Electrical Stimulation Of Frontal Cortex Research Articles

Role of presynaptic dopamine receptors in regulation of the glutamatergic neurotransmission in rat neostriatum

In experiments with the use of a push-pull cannula and simultaneous recording of electrical activity at the site of perfusion, the release of l-[ 3H]glutamic acid from rat neostriatum induced by K +-depolarization (60mM K + in perfusate) has been shown to be inhibited by replacing Ca 3+ in the perfusion medium by Co 2+. In contrast, release of l-[ 3H]glutamate induced by electrical stimulation of frontal cortex is enhanced by replacement of these cations. Application of dopamine (10 −5–10 −3 M), apomorphine (10 −4 M) or β-phenylethylamine (10 −3 M) as well as stimulation of the substantia nigra enhanced the basal release of l-[ 3H]glutamate. Haloperidol (10 −4 M) completely abolished the effects of apomorphine and β-phenylethylamine and partially abolished the effect of dopamine. The enhancement induced by apomorphine is strongly dependent on the presence of Na + in the perfusion medium. On the other hand, apomorphine (10 −4 M) and β-phenylethylamine (10 −3M) inhibited the release of glutamate induced by electrical stimulation of the frontal cortex and that by K +-depolarization (the latter was shown for apomorphine). This inhibition is also abolished by haloperidol. A possible functional role of endogenous dopamine in the regulation of glutamatergic neurotransmission in rat neostriatum is discussed.

Retrograde amnesia: Lack of attenuation with centrally administered adrenergic antagonists

Previous results indicate that pretraining peripheral injections of any of several adrenergic receptor antagonists can attenuate retrograde amnesia. The present experiment was an attempt to determine whether the attenuation of amnesia was due to peripheral or central actions of the adrenergic antagonists. This experiment examined the effects of intracerebroventricular (ICV) injections of these antagonists on the amnesia produced by supraseizure electrical stimulation of frontal cortex. Thirty minutes prior to training, rats received an ICV injection of an α-adrenergic (phenoxybenzamine, phentolamine, or piperoxane) or a β-adrenergic antagonist (propranolol) through a cannula in the lateral ventricle. After one-trial inhibitory (passive) avoidance training, the animals received stimulation of frontal cortex at an intensity that produces brain seizures and amnesia. The antagonists did not, in general, attenuate the amnesia produced by frontal cortex stimulation. One drug, propranolol, did attenuate the amnesia but this agent also impaired the brain seizure itself. Thus, the results suggest that adrenergic antagonists act to block the production of retrograde amnesia by interfering with peripheral aminergic responses to memory-impairing treatments.

Brain noradrenergic responses to training and to amnestic frontal cortex stimulation

Rats were trained in a one-trial inhibitory (passive) avoidance task prior to receiving supraseizure electrical stimulation of frontal cortex, a treatment that results in amnesia. Forebrain and brainstem norepinephrine (NE) concentrations decreased by 23% 10 min after footshock training. Posttraining frontal cortex stimulation resulted in a potentiation of the forebrain NE response (to 31–33% below control values) and in attenuation of the brainstem response (0–5% lower than control values). These results are consistent with previous findings that indicate that good retention performance is predicted by training and treatment conditions that result in approximately a 20% decrease in brain NE content as measured 10 min after training; deviations from this optimal level, presumably reflecting more or less NE release, predict poor retention in comparably trained and treated rats. Thus, memory storage processing appears to be sensitive to many manipulations that alter the endogenous posttraining brain NE response to footshock.

Extended retrograde amnesia gradients: Peripheral epinephrine and frontal cortex stimulation

This experiment examined the possibility that hormonal responses to training may increase the susceptibility of memory to an amnestic agent. As long as one week after training, rats that received a subcutaneous epinephrine injection shortly before electrical stimulation of frontal cortex exhibited amnesia on later retention tests. These findings suggest that retrograde amnesia gradients may reflect, in part, maximum susceptibility to amnesia shortly after training because the effects on memory of an amnestic agent are potentiated by the neuroendocrine response to training.

Electrophysiological correlates of frontal cortex-induced retrograde amnesia in rats

Experiment 1 investigated the electroencephalographic (EEG) changes occurring in rat cortex during afterdischarge activity elicited by electrical stimulation of frontal cortex. The EEG spike frequency of the primary afterdischarge (PAD) increased systematically with current level. Increases in current intensity, however, did not result in changes in the EEG spike frequency for the spontaneous secondary afterdischarge (SAD). Experiments 2 and 3 investigated the amnesic effects of frontal cortex stimulation. These experiments differed only in the motivational intensity of the aversive stimulus designed to produce an inhibitory avoidance response. The findings suggest that the degree to which abnormal brain activity interferes with memory storage processes is partially determined by the motivational intensity of the learning experience. That is, as the motivational intensity increases, the amount of frontal cortex stimulation (and concomitantly the degree of cellular dysfunction) must also increase in order to produce retrograde amnesia (RA).

Effects of stimulation of frontal cortex on neuronal activity in association and sensory areas of the cortex

Electrical stimulation of frontal cortex of anesthetized cat suppressed or abolished responses of polysensory cells in association cortex to subsequent peripheral stimuli. The same frontal shock train enhanced subsequent evoked activity of approximately half the cells studied in primary auditory and visual areas of the cortex.