[emfrefugee] Microwave exposure decreases brain hormone Norepinephrine. Decrease in Norepinephrine linked to Autonomic Nervous System Disorder, Memory Disturbances, ADHD, and Depression.

Microwave exposure has been shown to induce a decrease in levels of the brain hormone norepinephrine (Takahashi et al 1994).

J Auton Nerv Syst. 1994 Aug;48(3):213-9. Links

Aspects of hypothalamic neuronal systems in VMH lesion-induced obese rats.

Department of Neuropsychopharmacology (Tsumura), Gunma University School of Medicine, Japan.

To clarify neuronal disturbance in the hypothalamus reflecting the development of obesity in ventromedial hypothalamic nucleus (VMH)-lesioned rats, we investigated the contents of neurotransmitters in the hypothalamus after pretreatment by microwave irradiation , contents of neurotransmitter metabolites in third ventricle fluid and catecholamine contents in the adrenal gland. The hypothalamic contents of norepinephrine (NE) and dopamine (DA) were selectively decreased , but acetylcholine (ACh) and serotonin (5-HT) levels were not changed from those in controls. In the lateral part of the hypothalamus, also, a significant decrease of NE content was detected. On the other hand, NE and DA metabolites, MHPG, DOPAC and HVA were increased in the third ventricle fluid in VMH lesion-induced obese rats. Wet weight and content of epinephrine in the adrenal gland were decreased, though the content of NE was preserved. These results indicate that a disturbance of NE and DA neurons in the hypothalamus is involved in the development of VMH lesion-induced obesity. In addition, an increment of the activities of NE and DA systems in the central nervous system as a whole and some irregularity in the sympatho-adrenal system might contribute to VMH obesity .

This hormone is essential for control of the autonomic nervous system, and lack of it can lead to autonomic nervous system disorders. For example, if the autonomic nervous system is not working properly, the body will have trouble regulating its temperature - i.e. cooling itself when it is warm and heating itself when it is cold (Gandhi & Ross 1987).

1: Radiat Res. 1987 Jan;109(1):90-9. Links

Alterations in alpha-adrenergic and muscarinic cholinergic receptor binding in rat brain following nonionizing radiation.

Microwave radiation produces hyperthermia. The mammalian thermoregulatory system defends against changes in temperature by mobilizing diverse control mechanisms. Neurotransmitters play a major role in eliciting thermoregulatory responses. The involvement of adrenergic and muscarinic cholinergic receptors was investigated in radiation-induced hyperthermia. Rats were subjected to radiation at 700 MHz frequency and 15 mW/cm2 power density and the body temperature was raised by 2.5 degrees C. Of six brain regions investigated only the hypothalamus showed significant changes in receptor states, confirming its pivotal role in thermoregulation. Adrenergic receptors, studied by [3H]clonidine binding, showed a 36% decrease in binding following radiation after a 2.5 degrees C increase in body temperature, suggesting a mechanism to facilitate norepinephrine release. Norepinephrine may be speculated to maintain thermal homeostasis by activating heat dissipation. Muscarinic cholinergic receptors, studied by [3H]quinuclidinyl benzilate binding, showed a 65% increase in binding at the onset of radiation. This may be attributed to the release of acetylcholine in the hypothalamus in response to heat cumulation. The continued elevated binding during the period of cooling after radiation was shut off may suggest the existence of an extra-hypothalamic heat-loss pathway.

This could lead to feeling colder than one would normally when it is cold and feeling warmer than one would normally when it is warm (Way et al 1981).

Bioelectromagnetics. 1981;2(4):341-56. Links

Thermoregulatory physiologic responses in the human body exposed to microwave radiation.

