Norepinephrine brain

Rangel, S. and Leon, M. (1995) Early odor preference training increases olfactory bulb norepinephrine. Brain Res. Dev. Brain Res. 85, 187-191. 

Disulfiram and Fusaric Acid. Administration of these dopamine-/3-hydroxylase inhibitors produces an increase in REM sleep several hours after the drug administration. This is caused by depletion of norepinephrine brain levels. 

Hydroxydopamine (6-OHDA). Administration of 6-OHDA destroys catecholamine-containing neurons and therefore decreases norepinephrine brain levels. In turn, REM sleep is increased. 

Nadi NS, Head R, Grillo M, Hempstead J, Grannot-Reisfeld N, et al. 1981. Chemical deafferentation of the olfactory bulb Plasticity of the levels of tyrosine hydroxylase, dopamine and norepinephrine. Brain Res 213 365-377. 

Segal, M., Bar Sagie, D., and Mayevsky, A., 1980, Metabolic changes induced in rat hippocampal slices by norepinephrine. Brain Res. 202 387-399. 

Neuronal Norepinephrine Depleting Agents. Reserpine (Table 6) is the most active alkaloid derived from Rauwolfia serpentina. The principal antihypertensive mechanism of action primarily results from depletion of norepinephrine from peripheral sympathetic nerves and the brain adrenergic neurons. The result is a drastic decrease in the amount of norepinephrine released from these neurons, leading to decrease in vascular tone and lowering of blood pressure. Reserpine also depletes other transmitters including epinephrine, serotonin [50-67-9] dopamine [51-61-6] ... 

Methyldopa, through its metaboHte, CX-methyInorepinephrine formed in the brain, acts on the postsynaptic tt2-adrenoceptor in the central nervous system. It reduces the adrenergic outflow to the cardiovascular system, thereby decreasing arterial blood pressure. If the conversion of methyldopa to CX-methyl norepinephrine in the brain is prevented by a dopamine -hydroxylase inhibitor capable of penetrating into the brain, it loses its antihypertensive effects. 

Fig. 2. Biosynthetic pathway for epinephrine, norepinephrine, and dopamine. The enzymes cataly2ing the reaction are (1) tyrosine hydroxylase (TH), tetrahydrobiopterin and O2 are also involved (2) dopa decarboxylase (DDC) with pyridoxal phosphate (3) dopamine-P-oxidase (DBH) with ascorbate, O2 in the adrenal medulla, brain, and peripheral nerves and (4) phenethanolamine A/-methyltransferase (PNMT) with. Cadenosylmethionine in the adrenal...

The original monoamine hypothesis of depression states that depressions are associated with a deficiency of catecholamines, particularly norepinephrine, at functionally important adrenergic receptor sites in the brain. Elation conversely may be associated with an excess of such amines. The hypothesis was articulated in 1966 only after the mechanism of action of the tricyclic antidepressant desipramine and of the psychostimulants... 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

CBs, like OPs, can cause a variety of sublethal neurotoxic and behavioral effects. In one study with goldfish Carrasius auratus), Bretaud et al. (2002) showed effects of carbofuran on behavioral end points after prolonged exposure to 5 pg/L of the insecticide. At higher levels of exposure (50 or 500 pg/L), biochemical effects were also recorded, including increases in the levels of norepinephrine and dopamine in the brain. The behavioral endpoints related to both swimming pattern and social interactions. Effects of CBs on the behavior of fish will be discussed further in Chapter 16, Section 16.6.1. 

McCormick, DA, Pape, HC and Williamson, A (1991) Actions of norepinephrine in the cerebral cortex and thalamus implications for function of the central noradrenergic system. Prog. Brain Res. 88 293-305. 

Fontana, DJ, McMiller, LV and Commissaris, RL (1999) Depletion of brain norepinephrine differential influence on anxiol5dic treatment effects. Psychopharmacology 143 197-208. 

Weiss, JM, Goodman, PA, Lostito, BG, Corrigan, S, Charry, JM and Bailey, WH (1981) Behavioral depression produced by an uncontrollable stressor relationship to norepinephrine, dopamine and serotonin levels in various regions of rat brain. Brain Res. Rev. 3 167-205. 

These are four monoamines synthesized and seereted within many mammalian tissues, ineluding various regions in the brain, sympathetic nervous system, enlero-chromafhn cells of the digestive tract, and adrenal mednlla. These biogenic amines (indoleamine and catecholamines — dopamine, norepinephrine, and epinephrine) are synthesized within the cell from their precursor amino acids and have been associated with many physiological and behavioral functions in animals and humans. 

In an attempt to simulate in rats the dosage regimen commonly employed by abusers of amphetamines, METH was administered (10 or 15 mg/kg every 6 hours four to six doses), after which the animals were killed (Koda and Gibb 1971 Koda and Gibb 1973). TH activity and catecholamine con-eentrations were measured in various brain regions and in the adrenal. Neostriatal TH aetivity was depressed in a dose-dependent manner and reaehed its nadir at 36 hours. Dopamine (DA) and norepinephrine concentrations were initially elevated, but then deereased in parallel with TH aetivity. Adrenal TH aetivity was elevated, presumably because of stress assoeiated with the toxie doses of METH. 

Maker, H.S. Weiss, C. and Brannan. Amine-mediated toxicity The effects of dopamine, norepinephrine, 5-hydroxytryptamine, 6-hydroxy-dopamine, ascorbate, glutathione and peroxide on the in vitro activities of creatine and adenylate kinases in the brain of the rat. 

Javitch, J.A. Strittmatter, S.M. and Snyder, S.H. Differential visualization of dopamine and norepinephrine uptake sites in rat brain using [ HJmazindol autoradiography. J Neurosci 51 513-1521, 1985. 

MDMA produced a dose-related depletion of serotonin without altering the eoncentration of either dopamine or norepinephrine in the monkey brain (table 1). Even the lowest dose of MDMA produced a substantial depletion... 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

Locus ceruleus Nucleus of norepinephrine-containing neurons located in the brain stem that are responsible for physiologic response to stress and panic. 

BZ is usually disseminated as an aerosol with the primary route of entry into the body through the respiratory system the secondary route is through the digestive tract. BZ blocks the action of acetylcholine in both the peripheral and central nervous systems. As such, it lessens the degree and extent of the transmission of impulses from one nerve fiber to another through their connecting synaptic junctions. It stimulates the action of noradrenaline (norepinephrine) in the brain, much as do amphetamines and cocaine. Thus, it may induce vivid hallucinations as it sedates the victim. Toxic delirium is very common. 

Szot, R, Ashliegh, E. A., Kohen, R. etal. (1993). Norepinephrine transporter mRNA is elevated in the locus coeruleus following short- and long-term desipramine treatment. Brain Res., 618, 308-12. 

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