Catecholamine

Introduction to the Endocrine System

In Endocrine and Reproductive Physiology (Fourth Edition), 2013

Catecholamines

Catecholamines are synthesized by the adrenal medulla and neurons and include norepinephrine, epinephrine, and dopamine (Fig. 1-iii; Box 1-2). The primary hormonal product of the adrenal medulla is epinephrine, and to a bottom extent, norepinephrine. Epinephrine is produced past enzymatic modifications of the amino acid tyrosine. Epinephrine and other catecholamines are ultimately stored in secretory vesicles that are part of the regulated secretory pathway. Epinephrine is hydrophilic and circulates either unbound or loosely bound to albumin. Epinephrine and norepinephrine are like to poly peptide/peptide hormones in that they betoken through membrane receptors, called adrenergic receptors. Catecholamines have short biologic half-lives (a few minutes) and are inactivated by intracellular enzymes. Inactivated forms diffuse out of cells and are excreted in the urine.

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The Adrenal Gland

In Endocrine and Reproductive Physiology (Fourth Edition), 2013

Mechanism of Action of Catecholamines

Catecholamines act through membrane GPCRs (run into Affiliate 1). The individual types of adrenergic receptors were outset classified based on their pharmacology, and this classification scheme has been supported by genetics and molecular cloning. Adrenergic receptors are generally classified every bit α- and β-adrenergic receptors, and these are further divided into αone and αii receptors and βone, β2, and βthree receptors (Table seven-1). These receptors tin be characterized co-ordinate to the following:

1.

The relative potency of endogenous and pharmacologic agonists and antagonists. The α receptors and βthree receptors respond better to norepinephrine than epinephrine. The βi receptor responds every bit to the two catecholamines, whereas epinephrine is more potent than norepinephrine for the β2 receptor. A large number of synthetic selective and nonselective adrenergic agonists and antagonists now exist.

ii.

Downstream signaling pathways. Table vii-1 shows the chief pathways that are coupled to the unlike adrenergic receptors. This is an oversimplification because differences in signaling pathways for a given receptor have been linked to elapsing of agonist exposure and cell type.

3.

Location and relative density of receptors. Importantly, different receptor types predominate in dissimilar tissues. For case, although both α and β receptors are expressed past islet β cells, the predominant response to a sympathetic discharge is mediated by α2 receptors.

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Neuroendocrinology

Petra Netter , in International Encyclopedia of the Social & Behavioral Sciences (Second Edition), 2015

Hormones as Indicators of Neurotransmitter and Hypothalamic Activity

The catecholamines produced in the adrenal medulla mentioned to a higher place, practice not only act as hormones in the periphery, merely are also produced in neurons in the brain stimulating or inhibiting synthesis or release of hypothalamic and pituitary hormones as shown in Figure ane. Therefore, hormones can also be used as indicators of transmitter activity by the application of the and so-called neurotransmitter challenge tests: a specific pharmacological substance interim on the noradrenergic, dopaminergic, or serotonergic organisation is practical, which either interferes with synthesis, release, receptors, or metabolism of that item transmitter, and specific hormone responses on the pituitary level (PRL, GH, TSH) or on the level of glandular responses (mostly cortisol) can be measured in plasma or saliva (in urine only afterwards a delay of several hours, but contaminated past different intermediate effects). Hormone responses have to exist measured before and several times afterwards the challenge. Parameters of hormone responses are either measures of amplitude of hormone released (area under the response curve or highest difference from baseline) or parameters of slope of increase and turn down (see Reuter et al., 2002) or fourth dimension of onset of the hormone response. Challenge tests take been used in clinical equally well as in experimental inquiry to exam for disturbances and private differences in sensitivity of sure neurotransmitter systems, which are especially relevant in psychiatric diseases, since in that location is no direct access to the transmitter systems in the brain in humans. Examples of challenge tests with their substances for testing transmitter action and respective hormone responses are listed in Tabular array 3.