By introduction of an additional compartment in the hypothalamic region Stolwijk's thermoregulatory model has been modified to consider partial heating due to hot spots induced by microwaves. It was found that because of thermoregulatory action, the temperature of the hypothalamus will not increase drastically until the rate of energy deposition exceeds the threshold level of about 50 mW/g. The primary controlling mechanisms are blood flow and sweating. For an energy deposition rate of 10 mW/g in the hypothalamus the increase in blood flow in the skin is negligible and the temperature rise of the hypothalamus as compared with blood temperature is about 0.5 degrees C. It was found that exposure of the head to electromagnetic radiation, in general, causes a decrease in temperature of the trunk and skin. The results show that while the deposition of energy in the hypothalamus at the rate of 10 mW/g produced significant conductive and convective effects, the same total energy uniformly distributed over the cranial cavity produces less significant effects.

An abnormal decrease in norepinephrine levels has also been connected to short-term memory disturbances (Clinton et al 2006),

Psychopharmacology (Berl). 2006 Jan;183(4):404-12. Epub 2005 Nov 24.

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Desipramine attenuates working memory impairments induced by partial loss of catecholamines in the rat medial prefrontal cortex.

Mental Health Research Institute and Department of Psychiatry, University of Michigan, Ann Arbor, MI 48109, USA.

RATIONALE: The density of tyrosine hydroxylase-immunoreactive (TH-IR) axons in the prefrontal cortex of schizophrenic subjects may be reduced by as much as 50% in the deep cortical layers (Am J Psychiatry 156:1580-1589, 1999). Previously, we demonstrated that approximately 60% loss of TH-IR axons in the rat medial prefrontal cortex (mPFC) decreases local basal and stress-evoked extracellular dopamine (DA) concentrations, suggesting that moderate loss of DA axons in the mPFC is sufficient to alter the neurochemical activity of the remaining DA neurons (Neuroscience 93:497-505, 1999). OBJECTIVES: To further assess the functional consequences of partial mPFC DA depletion, we examined the effects of 6-hydroxydopamine lesions of the rat mPFC on behavior in a T-maze delayed-response task. We also assessed whether chronic administration of the norepinephrine (NE) uptake inhibitor, desipramine (DMI), attenuates lesion-induced deficits in T-maze performance. Previous research indicates that inhibition of NE transport in the mPFC results in a concomitant increase in extracellular DA and NE. RESULTS: Moderate loss of mPFC DA and NE (approximately 50 and 10% loss, respectively) was sufficient to impair delayed-response behavior, in part due to an increase in perseverative responding. Chronic DMI treatment (3 mg/kg delivered via osmotic pumps) impaired performance of control rats but attenuated the deficits in delayed-response behavior in rats previously sustaining loss of mPFC DA and NE (approximately 75 and 35% loss, respectively). CONCLUSION: These data suggest that moderate loss of DA and NE in the prefrontal cortex is sufficient to impair cognitive function, and these behavioral effects are attenuated by inhibition of the NE transporter.

ADHD (Arnsten & Li 2005)

Biol Psychiatry. 2005 Jun 1;57(11):1377-84.

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Neurobiology of executive functions: catecholamine influences on prefrontal cortical functions.

Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA. amy.arnsten@yale.edu

The prefrontal cortex guides behaviors, thoughts, and feelings using representational knowledge, i.e., working memory. These fundamental cognitive abilities subserve the so-called executive functions: the ability to inhibit inappropriate behaviors and thoughts, regulate our attention, monitor our actions, and plan and organize for the future. Neuropsychological and imaging studies indicate that these prefrontal cortex functions are weaker in patients with attention-deficit/hyperactivity disorder and contribute substantially to attention-deficit/hyperactivity disorder symptomology . Research in animals indicates that the prefrontal cortex is very sensitive to its neurochemical environment and that small changes in catecholamine modulation of prefrontal cortex cells can have profound effects on the ability of the prefrontal cortex to guide behavior. Optimal levels of norepinephrine acting at postsynaptic alpha-2A-adrenoceptors and dopamine acting at D1 receptors are essential to prefrontal cortex function. Blockade of norepinephrine alpha-2-adrenoceptors in prefrontal cortex markedly impairs prefrontal cortex function and mimics most of the symptoms of attention-deficit/hyperactivity disorder, including impulsivity and locomotor hyperactivity. Conversely, stimulation of alpha-2-adrenoceptors in prefrontal cortex strengthens prefrontal cortex regulation of behavior and reduces distractibility. Most effective treatments for attention-deficit/hyperactivity disorder facilitate catecholamine transmission and likely have their therapeutic actions by optimizing catecholamine actions in prefrontal cortex.

