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We studied the mechanisms of the antioxidant activity of a tryptamine derivative of securinine (TDS) and its influence on the dynamics of seizure activity in various models of experimental epilepsy. We found that the new TDS, which possesses an antioxidant and a chelating effect, has anticonvulsant action in lithium-pilocarpine-induced epilepsy and may be of interest as a potential scaffold for the development of new neuroprotective anticonvulsant drugs.

Pharmacology of Korean Red ginseng gives us unique possibility to develop new class of antiepileptic drugs today and to improve one’s biological activity. The chemical structures of ginsenosides (GS) have some principal differences from well-known antiepileptic new generation drugs. The antiepileptic effect of GS was also demonstrated in all models of epilepsy in rats (young and adult), which have studied, in all models of epilepsy including status epilepticus (SE), induced by lithium - pilocarpine. In our experiments in rats new evidences on protective effects were exerted as a result of premedication by GS. Pre-treatment of several GS could induce decrease of the seizures severity and brain structural damage (by MRI), neuronal degeneration in hippocampus. Wave nature of severity of motor seizures during convulsive SE was observed during lithium-pilocarpine model of SE in rats (the first increase of seizures was 30 min after the beginning of SE and the second - 90 min after. The efficacy of treatment on SE by ginsenoside as expected was observed after no less 3 weeks by daily GS i.p. administration. It is blocked SE or significantly decrease the severity of seizures during SE. The implication of presented data is that combination of ginsenosides from Korean Red ginseng and ginseng cell culture Dan25 that could be applied for prevention of epileptical status development. However, a development of optimal ratio of different ginsenosides (Rb1 Rc, Rg, Rf,) should consummate in the new antiepileptic drug development.

The dynamics of limbic epileptogenesis was studied using a model of electrical kindling from different rostrocaudal segments of the cortical nucleus of the amygdala (CoA). Statistically significant relationships were found between the rostrocaudal location of the site of focal stimulation of the CoA and the behavioral and electrographic manifestations of seizure activity. The data obtained suggest that different rostrocaudal segments of the CoA play different roles in the genesis of limbic epilepsy. Temporal lobe epilepsy (or limbic epilepsy) is the most common form of this disease in humans [3, 10, 11]. Patients with this form of epilepsy suffer from complex partial (focal) and secondarily generalized seizures. In most cases, pharmacological resistance develops that makes it difficult to efficiently control seizures or significantly decrease their frequency using anticonvulsant drugs [13]. Because of the high incidence of temporal lobe epilepsy, difficulties in its pharmacotherapy, and the diversity of associated structural and functional brain lesions, of particular interest are experimental studies in which the pathogenetic mechanisms of temporal epilepsy are analyzed using various animal models [9, 10]. Electrical kindling (low-level stimulation that causes a progressively increasing response when applied repeatedly) [8] is the most adequate chronic model of temporal epilepsy that closely follows the natural course of its development with respect to a number of parameters [3‐6, 9, 10]. The role of the CoA in initiating the epileptiform activity of the amygdaloid complex (AC) and of the entire brain remains largely obscure. Our early studies [4, 5] and a recent study by Pitkanen et al. [11] implicated the CoA in spreading the seizure activity, especially in generating mirror foci in the amygdala of the contralateral hemisphere. In contrast, Cain [7] presents evidence that the CoA is of little significance in the epileptogenic process. However, taken together, the fact that the CoA is morphologically closely related to the piriform cortex and to some other structures of the AC in the ipsi- and contralateral hemispheres, and the clinical data indicating that the mediobasal temporal lobe is involved in the genesis of human temporal lobe epilepsy put in doubt Cain’s point of view. In the rat AC, the CoA lies medial to the piriform cortex, being partially exposed on the basal surface of the brain [1, 2]. The CoA is elongated rostrocaudally. This makes it possible to perform separately microstimulation of its anterior and posterior subniclei, which are known for their complex and heterogeneous structure [2]. The CoA can be divided into the anterior CoA (CoAa), the periamygdaloid cortex (PAC), and the posterior CoA (CoAp), based on the differences in their neuron composition, cytoarchitectonics, histochemistry, afferentation, and involvement in the main conducting systems of the AC [1]. The purpose of this study was to determine whether the behavioral and electrographic manifestations of epileptogenesis depend on the rostrocaudal location of the site of focal stimulation.

