The effect of misgendering on body dissatisfaction and dietary restraint in transgender individuals: Testing a Misgendering-Congruence Process.

Objective: Despite research findings that transgender individuals have higher rates of body dissatisfaction and disordered eating than their cisgender peers, reasons for greater eating pathology remain unclear. We propose a Misgendering-Congruence Process by which being misgendered (i.e.

Beliefs About Emotion Are Tied to Beliefs About Gender: The Case of Men's Crying in Competitive Sports.

Gender and emotion stereotypes suggest that men do not and should not cry, yet men's crying seems to be particularly prominent in contexts such as competitive sports. In two studies, I investigated the possibility that men's crying is more frequent and seen as more acceptable in these settings because such contexts are perceived to be highly masculine, and can buffer men from the negative consequences associated with violating gender stereotypes. Specifically, I tested the hypotheses that (a) observers would perceive men's crying more positively in a masculine-stereotyped than a feminine-stereotyped setting, and following from this, (b) men would report being more likely to shed tears in a stereotypically masculine than a stereotypically feminine setting.

The Neurotoxin DSP-4 Induces Hyperalgesia in Rats that is Accompanied by Spinal Oxidative Stress and Cytokine Production.

Central neuropathic pain (CNP) a significant problem for many people, is not well-understood and difficult to manage. Dysfunction of the central noradrenergic system originating in the locus coeruleus (LC) may be a causative factor in the development of CNP. The LC is the major noradrenergic nucleus of the brain and plays a significant role in central modulation of nociceptive neurotransmission.

A Life without Hunger: The Ups (and Downs) to Modulating Melanocortin-3 Receptor Signaling.

Melanocortin neurons conserve body mass in hyper- or hypo-caloric conditions by conveying signals from nutrient sensors into areas of the brain governing appetite and metabolism. In mice, melanocortin-3 receptor (MC3R) deletion alters nutrient partitioning independently of hyperphagia, promoting accumulation of fat over muscle mass. Enhanced rhythms in insulin and insulin-responsive metabolic genes during hypocaloric feeding suggest partial insulin resistance and enhanced lipogenesis.

Melanocortin-3 receptors in the limbic system mediate feeding-related motivational responses during weight loss.

Objective: Appetitive responses to weight loss are mediated by a nutrient-sensing neural network comprised of melanocortin neurons. The role of neural melanocortin-3 receptors (MC3R) in mediating these responses is enigmatic. Mc3r knockout mice exhibit a paradoxical phenotype of obesity and reduced feeding-related behaviors in situations of nutrient scarcity.

Simultaneous analysis of vascular norepinephrine and ATP release using an integrated microfluidic system.

Background: Sympathetic nerves are known to release three neurotransmitters: norepinephrine, ATP, and neuropeptide Y that play a role in controlling vascular tone. This paper focuses on the co-release of norepinephrine and ATP from the mesenteric arterial sympathetic nerves of the rat.

New Method: In this paper, a quantification technique is described that allows simultaneous detection of norepinephrine and ATP in a near-real-time fashion from the isolated perfused mesenteric arterial bed of the rat.

Direct intranigral injection of dopaminochrome causes degeneration of dopamine neurons.

Parkinson's disease (PD) is characterized by progressive neurodegeneration of nigrastriatal dopaminergic neurons leading to clinical motor dysfunctions. Many animal models of PD have been developed using exogenous neurotoxins and pesticides. Evidence strongly indicates that the dopaminergic neurons of the substantia nigra pars compacta (SNpc) are highly susceptible to neurodegeneration due to a number of factors including oxidative stress and mitochondrial dysfunction.

Abnormal differentiation of dopaminergic neurons in zebrafish trpm7 mutant larvae impairs development of the motor pattern.

Transient receptor potential, melastatin-like 7 (Trpm7) is a combined ion channel and kinase implicated in the differentiation or function of many cell types. Early lethality in mice and frogs depleted of the corresponding gene impedes investigation of the functions of this protein particularly during later stages of development. By contrast, zebrafish trpm7 mutant larvae undergo early morphogenesis normally and thus do not have this limitation.

Interactions of neuropeptide y, catecholamines, and angiotensin at the vascular neuroeffector junction.

Work from our laboratory has established that angiotensin II (Ang II) produces a greater enhancement of the nerve stimulation (NS)-induced release (overflow) of both norepinephrine (NE) and neuropeptide Y (NPY) and a greater increase in perfusion pressure of the mesenteric arterial bed obtained from the spontaneously hypertensive rat (SHR) compared to age-matched Wistar-Kyoto (WKY) or Sprague-Dawley rats. The enhancement of NS-induced NPY release was blocked by the AT1 receptor antagonist EMD 66684 and the AT2 receptor antagonist PD 123319. Both captopril and EMD 66684 decreased NPY and NE overflow from SHR mesenteric beds, suggesting an endogenous renin-angiotensin system (RAS) is active in the mesenteric artery.

