus.…”

Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses

“…ADX also may reduce food intake through the increase of corticotrophin-releasing factor (CRF) mRNA expression in the paraventricular nucleus (PVN), since CRF is a well-known anorexigenic peptide (1, 2). CRF neurons in the PVN receive projections from neurons of the nucleus of the solitary tract (NTS) (6,35,45). This brain stem nucleus receives sensory information from gastrointestinal tract and abdominal viscera, as well as taste information from the oral cavity (19, 48), being involved in the satiety pathways.…”