models are used to study the genesis of epilepsy and on the other they are used to study changes in prolonged events. the question arises, therefore, of whether the resulting data of the models indicated an exaggerated defect responsible for the genesis of seizures or whether the data indicated systemic changes to normal tissue after prolonged seizure activity. calcium currents, normally prominent in ca1 hippocampal neurons are increased in response to status epilepticus. there is evidence that current in t-type calcium channels is increased specifically in apical dendrites. the hypothesis is that this phenomenon creates a situation in which fast sodium spikes in the soma back-propagate into the dendrites, whereby they detonate bursting. dendritic potentials (dps) also undergo changes. elicitation of dps during seizure activity showed that they were much smaller than controls. however, dps elicited just after seizure termination lasted for longer periods, indicating that suppression of the dp is correlated with the seizure activity itself. glutamate is an excitatory neurotransmitter capable of causing a metabolic injury to neurons. in the hippocampus, gabaergic neurons have been found vulnerable to excitotoxic action of glutamate at the kainate receptor. these receptors are most dense in sectors ca3 and ca2 of the hippocampus, where nanomolar (nm) concentrations of kainic acid have been associated with pronounced and persistent depolarization of ca3 pyramidal neurons. this involving the conduction of excitatory activity along the mossy fiber projections from the area dentate granule cells to the ca3 neurons. stimulation of this receptor type has been associated with paroxysmal spikes similar to seizures. plasticity in ca1 pyramidal cells and interneurons has been related to ca1 roles in epileptogenesis. ca1 is hyperexcitable when the ca3 region is damaged. reduction of both gabaa and gabab ipsps occurs. gaba interneurons, though intact, become less easily activated. seizure input from the ec to the dentate gyrus is filtered for both ictal and normal activity patterns, while ca3 cells impose an inter-ictal profile, reinforcing abnormal activity. hyperventilation leads to a marked surface negative direct current shift due to depolarization of the apical dendritic trees of the cortical pyramidal cells. this shift is likely to represent the increased excitability of the cortical neuronal networks and may explain the resultant potential epileptogenicity. certain anti-epileptic drugs have the opposing effect of reducing surface negativity in normal controls. temporal lobe epilepsy changes in expression of potassium channels and of potassium currents have been described in a model of temporal lobe epilepsy. in this model, there is downregulation of the a-type encoding kv4.2 channel. this channel is involved in limiting backpropagation of action potentials and in reducing the transfer of excitatory postsynaptic potentials (epsps) from apical dendrites into the soma. in the same model, the aforementioned upregulation of t-type calcium channels also has been shown to result in increased burst behavior in neurons in the hippocampus. infantile seizures and associated memory impairment neuronal death does not appear to contribute to the learning deficits in rats with infant seizures. ca3 neurons in the tetanus toxin model of early onset epilepsy, however, show a reduction in the branching complexity of basal dendrites as well as a decrease in the spine density on both the apical dendrites and the basal dendrites. similar data have been taken from epileptic human patients during surgical procedures. in neocortical and hippocampal foci, a decrease in length and branching complexity of dendritic arbors and a reduction in the branching complexity of the remaining dendrites were observed. the chronic alumina cream model of epilepsy in primates has produced similar data. because dendrites and their spines are sites of excitatory synaptic input onto neurons, the results suggest that the glutaminergic synaptic transmission may be reduced. as these are sites active in long-term potentiation (ltp) and other alterations in synaptic transmission that underlie learning and memory, changes at these sites could explain learning and memory deficits associated with both early-onset and long-term epilepsy. schizophrenia in individuals with schizophrenia, post-mortem analysis has indicated a decrease of gabaergic cells and activity in the hippocampus. human neocortical heterotopia heterotopia is the displacement of any organ or component thereof from its natural position. rat models of telencephalic internal structural heterotopia are used as a model for human neocortical heterotopia. in these models, the apical dendrites of the pyramidal neurons are not consistently radially oriented and may even be inverted. additionally, the dendrites near the edge of the heterotopic region often bend and