인체 ≫ 조절 ≫ 호르몬

호르몬 : 노르아드레날린, Norepinephrine

감정의 호르몬
- 트립토판 : 세로토닌, 멜라토닌
- 티로신 : 도파민, 노르아드네날린, 아드네날린




Norepinephrine (INN) (abbreviated norepi or NE), or noradrenaline (BAN) (abbreviated NA, NAd, or norad), is a catecholamine with multiple roles including as a hormone and a neurotransmitter.[3] Areas of the body that produce or are affected by norepinephrine are described as noradrenergic.

The terms noradrenaline (from the Latin) and norepinephrine (derived from Greek) are interchangeable, with noradrenaline being the common name in most parts of the world. However, to avoid confusion and achieve consistency, medical authorities[citation needed] have promoted norepinephrine as the favoured nomenclature, and this is the term used throughout this article.

One of the most important functions of norepinephrine is its role as the neurotransmitter released from the sympathetic neurons affecting the heart. An increase in norepinephrine from the sympathetic nervous system increases the rate of contractions.[4]

As a stress hormone, norepinephrine affects parts of the brain, such as the amygdala, where attention and responses are controlled.[5] Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. It increases the brain's oxygen supply.[6] Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus coeruleus.[7]

When norepinephrine acts as a drug, it increases blood pressure by increasing vascular tone (tension of vascular smooth muscle) through α-adrenergic receptor activation; a reflex bradycardia homeostatic baroreflex is overcome by a compensatory reflex preventing an otherwise inevitable drop in heart rate to maintain blood pressure.

Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in the secretory granules of the medullary chromaffin cells.[8] It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system, where it is released from noradrenergic neurons in the locus coeruleus. The actions of norepinephrine are carried out via the binding to adrenergic receptors.

Role in Decision Making

Cortical norepinephrine (NE) release during attention paradigms (patterns) can increase the alteration detection rate (number of times an alteration was selected) in multiple-cue probability learning during tasks involving giving predictive cues (such as auditory or visual), and thereby enhance subsequent learning.[12] A. J. Yu et al. developed a Bayesian framework to examine NE release in instances of "unexpected uncertainty," where a drastic alteration in sensory information produces a large disparity between top-down expectations and what actually occurs.[13] The model predicts that NE levels spike when the predictive context is switched, then subside. It has also been shown that lesions of the locus coeruleus (LC) impair this attentional shift.[13]

In a similar vein, several studies have implicated the LC-NE system in eliciting the P300, a cortical event-related potential that responds to environmental stimuli that have behaviorally-relevant, motivational, or attention grabbing properties.[14][15][16][17][18] The P300 may reflect updating of prior knowledge regarding stimuli relevant for accurate and efficient decision making. Several studies have searched for a P300 generator in the brain and have ultimately concluded that the potential must have a source that is distributed, synchronous and localized in cortex.[19] This definition is ideally satisfied both functionally and anatomically by the LC neuromodulatory system. Given its broad projection pattern and the correlation between NE release and increased sensory signal transmission,[20] it seems likely that noradrenergic cortical release is the neuronal mechanism of the P300.

Examination of the LC’s tonic firing pattern has led to speculation that it is important for the exploratory behavior essential for learning relations between sensory input, decision processing, motor output, and behavioral feedback.[21] Tonic activation within the range of 0–5 Hz has been shown to correlate with levels of drowsiness, accurate task performance, and when slightly more elevated, distractibility and erratic task performance. Furthermore, phasic activation of the LC is observed in response to both highly-salient unconditioned and task-relevant stimuli. The phasic response occurs after stimulation and precedes a behavioral response in a time-locked fashion.[22] As such, phasic activation of the LC-NE system is proposed to enhance signal processing and behavioral responses specifically to task-relevant stimuli. Given the contrasting functional roles of LC tonic and phasic activity, it is plausible that projections from this brain region are important for maintaining a balance between exploratory and goal-directed behaviors that regulate probabilistic environmental learning and corresponding decision making.

The LC-NE system receives convergent input from the orbitofrontal (OFC) and anterior cingulate cortices (ACC). The OFC has been associated with evaluation of reward. For example, Tremblay et al. found that the response magnitude of single-units in this region is varied with the hedonic value of a stimulus.[23] Additionally, neurons in this region are activated by rewarding stimuli but not by identification of the stimulus or corresponding response preparation. Activation of the ACC appears to reflect some evaluation of cost-benefit. Several studies show ACC activation in response to performance error, negative feedback or monetary loss.[24][25][26] Additionally, ACC responds to task difficulty.[27] Therefore, ACC activation may serve to integrate evaluations of task difficulty with corresponding outcome information to gauge the benefits of engaging an action in regards to a particular environmental stimulus. Conceivably, the functions of the ACC and OFC are directly related to decision-making, and their projections to LC may modulate the phasic release of NE in order to gain-modulate cortical responses to decision outcomes.

LC-NE may play a significant role in synchronizing cortical activity in response to a decision process. In computational modeling of decision, the most accurate and efficient decision mechanisms are mathematically defined random walk or drift-diffusion processes that utilize single-layer neural networks to calculate the disparity in evidence between two options.[28] NE release gated by the LC-NE system is elicited after neurons processing sensory information have presumably reached a decision threshold.[29] Thus, the phasic burst can alter activation in all cortical processing layers in a temporally-dependent manner, essentially collapsing the vast information processing circuit to the outcome of a single decision layer. Brown et al. found that the addition of a phasic LC mechanism was sufficient to yield optimal performance from a single layer decision network.[30]