Sensory circumventricular organs and brain homeostatic pathways

Abstract

Circumventricular organs (CVOs), small structures bordering the ventricular spaces in the midline of the brain, have common morphological and endocrine-like characteristics that distinguish them from the rest of the nervous system. Among their unique features are cellular contacts with two fluid phases--blood and cerebrospinal fluid--and neural connections with strategic nuclei establishing circuitry for communications throughout the neuraxis. A variety of additional morphological and functional characteristics of the CVOs implicates this group of structures in a wide array of homeostatic processes. For three of the circumventricular organs--the subfornical organ (SFO), the organum vasculosum of the lamina terminalis (OVLT), and the area postrema (AP)--recent findings demonstrate these structures as targets for blood-borne information reaching the brain. We propose that these three sensory CVOs interact with other nuclei in the maintenance of several homeostatic processes by way of neural and humoral links. We emphasize the collective role of brain CVOs in the maintenance of body fluid homeostasis as a model for the functional integration of these fascinating "windows of the brain" within central neurohumoral systems.

Evidence for a functional cardiac interaction between losartan and angiotensin‐(1–7) receptors revealed by orthostatic tilting test in rats

“…In this regard, it is known that losartan can cross the blood-brain barrier (Li et al, 1993;Polidori et al, 1996) or act at the area postrema, a circumventricular organ lacking a blood-brain barrier (Johnson & Gross, 1993). Also, losartan may act the rostral ventrolateral medulla, a key region involved in the tonic and reflex control of the sympathetic output (Tagawa et al, 2000) and where a high density of angiotensin receptors is present (Song et al, 1992).…”

Neural Pathways Underlying Lactate-Induced Panic

“…Brain regions analyzed for the number of c-Fos-ir nuclei were chosen based on previous studies implicating them in fear circuitry (Singewald and Sharp, 2000;Singewald et al, 2003) and central autonomic and/or osmotic regulation (see reviews (Johnson and Gross, 1993;Dampney, 1994)). Analysis of the number of c-Fos-ir nuclei in all brain regions analyzed using two-factor ANOVA with repeated measures revealed a lactate (F (1,19) …”

“…A critical component underlying sodium lactate's ability to induce panic-like cardiorespiratory responses in this panic model involves interactions between the CVOs (OVLT/ SFO), areas in the CNS that lack a blood-brain barrier and therefore serve as 'sensors' of changes in osmolarity, pH and other plasma parameters (Johnson and Gross, 1993), and the DMH/PeF which is a major target of these CVOs (Thompson and Swanson, 1998). Based on this, neurons in the CVOs are likely to react to sodium lactate infusions (Johnson and Gross, 1993) and propagate this signal to the DMH/PeF in both L-AG-and D-AG-treated rats.…”

“…Based on this, neurons in the CVOs are likely to react to sodium lactate infusions (Johnson and Gross, 1993) and propagate this signal to the DMH/PeF in both L-AG-and D-AG-treated rats. As predicted, the lactate challenge increased c-Fos responses in the OVLT of panic-prone and non-panic-prone rats equally.…”

“…Although 'osmosensitive' circumventricular organs (CVOs) such as the organum vasculosum of the lamina terminalis (OVLT) appear to be critical for relaying the lactate signal to the DMH/PeF (Johnson and Gross, 1993;Shekhar and Keim, 1997;Thompson and Swanson, 1998), the specific regions of the DMH/PeF involved and the downstream neural pathways through which this signal is propagated to behavioral centers to induce anxiety and elicit increases in heart rate (HR), mean arterial blood pressure (MAP) and respiration rate (RR) are poorly understood. Since evidence from previous studies suggested that disinhibiting the DMH elicits cardioexcitatory responses by mobilizing sympathetic outflow (see review (DiMicco et al, 2002)) and resetting the sensitivity of the baroreflex, which is parasympathetically mediated (see review McDowall et al, 2006), we hypothesized that disinhibition of the DMH/PeF alters lactate-induced behavioral, respiratory, and cardiovascular responses through efferent targets involved in central sympathetic and parasympathetic autonomic control (Dampney, 1994;Thompson and Swanson, 1998;Fontes et al, 2001).…”