Enhancement of synaptic facilitation during the progression of kindling epilepsy by amygdala stimulations

1. A quantitative analysis of facilitation during the kindling stimulation to the amygdala was conducted by measuring the area between the excitatory potential and the baseline in the averaged tetanic response recorded at the entorhinal cortex. The changes in facilitation were then compared with the development of electrographic afterdischarges (AD) and behavioral seizures in response to successive kindling stimulations. 2. Kindling train pulses (n = 99 or 100; duration: 0.5 ms; frequency: 10 Hz; intensity: AD threshold) were applied to conscious rats until at least one generalized seizure occurred or until 13 stimuli were delivered. 3. Facilitation of the entorhinal responses by kindling stimulation first occurred in the monosynaptic excitatory component and was then followed by a progressive increase in the polysynaptic component that was manifested as the later negative peaks. A clear progressive enhancement was observed in the facilitation by successive kindling stimulations, which also induced prolongation of the AD duration and progression of the seizure stages, indicating that activity-dependent enhancement of facilitation (EF) occurred during the progression of kindling epilepsy. 4. Quantitative analysis revealed that the EF that occurred with the progression of seizure stages was statistically significant (P < 0.001, Friedman test). The AD duration (r = 0.89) and the long-term potentiation (r = 0.85) of the entorhinal responses by single test amygdala stimuli showed a very good linear relation to the EF.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses of the Smooth Muscle Membrane of Guinea Pig Jejunum Elicited by Field Stimulation

Field stimulation of the jejunum elicited successively an action potential of spike form, a slow excitatory depolarization, a slow inhibitory hyperpolarization, and a postinhibitory depolarization as a rebound excitation. The slow depolarization often triggered the spike. The inhibitory potential showed lower threshold than did the excitatory potential. Both the excitatory potentials were abolished by atropine and tetrodotoxin. Effective membrane resistance measured by the intracellular polarizing method was reduced during the peak of the excitatory potential, but the degree of reduction was smaller than that evoked by iontophoretic application of acetylcholine. Conditioning hyperpolarization of the muscle membrane modified the amplitude of the excitatory potential. The estimated reversal potential level for the excitatory potenialt was about 0 mv. No changes could be observed in the amplitude of the inhibitory potential when hyperpolarization was induced with intracellularly applied current. Low [K]o and [Ca]o blocked the generation of the excitatory potential but the amplitude of the inhibitory potential was enhanced in low [K]o. Low [Ca]o and high [Mg]o had no effect on the inhibitory potential.

The Effects of Meprobamate on Perception

There is no discussion in Stevens' (16) or Osgood's (14) textbooks of experimental psychology of the contribution of cortical functions to the production of visual after-images. Woodworth (19) presents a theory of after-images involving the cortex in the first edition of his book. It is not repeated in the second edition. There is, however, a large number of reported studies indicating the importance of cortical functions in the production of after-images (e.g. 1, 3, 6, 9, 11, 12, 13, 15, 17). In view of these studies it was decided to use the afterimage in a further attempt to verify or disprove the drug action hypothesis advanced by Eysenck in a previous paper (2). This hypothesis stated that stimulant drugs increased excitatory potential and decreased inhibitory potential, while depressant drugs decreased excitatory potential and increased inhibitory potential.

Drugs and Personality

It is a well-known principle in psychology that the effects of sensory stimulation do not cease when the stimulus itself ceases. The so-called visual after-images are probably the best known of these after-effects, but almost equally well known are those induced by a rotating spiral. If a normal person fixates the centre of the rotating spiral for a period of time, and if then the motion of this spiral is suddenly stopped, an after-sensation of movement is well nigh universal. This after-sensation is opposite to the original motion in direction, just as the after-image produced by the fixation of a colour is usually the complementary colour to that which caused the original perception. There is little doubt that while peripheral factors play some part in these after-effects, central features also play a part, and it becomes tempting, therefore, to use phenomena of this type in attempts to verify or disprove the drug action hypotheses advanced by one of us in a previous paper. This hypothesis stated that stimulant drugs increased excitatory potential and decreased inhibitory potential, while depressant drugs decreased excitatory potential and increased inhibitory potential. The question now arises as to how this general postulate can be applied to the phenomena under discussion.