Electricity as a medium of psychic life: electrotechnological adventures into psychodiagnosis in Weimar Germany.

When electricity became a commodity in 1900, it furnished Germany with new attractions and revolutionized everyday life with all kinds of tools and gadgets; it also opened up a new space for investigating psycho-physical interaction, reviving ideas of a close linkage between psychic life and electricity. The paper traces the emergence of this electro-psychological framework beyond "electroencephalography," the recording of electrical brain waves, to "diagnoscopy," personality profiling by electric phrenology. Diagnoscopy opens a window onto the scientific and public cultures of electricity and psychical processes in Weimar Germany. It garnered enormous attention in the press and was quickly taken up by several institutions for vocational guidance, because it offered a rapid and technological alternative to laborious psychological testing or "subjective" interviewing. Academic psychology and leading figures in brain research reacted with horror; forging counter measures which finally resulted in this technique being denounced as quackery. A few years later, the press celebrated electroencephalography as a mind-reading device, whereas the neuroscientists remained initially skeptical of its significance and the very possibility of an "electroencephalogram" (EEG) before they adapted electroencephalography as a tool for representing various neuro-psychiatric conditions in patterns of recorded signals. The blending of psychophysiology and electrical engineering marks the formation of an electric epistemology in scientific as well as public understanding of the psyche. The transformations of electrodiagnosis from diagnoscopy to the EEG are indicative of a cultural shift in which electricity changed its role from being the power source for experimental apparatuses to becoming a medium of psychic processes.

Seizure-like events in disinhibited ventral slices of adult rat hippocampus.

Epileptic discharges lasting 2-90 s, were studied in vitro in slices from the ventral hippocampus of adult rats, in which inhibition was blocked acutely with bicuculline methiodide (BMI, 5-30 microM) and potassium ([K(+)](o)) raised to 5 mM. These seizure-like events (SLEs) comprised three distinct phases, called here primary, secondary, and tertiary bursts. Primary bursts lasted 90-150 ms. Secondary bursts lasted a further 70-250 ms, comprising a short series of afterdischarges riding on the same depolarization as the primary burst. Finally a train of tertiary bursts started with a peak frequency of 5-10 Hz and could last >1 min. Slices from the ventral hippocampus showed significantly higher susceptibility to SLEs than did dorsal slices. SLEs proved sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonists. They were insensitive to N-methyl-D-aspartate (NMDA) receptor antagonists; 50 microl D-2-amino-5-phosphonopentanoic acid (D-AP5) did block the transient secondary bursts selectively. SLEs were restricted to the hippocampus proper even if the entorhinal cortex was present. Entorhinal bursts could last <2 s and were only coupled with hippocampal bursts in a minority of slices. Reentry of epileptic bursts occasionally occurred during interictal discharges, but not during the later stages of SLEs. Full-length SLEs always started in CA3 region and could be recorded in minislices containing CA3 plus dentate hilus. Ion-sensitive microelectrodes revealed that interictal discharges were followed by short (2-3 s) [K(+)](o) waves, peaking at approximately 7.5 mM. SLEs were always accompanied by increases in [K(+)](o) reaching approximately 8.5 mM at the start of tertiary bursts; [K(+)](o) then increased more slowly to a ceiling of 11-12 mM. After the end of each SLE, [K(+)](o) fell back to baseline within 10-15 s. SLEs were accompanied by significant increase in synaptic activity, compared with baseline and/or interictal activity, estimated by the variance of the intracellular signal in the absence of epileptic bursts and action potentials (0. 38 mV(2), compared with 0.13 mV(2), and 0.1 mV(2), respectively). No significant increases were observed in the interval preceding spontaneous interictal activity. These studies show that focal assemblies of hippocampal neurons, without long reentrant loops, are sufficient for the generation of SLEs. We propose that a key factor in the transition from interictal activity to SLEs is an increase in axonal and terminal excitability, resulting, at least in part, from elevations in [K(+)](o).

On the structure of ictal events in vitro.

