Transcranial magnetic stimulation (TMS) is an increasingly common technique used to selectively modify neural processing. However, application of TMS is limited by uncertainty concerning its physiological effects. We applied TMS to the cat visual cortex and evaluated the neural and hemodynamic consequences. Short TMS pulse trains elicited initial activation (approximately 1 minute) and prolonged suppression (5 to 10 minutes) of neural responses. Furthermore, TMS disrupted the temporal structure of activity by altering phase relationships between neural signals. Despite the complexity of this response, neural changes were faithfully reflected in hemodynamic signals; quantitative coupling was present over a range of stimulation parameters. These results demonstrate long-lasting neural responses to TMS and support the use of hemodynamic-based neuroimaging to effectively monitor these changes over time.

The response of a neuron in striate cortex to an optimally oriented stimulus is suppressed by a superimposed orthogonal stimulus. The neural mechanism underlying this cross-orientation suppression (COS) may arise from intracortical or subcortical processes or from both. Recent studies of the temporal frequency and adaptation properties of COS suggest that depression at thalamo-cortical synapses may be the principal mechanism. To examine the possible role of synaptic depression in relation to COS, we measured the recovery time course of COS. We find it too rapid to be explained by synaptic depression. We also studied potential subcortical processes by measuring single cell contrast response functions for a population of LGN neurons. In general, contrast saturation is a consistent property of LGN neurons. Combined with rectifying nonlinearities in the LGN and spike threshold nonlinearities in visual cortex, contrast saturation in the LGN can account for most of the COS that is observed in the visual cortex.

. Cross-orientation suppression: monoptic and dichoptic mechanisms are different. J Neurophysiol 94: 1645-1650, 2005. First published April 20, 2005 doi:10.1152/jn.00203.2005. The response of a cell in the primary visual cortex to an optimally oriented grating is suppressed by a superimposed orthogonal grating. This cross-orientation suppression (COS) is exhibited when the orthogonal and optimal stimuli are presented to the same eye (monoptically) or to different eyes (dichoptically). A recent study suggested that monoptic COS arises from subcortical processes; however, the mechanisms underlying dichoptic COS were not addressed. We have compared the temporal frequency tuning and stimulus adaptation properties of monoptic and dichoptic COS. We found that dichoptic COS is best elicited with lower temporal frequencies and is substantially reduced after prolonged adaptation to a mask grating. In contrast, monoptic COS is more pronounced with mask gratings at much higher temporal frequencies and is less prone to stimulus adaptation. These results suggest that monoptic COS is mediated by subcortical mechanisms, whereas intracortical inhibition is the mechanism for dichoptic COS.

Summary: Purpose: Single and repeated hyperthermic seizures were induced in rats beginning at age 22 days to determine the neuroanatomic consequences to the hippocampus and to compare these changes with those in the hippocampi of patients with temporal lobe epilepsy (TLE) experiencing febrile seizures.Methods: Hyperthermic seizures were induced by placing rats in a bath of water at 45°C for 4 min. Seizures were visually observed, and some animals also were monitored electroencephalographically. Neurodegeneration was examined with a silver stain, whereas granule cell sprouting was detected with the Timm stain.Results: In a majority of rats, hyperthermia-induced tonicclonic seizures ranged in duration from 30 s to 6 min; the seizure duration increased with the number of seizures. No neurodegeneration was detectable in these animals, although there was sprouting of granule cell collaterals into the inner molecular layer (IML) of the dentate. In a small number of animals, the short seizures evolved into status epilepticus, and neuronal degeneration was present in the hippocampus and other parts of the temporal lobe, and the mediodorsal thalamus.Conclusions: This study confirms the relation between hyperthermia and seizure occurrence. It shows in particular that, as in the human, only prolonged seizures such as status epilepticus cause a pattern of neurodegeneration similar to that observed in human TLE. Key Words: Epilepsy- Hippocampus-Neurodegeneration-Sprouting-Status epilepticus.The possibility that febrile convulsions in early childhood (younger than 5 years) are an etiologic factor in human temporal lobe epilepsy has been proposed by many investigators (1,2). In particular, children with complicated, prolonged febrile convulsions or status epilepticus are thought to develop complex partial seizures (3-6) in later life. A possible neurologic consequence of febrile seizures in patients that later develop recurrent complex partial seizures is Ammon's horn sclerosis, sometimes also referred to as hippocampal sclerosis (7) or mesial temporal sclerosis (8). In the series of temporal lobe resections from patients with medically refractory temporal lobe epilepsy (TLE), a significant proportion of hippocampi showing these neuropathologic conditions are from patients with a history of febrile convulsions ($9-11). The study of Kim et al. (10; and unpublished data) further shows that those patients with a history of febrile convulsions also had more severe hippocampal neuronal loss than did those without.The hippocampi from patients with hippocampal scle- rosis show, in addition to neuronal loss and gliosis, other anatomic changes as well. Staining with the histochemical Timm stain or immunocytochemical staining for dynorphin reveals a band of stain corresponding to the inner molecular layer (IML) of the dentate. This band of staining is thought to be recurrent collateral sprouts from granule cell mossy fiber axons (12-15). Additionally, a series of reorganizational features involving neurotransmitters, receptors, secon...

Adaptation to a high-contrast grating stimulus causes reduced sensitivity to subsequent presentation of a visual stimulus with similar spatial characteristics. This behavioral finding has been attributed by neurophysiological studies to processes within the visual cortex. However, some evidence indicates that contrast adaptation phenomena are also found in early visual pathways. Adaptation effects have been reported in retina and lateral geniculation nucleus (LGN). It is possible that these early pathways could be the physiological origin of the cortical adaptation effect. To study this, we recorded from single neurons in the cat's LGN. We find that contrast adaptation in the LGN, unlike that in the visual cortex, is not spatial frequency specific, i.e., adaptation effects apply to a broad range of spatial frequencies. In addition, aside from the amplitude attenuation, the shape of spatial frequency tuning curves of LGN cells is not affected by contrast adaptation. Again, these findings are unlike those found for cells in the visual cortex. Together, these results demonstrate that pattern specific contrast adaptation is a cortical process.