C-fos expression in the rat brain after intraperitoneal injection of lithium chloride

Yamamoto, Takashi; Shimura, Tsuyoshi; Sako, Noritaka; Azuma, Shuji; Bai, Weiwei; Wakisaka, Sinichiro

doi:10.1097/00001756-199212000-00004

Cited by 118 publications

(72 citation statements)

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“…These findings are consistent with the conclusions derived from lesion studies that examined the role of the PBN in CTA (e.g., Reilly, 1999). Although the roles of the CNA and BLA in CTA are not fully understood (Reilly & Bornovalova, 2005), these structures show elevated c-Fos activity after a LiCl injection (Lamprecht & Dudai, 1995;Gu et al, 1993;Spencer & Houpt, 2001;Yamamoto et. al, 1992;Yamamoto et.…”

Section: Introductionsupporting

confidence: 86%

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C-fos expression in the rat brain following lithium chloride-induced illness

2007

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The present study examined c-Fos expression in selected brain areas consequent to administration of lithium chloride, the typical illness-inducing agent used in laboratory studies of conditioned taste aversion. The results replicated previous findings of significant c-Fos expression in the parabrachial nucleus, the central nucleus of the amygdala and the basolateral amygdala. New findings indicate significant lithium-induced c-Fos in the gustatory region of the thalamus and the bed nucleus of the stria terminalis but not in the insular cortex. The results are discussed with respect to the neural substrates of conditioned taste aversion.

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Section: Introductionsupporting

confidence: 86%

“…Prior studies have found increased c-Fos activity within the PBN after LiCl administration (Lamprecht & Dudai, 1995;Swank & Bernstein, 1994), with some researchers noting increased activity primarily within the lateral subnuclei (Yamamoto et. al, 1992).…”

Section: Introductionmentioning

confidence: 99%

C-fos expression in the rat brain following lithium chloride-induced illness

2007

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“…It is well-established that systemic injection of LiCl induces c-Fos in visceral and neuroendocrine relays of the rat brain (Houpt et al, 1994;Koehnle and Rinaman, 2007;Lamprecht and Dudai, 1995;Spencer and Houpt, 2001;Swank and Bernstein, 1994;Yamamoto et al, 1992), such as the nucleus of the solitary tract (NTS), the lateral parabrachial nucleus (PBN), the central nucleus of the amygdala (CeA), and the hypothalamic supraoptic (SON) and paraventricular nuclei (PVN). If D-cycloserine enhanced the central response to LiCl per se, then it might also increase levels of neuronal activation observed as c-Fos expression.…”

Section: Methodsmentioning

confidence: 99%

d-Cycloserine enhances conditioned taste aversion learning in rats

Nunnink

Davenport

Ortega

et al. 2007

Pharmacology Biochemistry and Behavior

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Conditioned taste aversion (CTA) is a form of associative learning in which the pairing of a taste with a toxin causes an animal to avoid the taste. NMDA receptor mediated neurotransmission has been implicated in CTA, but the role of the NMDA receptor glycine-binding site has not been examined. To examine the effects on CTA of the glycinergic NMDA receptor agonist D-cycloserine, rats received D-cycloserine (15 mg/kg, i.p.) or vehicle 15 min before 10-min access to 0.125% saccharin, followed by a low dose of LiCl (19 mg/kg, i.p.). CTA was measured with 24-h, 2-bottle preference tests between water and saccharin. Vehicle-treated rats formed a mild CTA that rapidly extinguished, while D-cycloserine-treated rats formed a stronger CTA that extinguished slowly. The effect of D-cycloserine was specific to the NMDA receptor glycine-binding site, because pretreatment with HA-966 (6 mg/kg), a partial glycinergic agonist, blocked enhancement by Dcycloserine. Three follow-up experiments suggest that the enhancement of CTA was not due to an aversive effect of D-cycloserine. First, saccharin paired with D-cycloserine (15 mg/kg) alone did not induce a CTA, although a higher dose (30 mg/kg) did significantly lower saccharin preference. Second, pretreatment with D-cycloserine did not increase the duration of "lying-on-belly" behavior induced by LiCl. Third, pretreatment with D-cycloserine did not increase c-Fos induction by either LiCl or vehicle injection in central visceral relays (the nucleus of the solitary tract, the parabrachial nucleus, the central nucleus of the amygdala, the supraoptic nucleus, and the paraventricular nucleus). These results confirm the participation of NMDA receptor, and specifically the glycine-binding site of NMDA receptor, in CTA learning.

