Synonym |
Neuromedin U-23 (rat) |
Species |
Rat |
Protein Accession |
P0C818 |
Purity |
Greater than 95% by HPLC analysis |
Endotoxin Level |
< 1 EU per 1 μg of protein |
Biological Activity |
Not determined |
Expression System |
Escherichia coli |
Fusion Tag |
None |
Predicted Molecular Mass |
2767 Da |
Formulation |
Lyophilized in 20mM Tris, 150mM NaCl, pH 7.5 |
Reconstitution |
Centrifuge vial before opening. Reconstitute in sterile ddH2O to a concentration of 0.1-1.0
mg/ml. |
Storage & Stability |
Store at -20°C. For long term storage, it is recommended to store at -80°C. Avoid repeated
freeze-thaw cycles. |
FAQ
What is Neuromedin U-23 (rat) and why is it significant in scientific research?
Neuromedin U-23
(rat) is a potent neuropeptide that consists of 23 amino acids, primarily found in the gut but also
expressed in the central nervous system. Its significance in scientific research stems from its diverse
role in physiological processes. This neuropeptide has been linked to a wide range of functions in
mammalian systems, including the regulation of smooth muscle contraction, blood pressure, and feeding
behavior. Moreover, Neuromedin U has been shown to play a critical role in the stress response, energy
homeostasis, and pain perception.
The study of Neuromedin U-23 provides insights into the complex
interactions between the nervous and endocrine systems, making it a focal point for research on
neuroendocrine signaling pathways. Researchers use Neuromedin U-23 in experimental studies to unlock the
mechanistic pathways through which it exerts its effects. Identifying these pathways guides the
development of therapeutic strategies for conditions like obesity, hypertension, and chronic pain, where
Neuromedin U signaling may be dysregulated.
Neuromedin U-23 also garners interest due to its
involvement in inflammatory processes. It influences immune activity, pointing to its potential role in
modulating immune responses. Understanding its functions could lead to novel approaches in managing
autoimmune disorders or inflammatory diseases. The use of Neuromedin U-23 in animal models, like rats,
allows researchers to explore its physiological roles in a controlled environment, offering
opportunities to decipher its functions that are conserved across species, including humans.
In
addition, Neuromedin U-23 is a candidate for biomarker discovery. Its levels can reflect physiological
and pathological states, potentially serving as an indicator of disease progression or response to
therapy. By understanding its precise role in cellular communication and systemic regulation,
researchers hope to employ Neuromedin U-23 in diagnostic and therapeutic applications, emphasizing its
significance in both physiological and pathological contexts.
How does Neuromedin U-23 affect
feeding behavior and energy homeostasis in rats?
Neuromedin U-23 (rat) plays a substantial role
in regulating feeding behavior and energy homeostasis, primarily through its actions in the central
nervous system. This neuropeptide has been identified in regions of the brain associated with the
control of appetite and energy expenditure, including the hypothalamus, which is a critical hub for
feeding regulation. Neuromedin U-23 is known to exert anorexigenic effects, meaning it reduces food
intake, which is a focal point for researchers studying obesity and metabolic disorders.
Upon its
release, Neuromedin U-23 interacts with specific receptors in the brain, such as Neuromedin U receptor 2
(NMUR2), to influence neuronal activities that regulate hunger signals. Studies have shown that
intracerebroventricular administration of Neuromedin U-23 in rats leads to a decrease in food
consumption. This action is believed to be mediated through the modulation of neuropeptide systems,
including those involving leptin and insulin, which are pivotal in maintaining energy
balance.
Furthermore, Neuromedin U-23 impacts energy homeostasis by influencing energy
expenditure and metabolic rates. Its effect on thermogenesis, particularly in brown adipose tissue,
suggests a mechanism through which it can increase energy expenditure, supporting its role in
maintaining body weight. This property makes Neuromedin U-23 a molecule of interest for developing
anti-obesity therapies that target energy balance rather than just appetite suppression.
