Rapid detection of fear in body expressions, an ERP study.

Recent findings indicate that the perceptual processing of fearful expressions in the face can already be initiated around 100-120 ms after stimulus presentation, demonstrating that emotional information of a face can be encoded before the identity of the face is fully recognized. At present it is not clear whether fear signals from body expressions may be encoded equally as rapid. To answer this question we investigated the early temporal dynamics of perceiving fearful body expression by measuring EEG. Participants viewed images of whole body actions presented either in a neutral or a fearful version. We observed an early emotion effect on the P1 peak latency around 112 ms post stimulus onset hitherto only found for facial expressions. Also consistent with the majority of facial expression studies, the N170 component elicited by perceiving bodies proved not to be sensitive for the expressed fear. In line with previous work, its vertex positive counterpart, the VPP, did show a condition-specific influence for fearful body expression. Our results indicate that the information provided by fearful body expression is already encoded in the early stages of visual processing, and suggest that similar early processing mechanisms are involved in the perception of fear in faces and bodies.

[The cortico-thalamic theory for generalised spike-wave discharges]. / Kortikotalamicheskaia teoriia proiskhozhdeniia generalizovannykh pik-volnovykh razriadov.

The origin of generalized absence epilepsy is still not known. In the last century, four theories have dominated the debate about the origin of the bilateral synchronous generalized spike-wave discharges associated with absence seizures: the "centrencephalic" theory [Penfield and Jasper], the "cortical" [Bancaud, Niedermeyer, Luders], the "cortico-reticular" theory [Gloor, Kostop[oulos, Avoli] and the "thalamic clock" theory [Buzsaki]. There is now some evidence that absence epilepsy, as studied in the WAG/Rij model, is a corticothalamic type of epilepsy. A new hypothesis is proposed which suggests that a cortical focus in the somatosensory cortex is driving the widespread corticothalamic networks during spontaneous absence seizures. This modern theory was given the name "hot spot' theory" [Meeren et al., 2002]. According to the present view three brain structures are critically involved and their integrity seems a minimal and sufficient condition for the occurrence of spike-wave discharges. Firstly, the reticular thalamic nucleus is involved and most likely its rostral pole. Secondly, the thalamocortical relay cells in the ventrobasal complex play a role and, thirdly and most importantly, the cerebral cortex with its epileptic zone. The zone in which the epileptic focus seems to be localised is located on the somato-sensory cortex, and more precisely in the area on which the peri-oral region including the upper lip, projects.

Auditory evoked potentials from auditory cortex, medial geniculate nucleus, and inferior colliculus during sleep-wake states and spike-wave discharges in the WAG/Rij rat.

OBJECTIVE: Click auditory evoked potentials (AEP) were simultaneously recorded from the auditory cortex (ACx), the medial geniculate nucleus (MGN), and the inferior colliculus (IC) in the freely moving WAG/Rij rat, to investigate state-dependent changes of the AEP in different anatomical locations along the auditory pathway. METHODS: AEPs obtained during active (AW) and passive wakefulness (PW), slow wave sleep (SWS), rapid-eye-movement sleep (REM) and generalized spike-wave discharges (SWD; a specific trait of the WAG/Rij rat, a genetic model for absence epilepsy), were compared. RESULTS: The early components in ACx, MGN and IC were stable throughout the sleep-wake cycle and SWD, apart from a slight increase in the IC during SWD. At all three locations a prominent enlargement of a later component (i.e., N32 in IC, N33 in MGN, and N44 in ACx) was found during SWS and SWD. CONCLUSIONS: The early AEP components are not modulated by the normal sleep-wake states, and are not impaired during SWD. A strong state-dependent modulation of a later AEP component occurs at all three anatomical locations investigated. This suggests that apart from the thalamic burst firing mode, additional mechanisms must exist for the enlargement of the AEP during EEG-synchronized states at the prethalamic and cortical level.

Magnetic source imaging in fixation-off sensitivity: relationship with alpha rhythm.

A patient in whom a variety of abnormal EEG findings can be elicited by elimination of central vision and fixation demonstrates fixation-off sensitivity. The underlying mechanisms of fixation-off sensitivity and its relationship with alpha rhythm remain unclear. To obtain a better understanding of this issue, we used a whole-head magnetoencephalograph to study an epileptic child with fixation-off sensitivity resulting in a 3-Hz, large-amplitude oscillation (300 microV) over the occipital regions on the EEG. Magnetic source localization revealed alpha activity around the calcarine fissure and surrounding parieto-occipital areas. Magnetic sources of abnormalities relating to fixation-off sensitivity, however, usually were located deeper in the brain, suggesting more extensively distributed sources, with involvement of the cingulate gyrus and the basomesial occipitotemporal region. Distributions of the sources of both types of activities show independent clusters but also an appreciable domain of overlap. Our findings indicate that abnormalities related to fixation-off sensitivity can emerge in thalamocortical networks, with larger and more anterior cortical distribution than those that generate alpha rhythm. Transition in the type of oscillation appears not only to depend on a change in cellular dynamics but also to be reflected in a different spatial distribution of the underlying neuronal networks.

Local morphine withdrawal increases c-fos gene, Fos protein, and oxytocin gene expression in hypothalamic magnocellular neurosecretory cells.