Brain damage and neuronal loss caused by traumatic brain injury, ischemic stroke, and symptomatic status epilepticus can lead to severe long-term consequences, such as impairment in learning and memory and cognitive functions, and development of chronic epilepsy. This can be the result of morphologic and functional changes underlying temporal lobe epilepsy. Epilepsy patients have increased risk of status epilepticus. It is a life-threatening condition when seizures last for more than 30 min and trigger processes leading to neuronal apoptosis and necrosis in various parts of brain. Administration of neuroprotective drugs preventing these pathologic processes could improve the prognosis for such patients. However despite of active research of neuroprotective drugs, the effective ways to prevent brain damage resulting from prolonged seizures are yet to be found. Studies of neuroprotective properties of classic and novel anticonvulsant drugs showed that most of them do not have the sufficient neuroprotective effect and are not able to prevent epileptogenesis. Thus the studies of other potential neuroprotective drugs seem to be promising.

In the late 90-s of the previous century the American Society of Epileptologists defined a priority for research as "possibilities to predict a seizure, early determinate and reduct". A method, which would allow the prediction of epileptical seizure's onset based on the EEG data registered with the patient with an epilepsy disease, would also allow implementing the new approach to treatment. If it became reliably possible to predict a moment of seizure, based on the EEG dynamics, one could create an automated closed loop system to prevent a seizure. In the article a number of works regarding this subject were reviewed. Also own results were discussed which were derived from analyses of brain electrical activity of rats with absence epilepsy and with the use of own developed software. Moreover specifics of absence initiation and course were discussed, as well as formation mechanism of thalamus-cortical loop, existing abilities of reduction not only absences, but also cognitive and emotional dissociations. Also described results of analyses of the EEG time series, that were derived by computation of correlation dimension with own developed software.

This review focuses on the modeling of status epilepticus in animal brain and modern data on the mechanisms of epileptical seizures initiation using the pilocarpine binding with the muscarinic cholinoreceptors (litium pilocarpine model). The character of epileptics seizures in developing brain and adult brain of rats were investigated. The lines of modulation and inhibition epileptics statues by sacricine and intranasal application of neuropeptide thyroliberin in ultra-low doses are demonstrated. The role of the short-term changes (signal regulated kinase signaling cascade, Kv 4.2 potassium channels, hippocampal and cortical spike-wave discharges) and the long-term changes (loss of selective type of interneurons, excitatory circuits by mossy fiber sprouting) that promotion the epileptic state and recurrent seizures in limbic structure are discussed.

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.

Thyroliberin (TRH) promoting endogeneous antidepressive effect is the most general regulator of the central mechanisms and visceral functions (especially respiration). Our group pioneered in applying the anticonvulsant action of TRH after local intranasal application). This application of TRH in ultra-low doses contrast the method of systemic TRH administration in the large doses). In our experiments intranasal application of 10(-8), 10(-10) and 10(-12) mol/l TRH significantly inhibited the severe epileptic motor fits in rats induced by PTZ. EEG also confirms beneficent effect of TRH (TRH suppressed SWD in cortex, amygdala and hippocamp). In the experiment that follows compared effects of TRH (pyroGlu-His-Pro-NH2) and its metabolite dipeptide His-Pro (10(-10), 10(-8) mol/l). The experiments make more precise that only TRH but not His-Pro posses the anticonvulsant properties. There is a good believe that medical potentialities of TRH have not been exhausted and its new possibilities of its usage will be revealed in epileptology.

Frontoparietal cortex and the thalamocortical circuit comprising reticular thalamic nucleus (RTN) and relay nuclei of the ventrolateral thalamus (VLT) are critical structures in the generation of spike-wave discharges (SWD) during absence seizures. The activity of these nuclei is under the control of the ascending cholinergic projections of nucleus basalis of Meynert. The aim of our study is to make an attempt to change the pattern of SWD in WAG/Rij rats by injecting of cholinotoxine AF64A to the area of RTN. Spontaneous SWD were registered in cortex of WAG/Rij rats with genetically determined absences. The spectral content of SWD was analyzed by means of the Fast Fourier Transformation (FFT) procedure. Unilateral injections of AF64A (1 nmol) to RTN led the decrease in duration and number of SWD comparing to the basal EEG recordings 2 days after the lesion. The FFT analysis showed the disappearance of 17-18 Hz spike on the side of the lesion compared with the intact side. The immunohistochemical study for acetylcholinetransferase (ChaT)-containing neurons showed the loss of ChaT-positive cells in the nucleus basalis area on the side of the lesion. The removal of cholinergic afferentation of RTN and cortex from nucleus basalis inhibits the SWD developing most likely due to the decrease of cortical excitability. Moreover, possibly cholinergic transmission is involved in the transforation of the synchronized phenomena (SWD) to another with close mechanism of generation.

