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9. Stress and Monoamine Neurons in the Brain
Pages 161-176

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From page 161...
... . These transmitters are found in brain neurons that are involved in the central nervous system's response to stress; indeed, some data indicate that TYR administration can enhance DA and NE synthesis in the brain and, as a result, reverse deficient performance in both rats and humans (Banderet and Lieberman, 1989; Lehnert et al., 1984~.
From page 162...
... However, given the diversity of effects of stress on the functional states of the various DA and NE receptor subtypes, the exact responses to TYR may not always be simple. Indeed, because of the incomplete body of data regarding the effects of stress on brain catecholamine receptors, their further study in this context would appear essential to an eventual understanding of the utility of TYR and other pharmacologic agents that stimulate DA and/or NE release as stress countermeasures.
From page 163...
... This relationship is tied to neuronal activity, however, because an increase in the brain TRP level produces a much larger stimulation of 5HT synthesis and release when the SHT neuron is active than when it is quiescent (Fernstrom et al., 1990; Sharp et al., 1992~. As discussed below, stress does not influence the activity of SHT-producing neurons, but it does increase brain TRP levels.
From page 164...
... The a2-receptor number and affinity have also been examined in a variety of rat brain regions following exposure to acute stressors and have been found to yield no simple effect. In different regions, acute stress is reported to reduce receptor number but not change affinity (hippocampus)
From page 165...
... (1981) reported that pretreatment of rats with a drug that inhibits phospholipase activity, and ultimately cyclic AMP generation, blocks the reduction in Preceptor number in the hypothalamus and brain stem that follows chronic stress in rats.
From page 166...
... Thus, the effects of agents that enhance NE synthesis and release (such as TYR) and that, as a result, produce particular functional effects following single stressful events, may not provide a reliable foundation for predicting functional changes under conditions of continued or repeated stress.
From page 167...
... observed that daily episodes of foot shock for 10 days continued to raise dihydroxyphenylacetic acid levels in the prefrontal cortex, corpus striatum, and brain stem. Similar findings were reported by MacLennan et al.
From page 168...
... synthesis and turnover in the rat brain. Acute stressors (e.g., immobilization or foot shock)
From page 169...
... Valine or TYR treatment also eliminated the stress-induced rise in neuronal S-hydroxyindole release (Joseph and Kennett, 19831. To summarize, the above evidence suggests that a single stressful event raises the amount of TRP taken up by the brain, possibly via the release of epinephrine into the circulation, causing brain TRP levels to rise and thus 5HT synthesis to increase.
From page 170...
... · Overall, given this diversity of catecholamine receptor responses to chronic stress and the relatively small number of studies that have defined them, it is presently impossible to conclude how brain circuits with catecholamine-producing neurons and postsynaptic receptors should respond to repeated stressful events. Additional studies should be encouraged, to define with more certainty the effects of stress on catecholamine receptors in particular brain regions and then to attempt to correlate such changes with functions specific to the affected regions.
From page 171...
... Cohen, and C.A. McLellan 1986 Foot shock induces time and region specific adrenergic receptor changes in rat brain.
From page 172...
... 1990 Aromatic amino acids and monoamine synthesis in the central nervous system: Influence of the diet.
From page 173...
... Cabib 1991 Repeated stressful experiences differently affect brain dopamine receptor subtypes.
From page 174...
... Kirk 1986 Effect of repeated restraint stress, desmethylimipramine or adrenocorticotropin on the alpha and beta adrenergic components of the cyclic AMP response to norepinephrine in rat brain slices.
From page 175...
... . But also, of course, stress caused striatocortical activation of corticosterone release.


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