PMID: 15950011 [PubMed - indexed for MEDLINE]

and depression (Meyer et al 2006; Charney 1988).

1: J Clin Psychiatry. 1998;59 Suppl 14:11-4. Links

Monoamine dysfunction and the pathophysiology and treatment of depression.

Charney DS.

Department of Psychiatry, Yale University School of Medicine, New Haven, Conn 06519, USA.

Alterations in noradrenergic and serotonergic function in the central nervous system (CNS) have been implicated in the pathophysiology of depression and the mechanism of action of antidepressant drugs. Based on changes in norepinephrine and serotonin metabolism in the CNS, it has been postulated that subgroups of patients with differential responses to norepinephrine and serotonin reuptake inhibitors may exist. Alpha-methylparatyrosine (AMPT), which causes rapid depletion of brain catecholamines, has been used as a noradrenergic probe to test the hypothesis that changes in neurotransmission through the catecholamine system may underlie the therapeutic response to norepinephrine reuptake inhibitors. Brain serotonin is dependent on plasma levels of the essential amino acid tryptophan. Rapid tryptophan depletion, in the form of a tryptophan-free amino acid drink, has been used as a serotonergic probe to identify therapeutically responsive subsets of patients. Using these probes, we have recently examined the behavioral effects of reduced concentrations of brain monoamines on depressed patients treated with a variety of serotonin selective reuptake inhibitors (SSRIs) or the relatively norepinephrine-selective antidepressant desipramine, during 3 different states: drug-free and depressed; in remission on antidepressant drugs; and drug-free in remission. The results of a series of investigations confirm the importance of monoamines in the mediation of depressed mood, but also suggest that other brain neural systems may have more of a primary role than previously thought in the pathophysiology of depression. Noradrenergic and serotonergic probes may be used in time to identify subsets of depressed patients to determine which patients might respond differentially to the new selective norepinephrine reuptake inhibitors or SSRIs.

1: Arch Gen Psychiatry. 2006 Nov;63(11):1209-16. Links

Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression.

Vivian M. Rakoff PET Imaging Centre and Mood and Anxiety Disorders Division, Clarke Division, Centre for Addiction and Mental Health and Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. jeff.meyer@camhpet.ca

CONTEXT: The monoamine theory of depression proposes that monoamine levels are lowered, but there is no explanation for how monoamine loss occurs. Monoamine oxidase A (MAO-A) is an enzyme that metabolizes monoamines, such as serotonin, norepinephrine, and dopamine. OBJECTIVE: To determine whether MAO-A levels in the brain are elevated during untreated depression. SETTING: Tertiary care psychiatric hospital. PATIENTS: Seventeen healthy and 17 depressed individuals with major depressive disorder that met entry criteria were recruited from the care of general practitioners and psychiatrists. All study participants were otherwise healthy and nonsmoking. Depressed individuals had been medication free for at least 5 months. MAIN OUTCOME MEASURE: Harmine labeled with carbon 11, a radioligand selective for MAO-A and positron emission tomography, was used to measure MAO-A DVS (specific distribution volume), an index of MAO-A density, in different brain regions (prefrontal cortex, anterior cingulate cortex, posterior cingulate cortex, caudate, putamen, thalamus, anterior temporal cortex, midbrain, hippocampus, and parahippocampus). RESULTS: The MAO-A DVS was highly significantly elevated in every brain region assessed (t test; P=.001 to 3x10(-7)). The MAO-A DVS was elevated on average by 34% (2 SDs) throughout the brain during major depression. CONCLUSIONS: The sizable magnitude of this finding and the absence of other compelling explanations for monoamine loss during major depressive episodes led to the conclusion that elevated MAO-A density is the primary monoamine-lowering process during major depression.

Paul Raymond Doyon
MAT (TESOL), MA Advanced Japanese Studies, BA Psychology
"All that is necessary for evil to triumph is for good men to do nothing"

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