Tabular array three. Principles of transmitter challenge tests, classes of substances used, and corresponding hormone responses

Principle of activity Serotonin (5-HT) Dopamin (DA) Noradrenaline (NE)
Substance (case) Hormone response Substance (instance) Hormone response Substance (example) Hormone response
Precursor for synthesis 50-Tryptophan PRL↑
Cortisol (↑)
GH (↑)		 l-Dopa (PRL ↓)
Blockade of synthesis Tryptophan depletion PRL ↓ AMPT (HVA ↓)
Release d-Fenfluramine PRL ↑
Cortisol (↑)		 Amphetamine (PRL ↓) Reserpine ?
Reuptake inhibition Citalopram, Fluoxetine Cortisol ↑ Mazindole (PRL ↑)!!∗
GH ↑		 Reboxetine Cort ↑
GH ↑
Receptor agonism Ipsapirone 5 – HT1a receptor Cortisol ↑ BromocriptineD2 receptor
Apomorphine D2D1 receptor		 PRL ↓
GH (↑)
PRL ↓
GH ↑		 α2:Clonidine TSH ↑
GH ↑
Receptor animosity Cyproheptadine – HT2a receptor Cortisol ↓ Fluphenazine DiiD1 receptor PRL ↑

!!∗ = dopamine increase would usually suppress PRL, hither: reverse effect, PRL = prolactin, Cort = cortisol, GH = growth hormone, HVA = homovanillic acid, AMPT = α-methylparatyrosin, TSH = thyroid stimulating hormone, v-HT = serotonin, D = dopamine; ? = no hormone response confirmed, weak or contradictory response or response only with higher doses, ↑ increase, ↓ decrease.

Modified from Netter, P., 2008. Neurochemische und endokrine Systeme in der experimentellen Emotionsforschung: Forschungsansätze und Grundlagen. In: Janke, W., Schmidt-Duffy, Yard., Debus, G., (Eds.), Experimentelle Emotionsforschung, Pabst Science Publishers, Lengerich, Berlin, p. 625.

As tin can exist seen from Table 3, tests may refer to synthesis, release, reuptake, and receptor agonistic and antagonistic effects demonstrating unlike levels of interference with the specific transmitter. Unfortunately, not all hormones suitable every bit possible indicators of transmitter actions take been tested for all transmitter principles of action and for all transmitter systems, and fifty-fifty, if and then, their effects on hormones may not exist positively correlated to each other (see e.one thousand., receptor agonists of dopamine). This may be due to the fact that pharmacological challenges by drugs may affect rate of synthesis, rate of release, sensitivity and number of receptors, sensitivity of the transporter (responsible for reuptake of the remaining transmitter from the synaptic cleft after binding of the transmitter to the postsynaptic receptors), and enzymatic catabolism of the transmitter. Then, unfortunately, when monitoring a hormone response, one is never certain to which of these processes the hormone response may exist attributable. This is even more the example when psychological responses, like performance, emotional reactions, or social beliefs are the target of interests, considering and so the challenge substance itself, the hormone elicited, and the genetic and personality dispositions of the person may exist responsible for variations in hormone responses. Yet, claiming tests have revealed insight into the relevance of serotonin, dopamine, and noradrenaline for personality related transmitter responsitivity and psychiatric diseases, most of which are based on disturbances of transmitter systems.

Similarly, hormones of the pituitary can be tested by awarding of respective hypothalamic stimulating hormones. For example, TRH awarding can bespeak either increased sensitivity of TSH represented by elevated TSH responses demonstrating hypofunction of the thyroid hormones (observed with the disease of myxedema) or, vice versa, reduced TSH responses indicating high thyroxin and T3 levels observed in hyperfunction of the thyroid equally observed with Morbus Basedow (an autoimmune disease). Past a more indirect pathway, the application of the corticosteroid dexamethasone can indicate a disturbed feedback loop of the HPA centrality (see Hypothalamic-Pituitary-Adrenal Centrality, Psychobiology of). Many more tests similar this make apply of the stimulation and feedback loops discussed above.