In
addition to nutritional influence, Neuromedin U-23 is implicated in the body's response to energy
deficits and surpluses, helping to maintain metabolic equilibrium. By studying Neuromedin U-23's effects
on appetite and energy expenditure in rat models, researchers can better understand its potential
application in managing human metabolic diseases. The implications of Neuromedin U-23 on feeding
behavior and energy regulation highlight its utility as both a research tool and a prospective target
for therapeutic intervention in metabolic health.
What are the known physiological effects of
Neuromedin U-23 on the cardiovascular system?
Neuromedin U-23 (rat) has been shown to exert
significant physiological effects on the cardiovascular system. This neuropeptide influences
cardiovascular functions by interacting with specific receptors expressed in cardiac and vascular
tissues. Studies demonstrate that Neuromedin U-23 can modulate the contraction of smooth muscles in the
blood vessels, which has direct implications for blood pressure regulation and cardiac
function.
Neuromedin U-23 has a pronounced vasoconstrictive effect, particularly on blood vessels
like the rat aorta. It induces vascular smooth muscle contraction, leading to increased vascular
resistance, which, in turn, elevates blood pressure. This vasoconstrictive action is part of the body's
complex mechanism to regulate blood flow and pressure, especially under conditions that require rapid
cardiovascular adjustments.
Furthermore, Neuromedin U-23 is involved in cardiac stress responses.
It may contribute to changes in heart rate and myocardial contractility, influencing the heart's
capacity to pump blood efficiently. Its effect on cardiovascular function is of interest particularly in
studying hypertension and other cardiovascular diseases where vascular tone regulation is
disturbed.
On a systemic level, Neuromedin U-23 impacts the sympathetic nervous system, which is
integral in cardiovascular regulation. It is thought to enhance sympathetic nervous activity,
potentially influencing heart rate and vascular tone. This connection illustrates Neuromedin U-23’s role
in integrating neuroendocrine signals with cardiovascular responses, supporting its involvement in
stress-related cardiovascular adaptations.
Research on rats allows scientists to explore these
cardiovascular effects in vivo, offering insights that can be extended to human physiology. The
potential therapeutic targeting of Neuromedin U signaling pathways could lead to novel treatments for
cardiovascular diseases, emphasizing the importance of understanding its precise role in the
cardiovascular system. By further elucidating these effects, researchers aim to develop interventions
that can mitigate cardiovascular dysfunction associated with disorders of vascular tone and blood
pressure regulation.
How does Neuromedin U-23 influence pain perception in
rats?
Neuromedin U-23 plays a notable role in modulating pain perception, with evidence
suggesting it acts as a modulator of nociceptive pathways in the central nervous system. This
neuropeptide interacts with receptors expressed in brain regions associated with pain processing,
contributing to our understanding of the neurochemical basis of pain perception.
Research
indicates that Neuromedin U-23 can influence both acute and chronic pain pathways. Its effects are
mediated through interactions with specific receptors like NMUR2, which are prevalent in pain-associated
circuitry. In experimental models, Neuromedin U-23 has been shown to exert pro-nociceptive effects,
meaning it can enhance the sensation of pain. This action highlights its potential role in signaling
pathways that amplify pain, suggesting Neuromedin U-23 might be involved in pain augmentation rather
than relief.
Neuromedin U-23's involvement in pain modulation is also linked to its interaction
with neuropeptides and neurotransmitters, such as substance P and calcitonin gene-related peptide
(CGRP), which are crucial mediators of pain and inflammation. Its influence on these chemical messengers
illustrates a complex interplay where Neuromedin U-23 can either directly or indirectly affect pain
signaling pathways.
Additionally, Neuromedin U-23 might play a role in stress-induced analgesia,
a phenomenon where the body's pain threshold is altered by stress. The neuropeptide's effect on pain
perception is thought to be context-dependent, varying with physiological states like stress,
inflammation, and injury. Understanding its precise mechanism in these contexts is vital for developing
pain management strategies that target Neuromedin U pathways.
The study of Neuromedin U-23 in
animal models provides valuable insights into its potential as a target for pain-relief therapies. By
exploring its role in pain perception, researchers can identify therapeutic angles to modulate
nociceptive signals, offering new avenues for treating chronic pain conditions that do not respond
adequately to current treatments. The prospect of modulating Neuromedin U-23 activity to either
attenuate or enhance pain responses underscores its importance in pain research and therapy
development.