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“…S1). Because LiCl promotes the formation of conditioned taste aversion and elevates Fos activity in the NTS and PBN by activating vagus nerves (30,31), we examined the effect of gastric vagotomy on LiCl-induced protection. The protective role of LiCl on feeding and body weight of AgRP-ablated mice was abolished completely in vagotomized mice as compared with controls treated with sham surgery (Fig.…”

Section: Pretreatment With Licl Reduces Fos Induction In the Pbn Aftermentioning

confidence: 99%

NR2B subunit of the NMDA glutamate receptor regulates appetite in the parabrachial nucleus

Zheng²,

Srisai

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Diphtheria toxin-mediated, acute ablation of hypothalamic neurons expressing agouti-related protein (AgRP) in adult mice leads to anorexia and starvation within 7 d that is caused by hyperactivity of neurons within the parabrachial nucleus (PBN). Because NMDA glutamate receptors are involved in various synaptic plasticity-based behavioral modifications, we hypothesized that modulation of the NR2A and NR2B subunits of the NMDA receptor in PBN neurons could contribute to the anorexia phenotype. We observed by Western blot analyses that ablation of AgRP neurons results in enhanced expression of NR2B along with a modest suppression of NR2A. Interestingly, systemic administration of LiCl in a critical time window before AgRP neuron ablation abolished the anorectic response. LiCl treatment suppressed NR2B levels in the PBN and ameliorated the local Fos induction that is associated with anorexia. This protective role of LiCl on feeding was blunted in vagotomized mice. Chronic infusion of RO25-6981, a selective NR2B inhibitor, into the PBN recapitulated the role of LiCl in maintaining feeding after AgRP neuron ablation. We suggest that the accumulation of NR2B subunits in the PBN contributes to aphagia in response to AgRP neuron ablation and may be involved in other forms of anorexia.feeding behavior | nausea | NR2B signaling N MDA receptors form glutamate-gated ion channels that mediate many forms of synaptic plasticity under physiological conditions and neuronal death under excitotoxic pathological conditions (1, 2). NMDA receptors are tetrameric complexes composed of two obligatory NR1 subunits and two regulatory NR2 and/or NR3 subunits. Multiple subtypes of NMDA receptors are identified with distinct pharmacological and biophysical properties that are predominantly determined by the type of NR2 subunit (NR2A to NR2D). NR2A and NR2B subunits are the most abundant subunits in the adult brain and differ in channel properties, synaptic localization, and protein interaction elements, all of which can contribute to the induction of synaptic plasticity (3). Some recent studies suggest that NMDA receptors play a major role in regulating feeding behavior and energy homeostasis. For example, antagonism of hindbrain NMDA receptors increases food intake, whereas activation of NMDA receptors in the nucleus tractus solitarius (NTS) is necessary for cholecystokinin-induced reduction of food intake (4, 5). Injection of NMDA receptor agonists into the lateral hypothalamus elicits feeding in satiated animals, whereas NMDA blockade suppresses food intake and can reduce body weight (6). Genetic inactivation of NR1 subunits specifically in agouti-related protein (AgRP) neurons results in marked loss of food intake and body fat and impaired feeding after a fast (7). These findings implicate NMDA receptor signaling within several neuronal circuits in the control of feeding and energy balance.Emerging evidence suggests that a complex neural network including GABAergic AgRP neurons in the hypothalamic arcuate nucleus plays a pivotal role in...

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C-fos expression in the rat brain after intraperitoneal injection of lithium chloride

Cited by 118 publications

References 0 publications

C-fos expression in the rat brain following lithium chloride-induced illness

C-fos expression in the rat brain following lithium chloride-induced illness

d-Cycloserine enhances conditioned taste aversion learning in rats

NR2B subunit of the NMDA glutamate receptor regulates appetite in the parabrachial nucleus

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