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Conflict Analysis

David LeMarquand , ... Robert O. Pihl , in Encyclopedia of Violence, Peace, & Conflict (Third Edition), 2022

Catecholamines (Norepinephrine, Dopamine) and Related Compounds

The catecholamines, NE (noradrenaline), and DA are formed from the amino acid tyrosine, which itself is derived from the amino acid phenylalanine. Jail cell bodies of the noradrenergic organisation are primarily located in the locus coeruleus. High concentrations of NE are also found in the hypothalamus. DA is present in high levels in the neostriatum, nucleus accumbens, and olfactory tubercle. In the CNS, the major metabolite of NE is 3-methoxy-4-hydroxyphenylglycol (MHPG). In the peripheral sympathetic nervous system, vanillylmandelic acrid (VMA) is the chief metabolite of NE. In the human brain, the primary metabolite of DA is homovanillic acid (HVA), with a smaller amount of 3,four-dihydroxyphenylacetic acid (DOPAC) and three-methoxytyramine formed. Free MHPG diffuses from the encephalon into the CSF and full general circulation, and then estimates of its concentration in the CSF are thought to reflect CNS noradrenergic neuronal activity. A proportion of CSF MHPG derives from the plasma, considering costless MHPG diffuses readily through membranes, so correction for the plasma contribution must be fabricated. Plasma and urinary gratis MHPG may exist useful indices of total body NE metabolism, but are not valid indices of encephalon NE metabolism, as the brain accounts for but approximately thirty% of the total torso production of MHPG. CSF HVA levels are taken as an index of DA metabolism in the CNS.

The few studies that have been done investigating CSF MHPG in tearing offenders suggest reduced levels of this neurochemical are associated with violent behavior. Impulsive arsonists (relative to habitually tearing offenders and nonviolent controls) and alcoholic violent offenders and impulsive burn-setters with histories of violent suicide attempts (relative to those without) accept low CSF MHPG. Low CSF MHPG also predicted recidivism in these individuals. Ii other studies have found no differences in CSF NE or MHPG concentrations between groups of impulsive versus nonimpulsive violent offenders, so the relationship between violence and CSF MHPG remains to exist confirmed.

The noradrenergic system contributes to the regulation of arousal and responsiveness to the environment. Increased locus coeruleus activity has been associated with reactivity to novel and particularly threatening stimuli, decreased activity with self-restitutive or vegetative activity such as eating, self-grooming, and sleeping. The few studies that did discover lower CSF MHPG in arsonists and impulsive fierce offenders may imply reduced arousal and reactivity in these individuals. This is consequent with psychophysiological studies of psychopaths showing reductions in sympathetic nervous arrangement arousal (due east.1000., skin conductance activity) compared to nonpsychopaths.

The relatively few studies investigating NE functioning in personality-disordered individuals suggest a positive correlation with aggression. CSF MHPG levels were positively correlated with cocky-reported assailment in personality-disordered military machine personnel (although the variance in aggression explained was low later decision-making for CSF 5-HIAA). In another report, growth hormone responses to the alpha-2-adrenergic agonist clonidine were positively correlated with sensation-seeking and take chances-taking behaviors and self-reported lifetime irritability (but not assaultiveness) in both personality-disordered patients and normal controls. (Note that there was no correlation betwixt growth hormone responses and overt aggression or impulsivity in this report.) In some other written report with personality-matted individuals, growth hormone responses to clonidine were associated with irritability and verbal hostility.

These results are difficult to reconcile with those found in violent offenders, which advise that increased NE office is related to assailment and violence. It has been suggested that reduced presynaptic and increased postsynaptic NE function are related to aggression. Increased presynaptic blastoff-2 NE receptor activity in the locus coeruleus (every bit has been suggested past increased locus coeruleus alpha-2 agonist binding in violent, but non irenic, suicides victims) may lead to reduced NE outflow (and thus reduced CSF MHPG) and an upregulation of postsynaptic alpha-two NE receptors, thus increasing growth hormone responses to clonidine. Overall, this might lead to an augmented blastoff-2 NE betoken in NE pathways in the presence of aversive, provocative stimuli, resulting in a heightened behavioral arousal (fight/flight response). Furthermore, alpha-ii heteroreceptors terminating on presynaptic 5-HT neurons may exist supersensitive, leading to greater inhibition of v-HT firing. Such a synthesis is intriguing and provides a number of testable hypotheses.

