Lateral parabrachial nucleus (LPB) is a critical region in the integration and transmission of peripheral nociception. The parabrachio-amygdaloid (P-Amy) pathway and parabrachio-ventral tegmental area (P-VTA) pathway is thought to be significant in regulation of pain-related negative emotions.
In a study of Quiao et al. from the Department of Anatomy and Histology and Embryology and K. K. Leung Brain Research Centre, Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China, retrograde tract tracers Fluorogold (FG) and tetramethylrhodamine-dextran (TMR) were stereotaxically injected into the right central amygdaloid nucleus (CeA) and right VTA, respectively. Then, part of these rats were performed with the spare nerve injury (SNI) in the controlateral side of FG and TMR injection. Afterwards, double- or triple-immunofluorescent histochemistry was used to examine FG/TMR double- and FG/TMR/FOS or FG/TMR/CGRP triple-labeled neurons in the LPB. The results showed that all of FG, TMR single- and FG/TMR double-labeled neurons were distributed in the LPB bilaterally with an ipsilateral predominance. The proportion of FG/TMR double-labeled neurons to the total number of FG- and TMR-labeled neurons was 10.78% and 13.07%, respectively. Nearly all of the FG/TMR double-labeled neurons (92.67%) showed calcitonin gene-related peptide (CGRP) immunopositive. On the other hand, in the SNI rats, about 89.49% and 77.87% of FG- and TMR-labeled neurons were FG/FOS- and TMR/FOS-positive neurons; about 93.33% of the FG/TMR double-labeled neurons were FOS-LI. Our results suggest that the part of CGRP immunopositive neurons in the LPB send projection fibers to both the CeA and VTA by the way of axon collaterals, which are activated by the nociceptive stimulation in the SNI condition, and may play an important role in the transmission of peripheral nociceptive information 1).
The other main brain entry of the information related to fluid and cardiovascular balance are the lamina terminalis (LT) and one of the sensory circumventricular organs (CVOs), the area postrema (AP). The LT, consisting of the median preoptic nucleus (MnPO) and the other two sensory CVOs—i.e., subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT) —is recognized as a site in the brain that is crucial for the physiological regulation of hydroelectrolyte balance. The SFO and OVLT lack a blood–brain barrier and contain cells that are sensitive to humoral signals, such as changes in plasma and cerebrospinal fluid sodium concentration (Vivas et al. 1990), osmolality (Sladek and Johnson 1983), and angiotensin II (ANG II) levels (Ferguson and Bains 1997; Simpson et al. 1978). Such unique features make the SFO and OVLT key brain regions for sensing the status of the body fluids and electrolytes. Humoral and neural signals that arrive to the two main brain entries—that is, the CVOs of the LT and within the hindbrain the AP-NTS—activate a central circuit that includes integrative areas such as the MnPO, the paraventricular (PVN), the supraoptic (SON), lateral parabrachial nucleus (LPBN), dorsal raphe nucleus (DRN), and neurochemical systems such as the angiotensinergic, vasopressinergic, oxytocinergic (OT), and serotonergic (5-HT) systems.
Once these signals act on the above-mentioned neurochemical networks, they trigger appropriate sympathetic, endocrine, and behavioral responses. Therefore, after a body fluid deficit, water and sodium intake and excretion need to be controlled to minimize disturbances of hydromineral homeostasis. In this context, hypovolemia and hyponatremia induced by body fluid depletion stimulate central and peripheral osmo–sodium receptors, taste receptors, volume and arterial/cardiopulmonary baroreceptors, and the renin–angiotensin system (RAS). This latter system, for example, acts mainly through the sensory CVOs and/or the AP to activate brain neural pathways that elevate BP, release vasopressin and aldosterone (ALDO), increase renal sympathetic nerve activity, and increase the ingestion of water and sodium 2).