PURPOSE: To analyze the cellular and network mechanisms of sustained seizures, we reviewed the literature and present new data on in vitro epileptiform events. We considered single and recurring synchronized population bursts occurring on a time scale from tens of milliseconds to 1 min. METHODS: We used intracellular and field potential recordings, together with computer network simulations, derived from three types of experimental epileptogenesis: gamma-aminobutyric-acidA (GABAA) blockade, low extracellular [Mg2+]o, and 4-aminopyridine (4-AP). RESULTS: In all three models, sustained depolarizing synaptic currents developed, either through N-methyl-D-aspartate (NMDA) receptors, depolarizing GABAA receptors, or both. Ectopic action potentials (APs), probably originating in axonal structures, occurred in 4-AP and (as shown by other researchers) after tetanic stimulation; ectopic APs, occurring at sufficient frequency, should also depolarize dendrites, by synaptic excitation, enough to trigger bursts. CONCLUSIONS: Ictal-like events appear to arise from two basic mechanisms. The first mechanism consists of sustained dendritic depolarization driving a series of dendritic bursts. The second mechanism consists of an increase in axonal and presynaptic terminal excitability driving a series of bursts analogous to interictal spikes.

Chronic focal epilepsy induced by intracerebral tetanus toxin.

A single, minute dose of tetanus toxin injected into mammalian cerebral cortex induces a chronic epileptic syndrome. Seizures lasting up to 3 minutes occur spontaneously and intermittently for several weeks to months. The cellular mechanisms of this model have been studied in detail using brain slices in vitro. Initially the release of the inhibitory neurotransmitter, GABA, is blocked, but after 2-4 weeks, other mechanisms take over. Intrahippocampal tetanus toxin models human complex partial seizures (temporal lobe epilepsy). It results in consistent behavioural changes analogous with those seen clinically, in spite of the limited neuronal loss found in only 10-30% of rats. Treatment with carbamazepine ameliorates both the seizures and their behavioural consequences. Tetanus toxin provides a versatile and long-lasting model of focal epilepsies.

The development of the myo-tendinous junction in the upper extremity of mouse embryos (days 15 p.c.--1 p.p.).

The development of the myo-tendinous junction in the upper extremity of mouse embryos of days 15 p.c. to 1 p.p. was studied electron microscopically. In the region of the myo-tendinous junction two cell types can be differentiated (muscle cells, fibroblasts) which undergo characteristic changes during the course of their development: The muscle cells show an increase in contractile material, the fibroblasts show a massive collagen production. The myo-tendinous junction is characterised by the appearance of four structures: 1. Irregular pattern of the plasma membrane resulting from intracellular membrane vesiculations in defined areas under the cell membrane on the longitudinal side as well as the end of the muscle fibre. These membrane vesiculations can break through to the cell membrane, thus leading to cell invaginations appearing in large amounts up to day 1 p.p. 2. Densifications of the plasma membrane towards the cell centre. 3. Insertion of the myofilaments of the muscle fibre at the desinfications of the plasma membrane (hemidesmosomes). 4. Insertion of collagen filaments in the extracellular space into the basement membrane which then also appears densified. The mechanical stress transmission seems therefore to be dependent upon the adhesion between myofibrils, plasma membrane, basement membrane and collagenous filaments.

[Electron microscopic study on blastema differentiation in the extremities of mice embryos to embryonic cartilage]. / Elektronenmikroskopische Untersuchungen an Mäuseembryonen über die Differenzierung des Blastems in den Extremitäten zum embryonalen Vorknorpel

Cartilage differentiation in the upper limb bud of the white mouse (NMRI) begins in the humerus anlage on day 12 + 13 h p.c.; cartilage differentiation in the phalanges begins on day 13 + 3 h p.c. Morphologically, differentiation can be characterized as follows: (1) cell densifications with an increase in contact structures between the cells in the blastema centre: (2) development of a two-layered cell densification: a central cartilage zone and a peripheral zone (perichondrium), between precartilage and prospective muscle anlage; numerous mitoses appear in this peripheral zone; (3) appearance of filaments and PG granula in the intercellular space as well as massive appearance of rough endoplasmic reticulum in the cytoplasm and, (4) increased distance between the cells coupled with the loss of specific contact structures and substance increase in the intercellular space.