Less evidence in humans implicates the dopaminergic system in vehement behavior. Studies on violent offenders have found no differences in CSF HVA levels in arsonists versus habitually violent offenders and irenic controls, bedevilled violent criminals who committed impulsive versus premeditated crimes, fierce offenders and impulsive burn down-setters with histories of serious violent suicide attempts compared to those with no such histories, or betwixt impulsive alcoholic violent offenders with hating personality disorder, impulsive alcoholic vehement offenders with intermittent explosive disorder, nonimpulsive alcoholic violent offenders, and healthy volunteers. Trigger-happy criminals with antisocial personality disorder had lower levels of CSF HVA compared to those with paranoid or passive-ambitious personality disorders. CSF DA levels and turnover were not different between five XYY assaultive patients and controls. No differences in CSF DOPAC or HVA have been plant between convicted violent criminals who committed impulsive versus premeditated crimes.

One study has found that violent alcoholic offenders had slightly college striatal DA reuptake site densities compared to irenic alcoholic offenders and nonalcoholic controls, suggesting that violence is associated with increased dopaminergic activity in the brain.

Finally, two studies suggested that violent male person offenders may be either college or lower in their levels of gratis or conjugated plasma phenylacetic acid, the major metabolite of phenylethylamine post-obit its breakdown by monoamine oxidase (MAO) B, compared to irenic offenders. Phenylethylamine, structurally related to amphetamine, has a like pharmacological response to the latter when administered following pretreatment with an MAO inhibitor. Information technology is synthesized from the amino acrid phenylalanine. It has been posited that increased phenylacetic acid levels in violent offenders may betoken increased phenylethylamine levels, the latter representing a compensatory increase to reduce ambitious tendencies, much the way amphetamine reduces hyperactivity in attending-deficit and hyperactive children.

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Energy Metabolism

In Endocrine and Reproductive Physiology (Fourth Edition), 2013

Glycogenolysis

Glucagon and catecholamines , acting through Gs-coupled receptors (glucagon receptor and β ii -adrenergic receptor, respectively) stimulate PKA, leading to the phosphorylation and activation of phosphorylase kinase and glycogen phosphorylase (Fig. 3-xi). Additionally, the loss of insulin signaling prevents the dephosphorylation and activation of glycogen synthase. Collectively, these actions lead to the increment in hepatic glucose-6-phosphate levels.

For glucose-six-phosphate to leave the liver through the Glut-2 transporter (and contribute to hepatic glucose production), it needs to be dephosphorylated to glucose. This reaction is catalyzed by glucose-six-phosphatase within the shine endoplasmic reticulum (run into Fig. 3-10). In the absence of insulin-PKB/AKT signaling, FOXO1 remains in the nucleus and stimulates glucose-vi-phosphatase factor expression (encounter Fig. 3-22).

Glycogenolysis supports hepatic glucose product for near 12-xvi hours at the beginning of a fast.

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Aging Mind: Facets and Levels of Analysis

Shu-Chen Li , in International Encyclopedia of the Social & Behavioral Sciences (Second Edition), 2015

Attenuated Neuromodulation

Amongst different neurotransmitter systems, the catecholamines, including dopamine (DA) and norepinephrine (NE), are important neurochemical underpinnings of historic period-related cerebral impairments for several reasons. Get-go, there is consensus for age-related decline in catecholaminergic function in the prefrontal cortex (PFC) and basal ganglia. Across the adult life span, dopaminergic function in the basal ganglia decreases past 5–10% each decade (see Schneider et al., 1996). Furthermore, many DA pathways in the basal ganglia are interconnected with the frontal cortex through the frontal-striatal circuits (Graybiel, 1990), hence are in close functional association with the PFC cognitive processes. 2d, research over the last two decades suggests that catecholamines modulate the PFC'due south utilization of briefly activated cortical representations of external stimuli to circumvent abiding reliance on environmental cues and to regulate attention to focus on relevant stimuli and advisable responses (see Arnsten, 1998 for review). Third, there are many findings indicating, specifically, functional relationships between age-related deficits in the dopaminergic system and deficits in various aspects of information processing. For instances, reduced dopamine receptor density in onetime rats' nigrostriatum decreases response speed and increases reaction time variability (MacRae et al., 1988). Drugs that facilitate dopaminergic modulation alleviate WM deficits of anile monkeys who suffer from 50% dopamine depletion in their PFC (see Arnsten, 1998 for review). In humans, age-related attenuation of dopamine D2 receptor's binding mechanism is associated with declines in processing speed and episodic retentivity (see Bäckman et al., 2006 for review).