What role does Neuromedin U-23 play in immune system regulation?
Neuromedin
U-23 is increasingly being recognized for its role in immune system regulation. This neuropeptide is
intertwined with the immune system through its expression and action in various immune cells, indicating
its significant involvement in immune responses and inflammation.
Neuromedin U-23's influence on
the immune system is evident in its capacity to modulate inflammatory responses. It has been shown to
affect the activity of immune cells such as macrophages and lymphocytes, which are key players in the
body's defense against infections and injury. By influencing cytokine release, Neuromedin U-23 can alter
the inflammatory milieu, impacting both the initiation and resolution of inflammation. For instance, it
may enhance the production of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-alpha)
and interleukins, which facilitate immune cell recruitment and activation.
Moreover, Neuromedin
U-23’s interaction with the immune system highlights its role in the neuro-immune axis. This connection
is pivotal, as it underscores how neuropeptides like Neuromedin U-23 can serve as a bridge between the
nervous and immune systems, facilitating communication and coordination in physiological processes and
stress responses.
The regulation of immune responses by Neuromedin U-23 is also linked to its
expression under stress conditions. Stress not only impacts neurological functions but also has
far-reaching effects on immune activity. Neuromedin U-23's role in mediating stress responses thereby
influences immune cell function, potentially affecting an organism's susceptibility to
diseases.
Research into NeuroMedin U-23's involvement in immune regulation holds promise for
therapeutic applications. By targeting Neuromedin U pathways, it may be possible to modulate immune
responses in chronic inflammatory diseases, autoimmunity, and other conditions where immune
dysregulation is a hallmark. Understanding the regulatory mechanisms driven by Neuromedin U-23 could
lead to the development of drugs that harness its modulatory effects, offering new strategies to treat
immune-related disorders.
The exploration of Neuromedin U-23's role in immune function continues
to provide deeper insights into the complex dynamics of neuroimmune interactions and their impact on
health and disease, indicating its potential as a therapeutic target in immunomodulation.
How is
Neuromedin U-23 linked to stress response mechanisms?
Neuromedin U-23 is intricately linked to
the body's stress response mechanisms, primarily through its involvement in the
hypothalamic-pituitary-adrenal (HPA) axis. This neuropeptide plays a pivotal role in modulating the
body's response to stress by influencing neuroendocrine pathways that regulate stress hormone production
and secretion.
Under conditions of stress, Neuromedin U-23 expression in the central nervous
system, particularly in the hypothalamus, is upregulated. This increase in expression is part of the
body's adaptive response to stress, where Neuromedin U-23 helps mediate the release of
corticotropin-releasing hormone (CRH). CRH, in turn, stimulates the pituitary gland to secrete
adrenocorticotropic hormone (ACTH), which ultimately leads to the release of cortisol from the adrenal
cortex. Cortisol is a critical hormone for stress adaptation, influencing metabolism, immune responses,
and energy utilization.
Additionally, Neuromedin U-23's role in stress responses extends to
behavioral adaptations. It modulates stress-related behaviors such as anxiety and alertness, through
interactions with various neuronal circuits and neurotransmitter systems. The peptide's influence on the
autonomic nervous system further supports its involvement in stress response, affecting physiological
parameters such as heart rate, blood pressure, and gastrointestinal function—typical markers of the
stress response.
Moreover, Neuromedin U-23 not only participates in acute stress responses but
also influences chronic stress adaptations. Its sustained expression under continuous stress conditions
can impact long-term physiological and psychological adaptations, making it a focus in the study of
chronic stress-related disorders and mental health conditions such as anxiety and depression.
The
research community is actively exploring Neuromedin U-23's potential as a target for modulating stress
responses, aiming to develop interventions that could mitigate the adverse effects of stress on health.
By understanding the pathways through which Neuromedin U-23 operates, particularly its regulatory
effects on the HPA axis and behavioral responses, new strategies can be devised to manage stress-related
health issues effectively.
Overall, Neuromedin U-23’s integration in stress response systems
highlights its significance in maintaining the balance between homeostasis and adaptability, marking its
importance in the broader context of stress physiology and potential therapeutic applications.