Hippocampal Spike Research Articles

Subcortical EEG changes in rhesus monkeys following experimental hyperextension-hyperflexion (whiplash).

A controlled study, involving EEG recordings from the scalp and chronically implanted electrodes in the cortex (ECoG), as well as from selected subcortical nuclei, was undertaken to investigate the neurophysiologic effects on rhesus monkeys following experimental whiplash (hyperextension of the head and neck). Sixteen animals, equally divided into four groups, were studied through the following protocol: (1) two animals within each group were whiplashed and then electrodes were implanted into the brain of one; (2) the second two animals were implanted with deep electrodes and then one was whiplashed. Weekly EEG follow-ups showed hippocampal spiking in three of the four whiplashed and then electrode-implanted animals and in one of implanted and then whiplashed animals 6 to 8 weeks postwhiplash. Several results deserve attention. (1) The "whiplash syndrome" owes part of its symptoms to EEG disturbances in the brain. (2) Prior to the onset of spiking, ie, 6 to 8 weeks postwhiplash, practically all scalp, cortical, and subcortical EEG recordings were normal. (3) When hippocampal EEG spiking did take place, only normal and mildly abnormal changes were seen in either the electrocorticogram (ECoG) or scalp electroencephalogram (EEG). (4) The growth and development of this trauma-induced hippocampal spiking followed the classic sequence for the spread of an epileptogenic focus. (5) This apparent subclinical form of posttraumatic epilepsy may be due to the combined effects of the whiplash plus the subcortical electrode placements further decreasing the already well-known, low-spiking threshold of the hippocampi.

Ephaptic interactions contribute to paired pulse and frequency potentiation of hippocampal field potentials

The contribution of ephaptic interactions to potentiation of the hippocampal CA1 extracellular population spike during paired pulse or frequency stimulation of stratum radiatum (SR) inputs was investigated using the in vitro hippocampal slice preparation. Records of the transmembrane potential revealed a depolarizing wave with an amplitude and latency that varied directly with that of the extracellular population spike. Paired pulse or repetitive stimulation of SR resulted in a potentiation of the population spike amplitude and a corresponding increase in the amplitude of the TMP depolarizing wave. Action potentials generated during the stimulus train consistently arose from the peak of the depolarizing wave. It is proposed that ephaptic interactions contribute to potentiation of the extracellular population spike through recruitment of subthreshold neurons within the population during repetitive afferent stimulation.

Verapamil counteracts the masking of long-lasting potentiation of hippocampal population spike produced by 2-amino-5-phosphonovalerate.

In transversely sectioned rat hippocampal slices the effects of 2-amino-5-phosphonovalerate (APV), presumably a selective N-methyl-DL-aspartate antagonist, were examined on the development of long-lasting potentiation (LLP) of the CA1 population spike produced by Schaffer collateral tetanization (100 Hz, 1 s). APF (100 nA, 5 min), when applied 150-200 micron away from the CA1 cell bodies (apical dendritic area), had no significant effect if the population spike was evoked at 0.1 Hz, but produced a depression of the population spike if a 100 Hz tetanus was given during its iontophoresis. This depressant effect of APV was counteracted by verapamil (0.33 microM, 3 min) and LLP induced by the 100 Hz tetanus was unmasked. It is suggested that APV does not antagonize LLP, but only masks it by allowing CA++ influx into CA1 neurones that induces a depression. The results also raise doubts as to the selectivity of APV as an amino acid antagonist.

Centrally administered N-terminal fragments of ACTH (1–10, 4–10, 4–9) display convulsant properties in rabbits

Electroencephalographic and behavioral effects of the following ACTH fragments: 1–4, 4–9, 4–11, 1–10, 4–10, 1–13, 1–17 and 1–24 were studied in rabbits. Sequences 4–9, 1–10 and 4–10 displayed some epileptic properties, i.e., they induced epileptic seizures (only electrographic or also behavioral) or increased hippocampal spiking. The 4–9 sequence seemed to be the common sequence responsible for these proconvulsant effects. The possible involvement of the enkephalinergic system is discussed.

The effect of amphetamine, nembutal, alpha-methyl-tyrosine, and parachlorophenylalanine on the sleep-related spike activity of the tortoise, Geochelone carbonaria, and on the cat ventral hippocampus spike.

The effect of amphetamine, nembutal, alpha-methyl-tyrosine, and parachlorophenylalanine on the sleep-related spike activity of the tortoise, Geochelone carbonaria, and on the cat ventral hippocampus spike.