follow the contour of the band. methods of studying effects the following list is adapted from lothman, et al. in-vivo imaging magnetic resonance imaging (mri) computerized tomography (ct) positron emission tomography (pet) film autoradiography single photon emission computerized tomography (spect) surface, subdural, and depth electroencephalography magnetoencephalography evoked potentials focal electrical stimulation afterdischarges physiological, psychological responses to stimulation single unit recording in-vitro physiology slices in-vitro imaging: standard light and electron microscopy histochemistry immunocytochemistry receptor autoradiography lesions destructive reversible cryolesions pharmacological seizure changes two methods are studying the relationship between seizures and dendritic impairment: seizures activate stress mechanisms including the excitatory neuropeptide corticotropin-releasing hormone (crh) from hippocampal neurons. crh has been shown to interfere with dendritic growth and differentiation. mice lacking this receptor possess exuberant dendritic trees. however, pyramidal cells exposed to crh during the first week of life had atrophied dendrites. these stress-related changes reduced synaptic plasticity and caused learning and memory deficits later in life. as antagonists for crh exist, there exists a potential to reverse or prevent these effects through pharmacological means. studies of recurrent febrile seizures have shown that seizures resulted in impaired learning and memory but also disrupted signaling that normally results in activation of camp response element binding factor (creb), a transcription factor. for rats tested in the inhibitory avoidance learning paradigm, normally an activation of creb occurs by phosphorylation at ser133. this activation is impaired following recurrent febrile seizures. a seizure-induced modification of a signaling cascade upstream of creb is suggested by this. adult rats with infant febrile seizures were treated with rolipram, a specific phosphodiesterase type iv inhibitor (pde4 inhibitor), which resultes in the activation of protein kinase a (pka) and is known to activate creb by the mitogen-activated protein kinase (mapk) pathway. rolipram treatment reversed the learning deficits in rats that had experienced recurrent febrile seizures. optical monitoring recording the activity of a single neuron at any given time at many locations in the dendritic tree has been accomplished using voltage-sensitive dyes with optical monitoring. signals are rapid but also small, and measurements from single cells require intense illumination. as the dyes are very phototoxic, the cells usually die after only a few action potentials. however, measurements from both somatic and dendritic patch recordings show that the peak membrane potential deflection during a paroxysmal depolarizing shift (pds) is 10mv greater in the apical trunk (supragranular location) than the soma. this is consistent with the anatomy of neocortical networks because the most powerful reciprocal layer connections are in supragranular layers 2 and 3. this may resolve the conflicting information suggesting that the activity spreads primarily at the supragranular layers or at the large layer 5 neurons. conventional studies with electron microscopy or golgi stains portrayed dendrites as stable structures. however, time-lapsed photography and two-photon microscopy have revealed dendrites as living, constantly changing tissues which are motile on a rapid time scale. electroencephalogram electroencephalogram (eeg) scalp signals are summed epsps and ipsps of nerve cells. eeg can only measure the potentials of cells arranged in organized layers and whose apical dendrites are oriented perpendicularly to the surface of the cortex (as they are in pyramidal cells). the potential measured by the eeg is the difference between the basal and apical parts of the active neurons that are oriented in such a way. the epsps that converge on the pyramidal neurons through direct afferent fibers ending in the upper part of the apical dendrites cause a flow of charged ions (a current) between points at different potentials within and outside neurons. the positive ions then enter the cell following concentration and electrical charge gradient and propagate to the rest of the neuron. epsps from the distal apical dendrites create a current starting from the apical part nearest to the synapse (where the magnitude is greater) toward the cell body because the resistance to this flow is less. the current perpendicular (or radial) to the apical dendrite is accompanied by a magnetic field that propagates orthogonally (or tangentially) to the current along the extracellular side of the cell membrane. this set of ionic and electrical functional alterations thus generates the fields of electromagnetic potentials or electromagnetic dipoles. these can be defined also as single equivalent dipoles.