We measured stimulation of c-fos and oxytocin gene expression during excitation of oxytocin cells induced by systemic or local morphine withdrawal. Female rats were made morphine-dependent by intracerebroventricular morphine infusion over 5 d. Morphine withdrawal, induced by systemic injection of the opioid antagonist naloxone (5 mg/kg) in conscious or anesthetized rats, increased the density of c-fos messenger RNA and of oxytocin heterogeneous nuclear RNA in supraoptic nucleus cells compared with those of nonwithdrawn rats; c-fos messenger RNA was also increased in the magnocellular and parvocellular paraventricular nuclei of withdrawn rats. Morphine withdrawal increased the number of Fos-immunoreactive cells in the supraoptic and magnocellular paraventricular nuclei of conscious or pentobarbitone-anesthetized rats. Morphine withdrawal also increased Fos-immunoreactive cell numbers in the parvocellular paraventricular nucleus of conscious but not anesthetized rats. Central administration of the alpha(1)-adrenoreceptor antagonist benoxathian (5 microg/min) did not prevent morphine withdrawal-induced increases in the numbers of Fos-immunoreactive neurons in the supraoptic or magnocellular paraventricular nucleus. Unilateral microdialysis administration of naloxone (10(-5) M) into the supraoptic nucleus of anesthetized morphine-dependent rats increased Fos-immunoreactive cell numbers compared with the contralateral nucleus. Finally, we investigated whether dependence could be induced by chronic unilateral infusion of morphine into a supraoptic nucleus; systemic naloxone (5 mg/kg) increased Fos-immunoreactive cell numbers in the morphine-infused nucleus compared with the contralateral nucleus. Thus, morphine withdrawal excitation increases c-fos and oxytocin gene expression in supraoptic nucleus neurons. This occurs independently from excitation of their ascending noradrenergic inputs, and both dependence and withdrawal can be induced within the supraoptic nucleus.

Cortical and thalamic visual evoked potentials during sleep-wake states and spike-wave discharges in the rat.

Flash visual evoked potentials (VEP) were simultaneously recorded from the primary visual cortex and the dorsal lateral geniculate nucleus in freely-moving WAG/Rij rats, to investigate whether the thalamic VEP shows the same state-dependent alterations as the cortical VEP. VEPs obtained during active and passive wakefulness (AW and PW), slow-wave sleep (SWS), REM sleep and during the occurrence of spike-wave discharges (SWD), a specific trait of the genetically epileptic WAG/Rij rat, were compared. The general architecture of the thalamic VEP resembles the cortical VEP, although its polarity is reversed. This facilitated the interpretation of components in terms of underlying neuronal events. The primary excitation peak is differently modulated in cortex and thalamus. Whereas the thalamic component (P30) is not affected by brain-state, the cortical component (N1) shows a strong increase in latency during SWS and SWD. In contrast, the modulation of later components is highly similar for cortex and thalamus. VEPs obtained during AW and REM resemble each other. During SWS and SWD there is a considerable, and during PW a moderate, enlargement of primarily inhibitory components. After-discharges are enhanced during SWS, SWD and REM. No evidence is found for a major impairment of sensory transmission during SWD.

Stimulation of expression of the oxytocin gene in rat supraoptic neurons at parturition.

We measured expression of the oxytocin gene in the supraoptic nucleus (SON) during pregnancy, parturition and lactation to examine its relationship to states of accumulation or depletion of oxytocin stores and to conditions of strong excitation of oxytocin neurons. The primary transcript (heterogeneous nuclear RNA, hnRNA) of the oxytocin gene was measured using a 3H-cDNA probe against intron 1 for in situ hybridisation. Autoradiographs of the SON showed the hnRNA as discrete clumps of silver grains within the nucleus of each neuron. The number of cells expressing oxytocin hnRNA did not change during pregnancy but increased during parturition; 10-day lactating animals showed similar increases. Oxytocin mRNA was also measured by in situ hybridisation using a 3H- or 35S-labelled oligonucleotide probe against exon C: hybridisation was seen over the cytoplasm of supraoptic neurons, but no differences were measured between virgin, mid-pregnant, preparturient, parturient or 2-day lactating rats. The data suggest that enhanced oxytocin gene transcription is not necessary to increase oxytocin stores in pregnancy. However, acute stimulation of magnocellular oxytocin neurons at parturition, which strongly increases neuron activity and secretion, results in a rapid increase in the number of cells expressing oxytocin hnRNA, and increased expression is sustained in lactation.

Central endogenous opioid inhibition of supraoptic oxytocin neurons in pregnant rats.

Naloxone increases oxytocin secretion in pregnant rats, suggesting restraint by endogenous opioids but we have previously reported that oxytocin nerve terminals in the neural lobe become desensitized to opioid actions in late pregnancy. Therefore, we sought evidence for opioid inhibition on oxytocin cell bodies and their inputs at this time. In conscious 21 d pregnant rats naloxone increased the number of neurons expressing Fos (an indicator of neuronal activity) in the supraoptic nucleus (SON) but had no effect on 16 d pregnant or virgin rats. Release of oxytocin within the SON, measured by microdialysis in conscious rats, was also increased by naloxone in late pregnancy but not before. Nor-binaltorphimine, a specific kappa- opioid antagonist, did not increase Fos or affect oxytocin release within the SON in any group. In anesthetized rats the firing rate of SON neurons was recorded and oxytocin neurons identified by an excitatory response to intravenous cholecystokinin. Naloxone potentiated the cholecystokinin-induced firing rate response on day 21 of pregnancy but not in 16 d pregnant or virgin rats. Blood sampling in anesthetized rats showed that naloxone also increased the oxytocin secretory response to cholecystokinin in late pregnant rats. We conclude that in late pregnancy, after day 16, endogenous opioids inhibit oxytocin neurons either directly, on their cell bodies, or presynaptically on inputs. These endogenous opioids do not act through kappa- opioid receptors since nor-binaltorphimine was ineffective, but may act via mu-opioid receptors. Thus, the opioids restrain premature oxytocin secretion until parturition when there is a high demand for it.