Alcohol-related electrophysiology

Considerable effort has been expended to determine the electrophysiological actions of ethanol (EtOH) on nervous tissue. However, the site and mechanisms of EtOH intoxication, tolerance and dependence remain largely unknown. We and our co-workers have used two central mammalian models to clarify these problems: the rat cerebellar Purkinje cell (CPC) and the rat hippocampal pyramidal cell (HPC). Direct application of EtOH to CPCs via micro-electroosmosis or micropressure depresses spontaneous discharge weakly, while tetrahydropapaveroline (THP) depresses firing markedly. Single IP injections of EtOH (1–4 g/kg) increase the frequency of climbing-fiber (CF)-evoked bursts in CPCs but only occasionally increase simple-spike rates. However, CPCs of rats chronically treated with EtOH for 11–14 days and recorded 0–3 hrs after the last EtOH dose do not differ from controls. Rats chronically treated and then withdrawn from EtOH show significant decreases in CF activity and simple-spike rates 3–32 hrs after the last EtOH dose. These changes in CPC firing may be neuronal correlates of EtOH intoxication, tolerance and dependence. In the hippocampus, with direct application of EtOH to HPCs in vivo about half of the cells are excited and half inhibited. Salsolinol excites most HPCs, in parallel with opiate actions. THP is mostly inhibitory. EtOH and salsolinol excitatory effects are often antagonized by naloxone. With intracellular recording in the hippocampal slice, EtOH perfusion (10–400 mM) has mixed de-polarizing/hyperpolarizing actions, depending on dose and time of application. Excitations may arise from depolarization, increase in membrane resistance, enhancement of evoked EPSPs or block of IPSPs, in contrast to opiate actions which are always associated with reduction in IPSPs. In vivo, systemic EtOH (3 g/kg, IP) significantly enhances both excitatory and inhibitory responses to stimulation of afferent pathways to HPCs. The excitatory EtOH actions on HPCs may relate to the hippocampal EEG spiking sometimes elicited by low doses of EtOH. However, further studies are needed to verify a link with opiate-like mechanisms.

Electrophysiological semeiology of sleep

The main characteristics of electroencephalograms, electro-oculograms and electromyograms in human sleep are described. This electrophysiological semeiology permits the identification of the different stages in normal sleep. In animals, sleep is generally less differentiated; the possibility of recording subcortical structures allows the observation of additional phenomena such as hippocampal theta activity and PGO spikes. Evoked brain electrical activity is less well known than the spontaneous activity in sleep. Recent technological developments offer many interesting possibilities in the processing of the EEG and other physiological signals.

Effects of sleep deprivation on sleepiness, sleep intensity, and subsequent sleep in the rat.

The effects of 24 hr of sleep deprivation on cortical EEG and ventral hippocampus EEG recordings, ventral hippocampus spike rates, sleep stages percentages, and bout length measures were studied in rats. Two groups, differing only in the rate and distance they were forced to walk during deprivation by the water wheel method, were recorded continuously (23 hr per day) for one baseline, one deprivation, and two recovery days. During deprivation, microsleeps, increased hippocampal spike rates, and increased amplitude of the EEG recordings all suggested the intrusion of sleep processes. Nonetheless, there was no evidence to support the idea that these animals were not substantially deprived of sleep. No important differences were found in the recovery data of the two groups, even though one group walked three times as far as the other during deprivation. This supports the idea that, in conjunction with large amounts of sleep deprivation, changes in exercise and energy depletion may have little effect on sleep measures. During recovery, increased hippocampal spike rates and bout lengths, as well as increases in EEG amplitude, were interpreted in terms of increased sleep "intensity." High amplitude NREM sleep rebounded first, followed by rebounds in both paradoxical sleep and low amplitude NREM sleep. This pattern was compared to patterns previously reported for humans, cats, and rats. Finally, the tendency for some measures to fall below their baseline levels after an initial rebound was discussed in terms of "sleep inhibition" and servomechanism theory.

Electrographic and behavioral study of convulsants in the cat.

Electrical activity from six sites in the cat brain was monitored before and after systemic and intracerebral administration of graded doses of local anesthetics, pentylenetetrazol and morphine, and correlated with behavioral changes. Results suggest that the amygdaler hypersynchronous fast-ware response evoked by convulsant doses of local anesthetics is due to a lowering of this site's threshold to olfactory inputs. Intracerebral infusion of butacaine into the ventral hippocampus elicited electrographic pattern changes very similar to that induced by systemic administration of local anesthetics. Infusion of pentylenetetrazol into the mesencephalic reticular formation elicited an overall, attenuated electrographic pattern almost identical to that induced by systemic administration of this drug. Morphine given in excitant dosages subcutaneously elicited isolated hippo-campal spiking; the hippocampus also had the lowest threshold to this drug of three sites infused.

Effect of drugs on the spike complication of hippocampal field potentials

Drugs were applied to the alvear surface of the dorsal hippocampus with pieces of filter paper soaked in suitable solutions, and their effect on the hippocampal spike complication was examined. The size of the spike complication, for a given stimulus strength, was decreased by procaine and tetrodotoxin, and increased by aconitine. When stimuli below threshold for the spike complication were used, a short number of pulses at a 10 per sec rate caused this potential to appear; this number of pulses was increased by procaine, tetrodotoxin and tetraethylammonium, and decreased by aconitine and veratrine. These results suggest that spike complications are the envelopes of Na + spikes, and that an accumulation of extracellular K + favors their appearance.

Effect of barbiturate sleep on the electrical activity of the hippocampus of patients with temporal lobe epilepsy: A preliminary report

Electroencephalograms and direct records from the temporal, central, frontal and hippocampal surfaces of three patients with temporal lobe epilepsy are presented. Light sleep and drowsiness induced by Evipan resulted in sinusoidal slow rhythms of the hippocampus most pronounced during waking up from anaesthesia. This hippocampal synchronization showed some similarity to the hippocampal “arousal reaction” described in animals; it displayed a contrast with the simultaneous desynchronization of neocortical regions. Hippocampal spike discharges could be intensely activated by light sleep and drowsiness during waking up. Awakening caused by strong peripheral stimulation proved to be more effective than spontaneous lightening of anaesthesia. An inverse relation between sleep activation of hippocampal discharges and of temporal neocortical spikes was observed in a case with sclerosis of Ammon's horn. Background irregular or rhythmic slow waves, as well as spike discharges in hippocampus, were abolished by deep sleep.