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The Thyroid Gland

In Endocrine and Reproductive Physiology (Fourth Edition), 2013

Cardiovascular Furnishings

Maybe the near clinically of import deportment of thyroid hormone are those on cardiovascular physiology. T3 increases cardiac output, ensuring sufficient oxygen delivery to the tissues (Fig. 6-10). The resting heart rate and the stroke book are increased. The speed and force of myocardial contractions are enhanced (positive chronotropic and inotropic effects, respectively), and the diastolic relaxation time is shortened (positive lusitropic outcome). Systolic blood pressure is modestly augmented, and diastolic blood pressure is decreased. The resultant widened pulse pressure reflects the combined effects of the increased stroke volume and the reduction in total peripheral vascular resistance that result from blood vessel dilation in skin, muscle, and heart. These effects in turn are partly secondary to the increment in tissue product of rut and metabolites that thyroid hormone induces (see later). In addition, nonetheless, thyroid hormone decreases systemic vascular resistance by dilating resistance arterioles in the peripheral circulation. Total blood book is increased by activating the renin-angiotensin-aldosterone axis and thereby increasing renal tubular sodium reabsorption (see Chapter 7).

The cardiac inotropic effects of T3 are indirect, through enhanced responsiveness to catecholamines (encounter Chapter 7), and straight (Fig. 6-11). Myocardial calcium uptake is increased, which enhances contractile force. Thyroid hormone inhibits expression of the Na-Ca antiporter, thereby increasing intramyocellular Ca2   + concentrations. T3 increases the velocity and strength of myocardial contraction. Tiii promotes the expression of the faster and stronger α-isoform and represses the slower, weaker β-isoform of cardiac myosin heavy chain. T3 also increases the ryanodine Ca 2   + channels in the sarcoplasmic reticulum, promoting Caii   + release from the sarcoplasmic reticulum during systole. The calcium adenosine triphosphatase (ATPase) of the sarcolemmal reticulum (SERCA) is increased past T3, which facilitates sequestration of calcium during diastole and shortens the relaxation time.

Clinical Box half-dozen-viii

Thyroid hormone levels in the normal range are necessary for optimal cardiac functioning. Hypothyroidism in humans reduces stroke volume, left ventricular ejection fraction, cardiac output, and the efficiency of cardiac office. The latter defect is shown by the fact that the stroke work index [(stroke book/left ventricular mass) × superlative systolic claret pressure] is decreased even more than than is myocardial oxidative metabolism. The rise in systemic vascular resistance may contribute to this cardiac debility. On the other paw, hyperthyroidism increases cardiac output and reduces peripheral resistance, generating a widened pulse force per unit area. T3 increases UCP2 and UCP3 in cardiac muscle, which uncouples ATP production from oxygen use during the β-oxidation of free fatty acids. This can cause high-output cardiac failure. When aging individuals develop hyperthyroidism, the cardiac effects of thyroid hormone may include rapid atrial arrhythmias, flutter, and fibrillation.

