Electrical stimulation of brain

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. 

The effects of DBS on the cortex-basal-ganglia-thalamus-cortex motor loop appear to be more complex than initially believed. The paradox of DBS is that electrical stimulation of brain tissue (which presumably induces brain activation), has a similar effect as that of a surgical lesion of that same structure (which effectively destroys brain tissue). These two realities are hard to reconcile. As indicated by [64] the ultimate elucidation of this paradox depends on the nature of the complex and interactive neural connections in the brain that communicate through electrical and chemical processes. There is an emerging view that DBS has both excitatory and inhibitory effects on how brain circuits communicate with one another depending on the distance from the electrode, the cell structures activated and the direction of the activation (ortho- versus anti-dromic). The effect appears to modulate the activity of a network as well as neural firing patterns. Long term effects on neurotransmitters and receptor systems cannot be excluded [64]. 

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. 

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. 

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-... 

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. 

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

Lamprea MR, Cardenas FP, Vianna DM, Castilho VM, Cruz-Morales SE, Brandao ML (2002) The distribution of fos immimoreactivity in rat brain following freezing and escape responses elicited by electrical stimulation of the inferior colliculus. Brain Res 950 186-194 Lechner HA, Squire LR, Byrne JH (1999) 100 years of consolidation—remembering Muller and Pilzecker. Learn Mem 6 77-87... 

We propose that the therapeutic efficacy of ECT may be related to activation of specific brain areas and the whole brain need not convulse for an antidepressant effect. It is possible that neural discharge in specific brain regions [Bolwig 1984], and not the convulsion, is the key factor for ECT s antide-pressive effects. External electrical stimulation as used for ECT may depolarize deep brain regions only by induction of convulsion. Local electrical brain stimulation in humans is not possible, of course ECT initiates massive discharge in the central nervous system [Lerer et al. 1984], and activation of no specific brain area has been proven to be the cause for ECT s therapeutic action. Local electrical stimulation of various brain regions for examination of antidepressive effect in animal models of depression would be a tedious and complicated task. 

Postictal inhibition has been demonstrated after bilateral ECS through ear-clip electrodes as well as after direct electrical stimulation of specific brain areas [for review, see Krauss and Fisher 1993]. TMS might exert anticonvulsive effects by stimulation of brain areas that are responsible for seizure inhibition. Alternatively, TMS might inhibit by direct inhibition of neural excitability in brain regions that are responsible for seizure initiation and spreading. Indeed, the TMS-induced decrease in postsynaptic action potentials hints that TMS might generate direct inhibitory mechanisms on neural excitability. 

In 1974, Liebeskind showed the existence of a central pain-suppressive system, and was able to produce analgesia by electrical stimulation of the periventricular gray matter within the brain. This electroanalgesia could be reversed by opiate antagonists, and showed a cross-tolerance with morphine-induced analgesia. These results indicated the existence of a neuronal system that uses an endogenous neuromodulator or neurotransmitter with opiate-like properties. 

Young, Shelly D., and Adrian C. Michael. 1993. "Voltammetry of Extracellular Dopamine in Rat Striatum During ICSS-Like Electrical Stimulation of the Medial Forcbrain Bundle." Brain Research 600 305-7. 

Luigi Rolando (1773-1831), Italian anatomist, achieves the first synthetic electrical stimulation of the brain. 

---