Lesions of medullary catecholaminergic neurons increase salt intake in rats

Colombari, Débora S. A.; Pedrino, Gustavo Rodrigues; Freiria-Oliveira, André Henrique; Korim, Willian S.; Maurino, Isabela; Cravo, Sérgio L.

doi:10.1016/j.brainresbull.2008.04.001

Cited by 15 publications

(11 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Anti-TH immunostaining was eliminated by preabsorption of the antibody with a high concentration of TH [27], as well as following toxin-induced lesions of catecholamine neurons [28]. The antibody was characterized in Western blot analyses by Immunostar (Hudson, WI), and was shown to recognize the expected single band of 60 kD in cell extracts of HEK293 cells transiently transfected with cDNA of human TH isoform without cross-reactivity with dihydropterdine reductase, dopamine- β- hydroxylase, phenylethanolamine-N-methyltransferase, phenylalanine hydroxylase, or tryptophan hydroxylase or related enzymes.…”

Section: Methodsmentioning

confidence: 99%

5-HT2C Receptors Localize to Dopamine and GABA Neurons in the Rat Mesoaccumbens Pathway

2011

View full text Add to dashboard Cite

The serotonin 5-HT2C receptor (5-HT2CR) is localized to the limbic-corticostriatal circuit, which plays an integral role in mediating attention, motivation, cognition, and reward processes. The 5-HT2CR is linked to modulation of mesoaccumbens dopamine neurotransmission via an activation of γ-aminobutyric acid (GABA) neurons in the ventral tegmental area (VTA). However, we recently demonstrated the expression of the 5-HT2CR within dopamine VTA neurons suggesting the possibility of a direct influence of the 5-HT2CR upon mesoaccumbens dopamine output. Here, we employed double-label fluorescence immunochemistry with the synthetic enzymes for dopamine (tyrosine hydroxylase; TH) and GABA (glutamic acid decarboxylase isoform 67; GAD-67) and retrograde tract tracing with FluoroGold (FG) to uncover whether dopamine and GABA VTA neurons that possess 5-HT2CR innervate the nucleus accumbens (NAc). The highest numbers of FG-labeled cells were detected in the middle versus rostral and caudal levels of the VTA, and included a subset of TH- and GAD-67 immunoreactive cells, of which >50% also contained 5-HT2CR immunoreactivity. Thus, we demonstrate for the first time that the 5-HT2CR colocalizes in DA and GABA VTA neurons which project to the NAc, describe in detail the distribution of NAc-projecting GABA VTA neurons, and identify the colocalization of TH and GAD-67 in the same NAc-projecting VTA neurons. These data suggest that the 5-HT2CR may exert direct influence upon both dopamine and GABA VTA output to the NAc. Further, the indication that a proportion of NAc-projecting VTA neurons synthesize and potentially release both dopamine and GABA adds intriguing complexity to the framework of the VTA and its postulated neuroanatomical roles.

show abstract

Section: Methodsmentioning

confidence: 99%

5-HT2C Receptors Localize to Dopamine and GABA Neurons in the Rat Mesoaccumbens Pathway

2011

View full text Add to dashboard Cite

show abstract

“…Acting on forebrain ␣ 1 -or hindbrain ␣ 2 -adrenoceptors, norepinephrine facilitates both behaviors. In contrast, acting on forebrain ␣ 2 -adrenoceptors, norepinephrine inhibits them (10,11,28,40,93,125). Similar to norepinephrine, either intracerebroventricular or forebrain parenchimal injections into the lateral hypothalamus, medial septal area, or preoptic area of ␣ 2-adrenoceptor agonists (e.g., ␣-methylnorepinephrine) or of ␣ 2 -adrenergic-imidazoline receptor agonists (e.g., clonidine or moxonidine) also inhibit water and sodium intake (39,40,47,93,125).…”

Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

.-In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review. sodium intake; angiotensin; electrolyte balance; thirst ANIMALS CONSTANTLY LOSE WATER and electrolytes to the external environment, but specific autonomic, hormonal, and behavioral mechanisms operate continuously to adjust and restore body fluid-electrolyte balance. The rate of loss from the kidneys is primarily controlled by neural and hormonal actions, but loss may also occur passively through the largely uncontrolled processes of respiration (evaporation), perspiration, transpiration, and salivation. These later modes of loss are referred to as insensible loss because they cannot be easily measured. Severe loss of both sodium and water may also occur in disorders associated with emesis and diarrhea. However, despite such ongoing challenges, the osmolarity and volume of body fluids are maintained within reasonably narrow limits, thus allowing normal metabolic and cardiovascular functions. Although renal mechanisms can slow water and sodium loss, the restoration of fluid homeostasis is only made possible by the mobilization of behaviors that result in the ingestion of water and sodium (usually NaCl). The behavioral responses of seeking out and consuming water and salty substances involve the motivational states of thirst and salt appetite. Salt appetite is also frequently referred to as sodium appetit...

show abstract

“…Furthermore, lesion of A1 noradrenergic neurons prevented the renal sympathoinhibition induced by hypernatremia (4). Additionally, we have demonstrated that these noradrenergic cells were part of an inhibitory circuit involved in the control of NaCl intake induced by ANG II-dependent mechanisms (37). These studies represent the initial observation that A1 noradrenergic neurons are involved in autonomic, cardiovascular and behavioral adjustments induced by changes in circulating volume.…”

Section: The Caudal Ventrolateral Medullamentioning

confidence: 55%

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Cravo

Lopes

Pedrino

2011

Braz J Med Biol Res

View full text Add to dashboard Cite

Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of multiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data suggesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.

show abstract

Lesions of medullary catecholaminergic neurons increase salt intake in rats

Cited by 15 publications

References 32 publications

5-HT2C Receptors Localize to Dopamine and GABA Neurons in the Rat Mesoaccumbens Pathway

5-HT2C Receptors Localize to Dopamine and GABA Neurons in the Rat Mesoaccumbens Pathway

Role of the lateral parabrachial nucleus in the control of sodium appetite

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Contact Info

Product

Resources

About