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Reinforcement: Neurochemical Substrates

Larry Stein , in International Encyclopedia of the Social & Behavioral Sciences (Second Edition), 2015

Reinforcing Neurons – Brain Cocky-Stimulation Show

The idea that behavioral reinforcement is specialized neurochemically and is mediated past encephalon catecholamine systems has guided research in this field for 50 years ( Stein, 1962, 1968). More specific hypotheses – that dopamine, norepinephrine, and opioid-peptide encephalon cells may serve as reinforcing neurons – extend this thought and are supported past evidence from brain self-stimulation and drug cocky-administration experiments (Olds, 1975; Crow, 1972; Stein, 1964, 1978; Wise, 1982, 2004, 2008). In self-stimulation experiments, animals piece of work to deliver electric stimulation to their own brains through permanently indwelling electrodes much as hungry or thirsty rats work to obtain natural reinforcers, such as food or water (Figure 1). In the absence of other sources of reward, the reinforcement for cocky-stimulation behavior must arise from the neuronal activity that is excited by the electrical stimulus. Accordingly, it is tempting to assume that some of the neurons under the electrode tip actually are the reinforcing neurons that mediate the furnishings of natural rewards, or at to the lowest degree are neurons that directly excite them.

Figure ane. Diagram of self-stimulation experiment. When the rat presses on lever, it triggers a reinforcing electrical stimulus to its encephalon.

 Reprinted with permission from Olds, J., 1956. Pleasance centers in the brain. Scientific American 195, 105–116.

High self-stimulation rates are observed when electrodes are implanted in regions containing dopamine or opioid peptide jail cell bodies or pathways. In detail, self-stimulation tightly overlaps the distribution of dopamine cells in the ventral tegmental area and substantia nigra. Cocky-stimulation closely follows the anteriorly projecting dopamine fibers through the hypothalamus, only it correlates somewhat less closely with the dopamine concluding fields in the forebrain. Similarly, mapping of opioid peptide sites for self-stimulation is consequent with the idea that certain beta-endorphin and dynorphin neurons are involved in self-stimulation. Involvement of norepinephrine neurons in self-stimulation is more than controversial. Although many laboratories report self-stimulation from sites in or near the locus coeruleus and its dorsal packet projection, in that location is no general agreement that the noradrenergic neurons which brand up this nucleus are responsible for the reinforcing effect. Nonetheless, noradrenergic neurons in the locus coeruleus and other nuclei innervate the ventral tegmentum and provide excitatory bulldoze to midbrain dopamine neurons. Thus, electric stimulation of these noradrenergic sites, at the very least, could reinforce behavior via a dopaminergic pathway.

The catecholamine-opioid peptide reinforcement hypothesis also is firmly supported past pharmacological experiments. Significantly, selective antagonists of dopamine and opioid peptide receptors, such as pimozide and naloxone, respectively, reduce self-stimulation rates in patterns that resemble the extinction of behavior subsequently reward omission (Wise, 2004; Trujillo et al., 1989). Thus, the antagonist drugs appear to act past blocking or weakening a chemically coded reinforcement message. In the disputed case of norepinephrine, selective inhibition of its biosynthesis by disulfiram and related agents decreases or eliminates self-stimulation over the same time course as the depletion of norepinephrine stores. Furthermore, intraventricular infusions of l-norepinephrine restore normal rates of self-stimulation within a few minutes, presumably later the exogenous transmitter diffuses to and replenishes reinforcement-relevant stores (Wise and Stein, 1969). Similar infusions of the unnatural isomer d-norepinephrine or dopamine (whose stores are not depleted past disulfiram) fail to restore self-stimulation. An alternative interpretation of these results (Roll, 1970) – that norepinephrine is not a reinforcement transmitter, merely acts but to arouse disulfiram-sedated rats – has gained a widespread currency (e.chiliad., Wise, 2008). Simply the arousal hypothesis is challenged by much other prove. First, sedation itself is not adequate to reduce self-stimulation behavior; in fact, heavily sedative doses of barbiturates or benzodiazepines do not suppress, and sometimes fifty-fifty increase, rates of self-stimulation. Second, physical handling of the rats, priming trains of stimulation given by the experimenter, and control infusions of saline or other substances, which also produce arousal, neglect to restore normal rates of cocky-stimulation. Indeed, even response-independent noradrenergic receptor stimulation by infusion of norepinephrine agonists (eastward.yard., clonidine and oxymetazoline) is ineffective. The agonist infusions might be arousing, but even so do not restore self-stimulation (arguably, because response-independent activation of noradrenergic receptors confuses the obligatory contingency relationship between cocky-stimulation responses and the electrically induced release of reinforcement transmitter).

