Electrical brain stimulation

A number of procedures are known to cause release of prostaglandins in the brain. Electrical stimulation, trauma, hypoxia, ischaemia, hypoglycemia, convulsion, pyrogen fever aU cause a rapid increase in free arachidonic acid and stimulation of prostaglandin biosynthesis. For general reviews of eicosanoids in the nervous system, see refs. 201 203. 

In 1954, experiments by Olds and Milner revealed that the brain has specialized centers for reward functions. In these studies electrical stimulation of certain brain sites was found to be highly rewarding in the sense that rats operantly respond for electrical stimulation of these brain sites, often to the exclusion of any other activity. A neurotransmitter system that is particularly sensitive to electrical self-stimulation is the mesolimbic dopamine projection that originates in the ventral tegmental area and projects to structures closely... 

Fiorino, DF, Coury, A, Fibiger, HC and Phillips, AG (1993) Electrical stimulation of reward sites in the ventral tegmentum area increases dopamine transmission in the nucleus acumbers of the rat. Behav. Brain Res. 55 131-141. 

Not a great deal is known about factors that actually activate tryptophan hydroxylase. In particular, the relative contribution of tryptophan supply versus factors that specifically modify enzyme activity under normal dietary conditions is unknown. However, removal of end-product inhibition of tryptophan hydroxylase has been firmly ruled out. Also, it has been established that this enzyme is activated by electrical stimulation of brain slices, even in the absence of any change in tryptophan concentration, and so other mechanisms are clearly involved. 

These are normally based on the use of either electrical stimulation or chemical convulsants. When applied generally, i.e. an electric shock to the whole brain or convulsants injected systemically, the resulting convulsions are indicative of generalised seizures. If they are applied locally to specific brain areas, the same approaches induce activity indicative of partial seizures. Also some animals can be bred in which seizures either occur spontaneously or can be induced easily by appropriate sensory stimulation. 

Goddard, G.V. McIntyre, D. and Leech, C. A permanent change in brain function resulting from daily electrical stimulation. Exp Neurol 25 295-330, 1969. 

Houdouin, F., Cespuglio, R. 8r Jouvet, M. (1991). Effects induced by the electrical stimulation of the nucleus raphe dorsalis upon hypothalamic release of 5-hydroxyindole compounds and sleep parameters in the rat. Brain Res. 565, 48-56. 

Thakkar, M., Portas, C. McCarley, R. W. (1996). Chronic low-amplitude electrical stimulation of the laterodorsal tegmental nucleus of freely moving cats increases REM sleep. Brain Res. 723, 223-7. 

Fiorino DF, Coury A, Fibiger HC and Phillips AG (1993). Electrical stimulation of reward sites in the ventral tegmental area increases dopamine release in the nucleus accumbens of the rat. Behavioral Brain Research, 55, 131-141. 

FIGURE 53-1 Illustrative drawing of the temporal lobe system in the human brain. (A) Anatomical sites, marked by black dots, within the temporal lobe where electrical stimulation evoked experiential responses in Penfield s patients. (B) The location of the hippocampus and amygdala inside the temporal lobe. 

Halgren, E. Walter, R. D., Cherlow A. G. and Crandall, P. H. Mental phenomena evoked by electrical stimulation of the human hippocampal formation and amygdale. Brain 101 83-117,1978. 

The amygdala is perhaps the best-studied, and most strongly implicated, brain structure in anxiety and fear. Electrical stimulation of the amygdala produces fear-like behavioral and physiological responses in animals, and increases the suggestive experience of fear in human subjects. Additionally, amygdala stimulation leads to corticosterone secretion and HPA-axis activation in animals, probably via outputs to the hypothalamus and the bed nucleus of the stria terminalis. It has been suggested... 

The metabolism of norepinephrine is reported to be altered by other drugs used in the treatment of the affective disorders and a number of studies have shown a change in the metabolism of norepinephrine as a result of Li+ treatment. In rat brain, acute Li+ treatment enhances the uptake of norepinephrine in synaptosomes [151] and the enhanced turnover of this neurotransmitter may be due to an increase in its deamination in the brain, although Li+ also causes a slight increase in the levels of the amino acid precursor, tyrosine, in the brain and plasma of rats [152]. Also, acute Li+ treatment induces a decrease in the release of norepinephrine after electrical stimulation of rat brain [153]. Interest-... 

Katz, R. 1., and Kopin, 1. J. (1969) Effect of D-LSD and related compounds on release of norepinephrine-3H and serotonin-3H evoked from brain slices by electrical stimulation. Pharmacol. Res. Commun., 1 54-62. 

Olds, J. and Milner, P. (1954) Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. J. Comp. Physiol. Psychol. 47, 419-427. 

Pedata F, Pepeu G, Spignoli G. (1984). Biphasic effect of methyixanthines on acetylcholine release from electrically-stimulated brain slices. Br J Pharmacol. 83(1) 69-73. 

Segal M, Sandberg D. (1977). Analgesia produced by electrical stimulation of catecholamine nuclei in the rat brain. Brain Res. 123 369-72. 

---