Dopaminochrome induces caspase-independent apoptosis in the mesencephalic cell line, MN9D.

Parkinson's disease is characterized by a deficiency in motor cortex modulation due to degeneration of pigmented dopaminergic neurons of the substantia nigra projecting to the striatum. These neurons are particularly susceptible to oxidative stress, perhaps because of their dopaminergic nature. Like all catecholamines, dopamine is easily oxidized, first to a quinone intermediate and then to dopaminochrome (DAC), a 5-dihydroxyindole tautomer, that is cytotoxic in an oxidative stress-dependent manner.

Inhibitory effects of angiotensin-(1-7) on the nerve stimulation-induced release of norepinephrine and neuropeptide Y from the mesenteric arterial bed.

Neuropeptide Y (NPY) is a cotransmitter with norepinephrine (NE) and ATP in sympathetic nerves. There is evidence for increased activity of the sympathetic nervous system and the renin-angiotensin system (RAS), as well as a role for NPY in the development of hypertension in experimental animal models and in humans. Angiotensin II (ANG II) is known to facilitate sympathetic neurotransmission, an effect greater in spontaneously hypertensive rats (SHR) than normotensive Wistar-Kyoto (WKY) rats.

Cytotoxicity of dopaminochrome in the mesencephalic cell line, MN9D, is dependent upon oxidative stress.

Parkinson disease is a specific form of neurodegeneration characterized by a loss of nigra-striatal dopaminergic neurons in the midbrain of humans. The disease is also characterized by an increase in oxidative stress and a loss of glutathione in the midbrain region. A potential link between all these factors is the oxidation of dopamine to dopaminochrome (DAC).

Norepinephrine increases blood pressure but not survival with anthrax lethal toxin in rats.

Objectives: The response of anthrax lethal toxin (LeTx) induced shock and lethality to conventional therapies has received little study. Previously, fluids worsened outcome in LeTx-challenged rats in contrast to its benefit with lipopolysaccharide (LPS) or Escherichia coli. The current study investigated norepinephrine treatment.

Nerve stimulation induced overflow of neuropeptide Y and modulation by angiotensin II in spontaneously hypertensive rats.

The sympathetic nervous system and renin-angiotensin system are both thought to contribute to the development and maintenance of hypertension in experimental models such as the spontaneously hypertensive rat (SHR). We demonstrated that periarterial nerve stimulation (NS) increased the perfusion pressure (PP) and neuropeptide Y (NPY) overflow from perfused mesenteric arterial beds of SHRs at 4-6, 10-12, and 18-20 wk of age, which correspond to prehypertensive, developing hypertensive, and maintained hypertensive stages, respectively, in the SHR. NS also increased PP and NPY overflow from mesenteric beds of Wistar-Kyoto (WKY) normotensive rats.

MAO-B elevation in mouse brain astrocytes results in Parkinson's pathology.

Age-related increases in monoamine oxidase B (MAO-B) may contribute to neurodegeneration associated with Parkinson's disease (PD). The MAO-B inhibitor deprenyl, a long-standing antiparkinsonian therapy, is currently used clinically in concert with the dopamine precursor L-DOPA. Clinical studies suggesting that deprenyl treatment alone is not protective against PD associated mortality were targeted to symptomatic patients.

Oxidative stress attenuates NO-induced modulation of sympathetic neurotransmission in the mesenteric arterial bed of spontaneously hypertensive rats.

Current evidence suggests that hyperactivity of the sympathetic nervous system and endothelial dysfunction are important factors in the development and maintenance of hypertension. Under normal conditions the endothelial mediator nitric oxide (NO) negatively modulates the activity of the norepinephrine portion of sympathetic neurotransmission, thereby placing a "brake" on the vasoconstrictor ability of this transmitter. This property of NO is diminished in the isolated, perfused mesenteric arterial bed taken from the spontaneously hypertensive rat (SHR), resulting in greater nerve-stimulated norepinephrine and lower neuropeptide Y (NPY) overflow from this mesenteric preparation compared with that of the normotensive Wistar-Kyoto rat (WKY).

Stable RNA interference of synaptotagmin I in PC12 cells results in differential regulation of transmitter release.

In sympathetic neurons, it is well-established that the neurotransmitters, norepinephrine (NE), neuropeptide Y (NPY), and ATP are differentially coreleased from the same neurons. In this study, we determined whether synaptotagmin (syt) I, the primary Ca(2+) sensor for regulated release, could function as the protein that differentially regulates release of these neurotransmitters. Plasmid-based RNA interference was used to specifically and stably silence expression of syt I in a model secretory cell line.