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Our Ethical and Moral Responsibility

Zenithson Ng , ... Jose Peralta , in Handbook on Animal-Assisted Therapy (Quaternary Edition), 2015

26.4.iv Other Measures of Animal Welfare

Researchers have attempted to mensurate numerous other physiologic parameters to assess animal welfare. These accept included alterations in neuroendocrine responses such as catecholamines, dopamine, and B-endorphins; immune response such as white blood cell count and immunoglobulin A; and acute-phase protein response such as prolactin, haptoglobin, and C-reactive poly peptide ( Odendaal & Meintjes, 2003; Siracusa et al., 2010). Additionally, cardiovascular responses such as modify in eye charge per unit variability (Bergamasco et al., 2010; von Borell et al., 2007; Gehrke, Baldwin, & Schiltz, 2011) and blood force per unit area (Vincent & Michell, 1996) accept been associated with stress and measured in response to human interaction. However, these outcomes tin can often be difficult to assess and correlate with brute welfare due to challenges in collecting samples and their inherent multifactorial variability. There is no consensus as to which is the single best test (Mostl & Palme, 2002), and it is likely that a combination of various parameters will help to elucidate a more consummate understanding of stress and welfare in animals (Hiby et al., 2006). Cut-border enquiry should focus on correlating these physiologic indicators of stress and discovering novel methods to collect such parameters.

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Interoception

André Schulz , in International Encyclopedia of the Social & Behavioral Sciences (Second Edition), 2015

Stress Hormones

Certain stress hormones are considered to play an important role in the processing of interoceptive signals. First, the activation of the autonomic nervous system may result in a release of catecholamines, such as epinephrine. Although catecholamines do non cross the blood–brain barrier and, therefore, cannot modulate the processing of interoceptive signals at the level of the CNS, epinephrine binds to beta1-adrenergic receptors at the myocardium. The binding of epinephrine to beta1-adrenoceptors causes positive inotropic (increased contractibility), chronotropic (increased centre rate), and dromotropic effects (faster depolarization), which lead to an increase of SV and a decrease of the PEP ( Schachinger et al., 2001). It was repeatedly shown that cardiodynamic parameters, such equally PEP or SV, are associated with the accuracy in heartbeat detection tasks (Schandry et al., 1993). It is likely that the increased stimulation of arterial baroreceptors caused by increased SV is responsible for this issue. Furthermore, peripheral sympathetic activation induced via beta1-adrenergic agents and primal sympathetic activity elicited by alpha1-adrenergic agents increases heartbeat perception accuracy (Moor et al., 2005). Second, cortisol, the final product of HPA axis activation, may also take the potential to modulate interoceptive signal processing. A dose of iv mg of intravenously administered cortisol may induce higher heartbeat-evoked potentials in a state of high alertness compared with a state of low alertness (Schulz et al., 2013b). This effect may feed into a savage circle of increased attentional focus on physical symptoms, increased anxiety and higher levels of cortisol, which may stand for possible psychoneuroendocrine mechanism underlying psychological feed-frontward models of somatosensory amplification. Interestingly, cortisol does not bear upon the cardiac modulation of startle, suggesting that this effect is limited to the cortical representation of interoceptive signals, simply does not modify the brainstem processing of afferent actual signals (Schulz et al., submitted). In contrast to catecholamines, cortisol crosses the blood–brain barrier and affects cells in the entire body, including the CNS. The described results can exist attributed to activity in the thalamus, which represents a major relay center for exteroceptive and interoceptive sensory data, and was demonstrated to be affected past cortisol administration. The importance of the HPA axis for altered perception of physical sensations is farther underlined by the fact that dysregulation of the HPA axis tin be observed in many body-related mental disorders, such every bit somatoform disorders (Rief and Barsky, 2005) or depression (Terhaar et al., 2012).

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