Neuropeptide Y-induced enhancement of the evoked release of newly synthesized dopamine in rat striatum: mediation by Y2 receptors.

The purpose of the present study was to determine whether or not activation of neuropeptide Y (NPY) receptors resulted in an enhancement or attenuation of the KCl (50 mM) evoked release of [3H]dopamine newly synthesized from [3H]tyrosine in superfused striatal slices and, if so to identify the NPY receptor subtype mediating the effect. Rat striatal slices were prepared and placed in microsuperfusion chambers and continuously superfused with physiological buffer containing 50 microCi/ml of l-3-5-[3H]tyrosine. Superfusate effluents were collected and analyzed for [3H]dopamine by liquid scintillation spectrometry following amberlite CG50 and alumina chromatography.

A role for nitric oxide-mediated peroxynitrite formation in a model of endotoxin-induced shock.

The aim of the present study was to assess the relative contributions of peroxynitrite formation following induction of nitric-oxide synthase (iNOS) in the pathophysiology of endotoxin-induced shock in the rat. To this end, we used a selective inhibitor of iNOS, N-(3-(aminomethyl)benzyl)acetamidine (1400W), and a peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron III chloride (FeTTPs). Intravenous (i.

Influence of cold stress on neuropeptide Y and sympathetic neurotransmission.

Chronic cold stress of rats (4 degrees C; 1-3 weeks) induced a marked increase in gene expression (adrenal medulla; superior cervical ganglia), tissue content (mesenteric arterial bed) and nerve stimulation-induced overflow of NPY-immunoreactivity (NPYir) from the perfused mesenteric arterial bed. In contrast increased NPY neurotransmission was offset by an apparent decrease in the evoked overflow of norepinephrine (NE) due to a presumed deactivation of NE by nitric oxide (NO), despite increased sympathetic nerve activity. The net effect of these offsetting system was no change in basal or the evoked increase in perfusion pressure (sympathetic tone).

Cannabinoids augment the release of neuropeptide Y in the rat hypothalamus.

Little is known about the mechanism of action behind the orexigenic activity of cannabinoids. Neuropeptide Y (NPY) is one of the most potent orexigenic factors and is a key mediator in the hypothalamic control of food intake. We examined the effect of cannabinoids on NPY release using a rat hypothalamic explant model.

Neuropeptide Y induced modulation of dopamine synthesis in the striatum.

The purpose of the present study was to determine whether the activation of NPY receptors alters catecholamines (CA) synthesis in the central nervous system and, if so, to identify the NPY receptor subtype(s) mediating this effect. Tyrosine hydroxylation, the rate-limiting step in CA synthesis, was assessed by measuring the accumulation of 3,4-dihydroxyphenyalanine (DOPA) by high pressure liquid chromatography coupled to electrochemical detection (HPLC-EC) in rat striatal dices following incubation of the tissue with the aromatic L-amino acid decarboxylase inhibitor m-hydroxybenzyl hydrazine (NSD 1015). Treatment with NSD 1015 resulted in an increase in DOPA accumulation that was increased even further following depolarization with a high potassium (KCl) buffer.

The separation and quantification of aminochromes using high-pressure liquid chromatography with electrochemical detection.

There is increasing evidence that oxidative stress plays an important role in the pathogenesis of many neurodegenerative diseases including Parkinson's disease (PD). In particular there is support for the participation of oxidized catecholamines in PD. Catecholamines are highly reactive and are readily oxidized to aminochromes.

Modulation of neurotransmitter release by NO is altered in mesenteric arterial bed of spontaneously hypertensive rats.

Nitric oxide (NO) reacts with catecholamines resulting in their deactivation. In the present study with the use of the perfused mesenteric arterial bed as a model of the sympathetic neuroeffector junction, the NO synthase (NOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) resulted in the enhancement of the periarterial nerve stimulation-induced increase in perfusion pressure and norepinephrine overflow while decreasing neuropeptide Y (NPY) overflow. These changes were prevented by l-arginine, demonstrating that the effects of l-NAME were specific to the inhibition of NOS.

Severity of sepsis alters the effects of superoxide anion inhibition in a rat sepsis model.

Previous analysis showed that selective inhibitors of five different host inflammatory mediators administered for sepsis, although beneficial with severe sepsis and high-control mortality rates, were ineffective or harmful with less severe sepsis. We hypothesized that severity of sepsis would also influence inhibition of superoxide anion, another inflammatory mediator. To test this, 6-h infusions of M40401, a selective SOD mimetic, or placebo were given to antibiotic-treated rats (n=547) starting 3 h after challenge with differing doses of intravenous Escherichia coli designed to produce low- or high-control mortality rates.