A current status of knowledge about high-frequency (140-200 Hz) ripple oscillations in the CA1 hippocampal subfield is summarized and considered in the context of two-stage model of the hippocampal memory processing. A large body of evidence suggests highly-selective recruitment of pyramidal cells and interneurons in the generation of the oscillatory pattern after co-operative sharp-wave-related discharge of CA3 pyramidal neurons. We also discuss a role of transmission via gap junctions in the mechanisms of ripple oscillations as well as their adaptive aminergic (histaminergic) modulation. Patterns of neuronal firing in the hippocampus observed during ripple oscillations reproduce space-dependant neuronal activity from the previous waking period. Together with a data about efficacy of high-frequency stimulation for induction of synaptic modification it points out a role for ripples in the formation of long-term memory. Focal ultra fast ripples (up to 500 Hz) have been shown to participate in the development of temporal lobe epilepsy.

This report addresses the verification of the hypothesis that arginine-vasopressin affects the formation of hyperthermia-evoked convulsions in early ontogenesis in rats on days 3, 5, 7, and 9 of postnatal life. The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin. Arginine-vasopressin (10 microg/rat) and PACAP (0.01 microg/rat) decreased the latency of generalized tonic-clonic convulsions and the time of truncal generalization of convulsive activity on days 3 and 5 of rat development. Animals given arginine-vasopressin (0.1-10 microg/rat) sowed significant increases in the duration of generalized convulsions to the level of status epilepticus on day 9 of life. Conversely, administration of higher doses of PACAP (0.1 microg/rat) increased the threshold of tonic-clonic convulsions on days 3 and 5 and decreased it on days 7 and 9 of postnatal development. The indirect involvement of PACAP in the mechanisms of experimental febrile convulsions is suggested to act via changes in arginine-vasopressin neurosecretion.

Progesterone and oestradiol serum level was investigated in WAG/Rij rats with genetically determined absences. Blood samples were drawn before and after the pregnancy following the parturition. The serum concentration of progesterone increased after the 3rd day of pregnancy. There is no increasing of oestradiol during pregnancy as large as this. The progesterone is kept high to the 18th day of pregnancy and drastically decreased before the parturition. Common duration of absences--spontaneous spikewave discharges (SWD), frequency and the duration of every SWD decreased from 3rd to 19th days of pregnancy before the parturition. On the basis of these data and modern investigations, regulation of GABAA receptor expression during pregnancy by progesterone (Brusaartd A. B. et al., 1999) it can be assumed that the changes in the parameters of SWD are possibly correlated with the progesterone changes in serum during pregnancy in WAG/Rij rats.

Thyroliberin (TRH) promoting endogenous antidepressive effect is the most general regulator of the central mechanisms and visceral functions (especially respiration). Our group pioneered in applying the anticonvulsant action of TRH after local intranasal application. This application TRH in ultra-low doses contrast the method of systemic TRH administration (i.v., i.m. or oral in the large doses--mg). In our experiments intranasal application of 10(-9) M, 10(-10) M and 10(-12) M TRH significantly inhibited the severe epileptic motor fits in rats induced by pentylenetetrazole (PTZ). Beneficent effect of TRH is also confirmed by EEG (TRH suppressed SWD in cortex, amygdala and hippocamp). In the experiment that follows compared effects of TRH (pyroGlu-His-Pro-NH2) and its metabolite dipeptide cHis-Pro-NH2 (10(-10) M, 10(-5) M). The experiments make more precise that only TRH but not His-Pro posses the anticonvulsant properties. There is a good believe that medical potentialities of TRH have not been exhausted and its new possibilities of its usage will be revealed in epileptology.

Arginine-vasopressin reduced the tonic-clonic seizures' latency as well as the duration of the seizures brain-stem generalisation on the 3rd and 5th postpartum days in rats. The reduced latency was also observed after the PACAP38 low doses administration, whereas higher doses diminished and then enhanced the threshold of generalised hyperthermia-induced seizures on the 3rd and 5th days and the 7th and 9th days, resp. The arginine-vasopressin-treated animals had a dramatically enhanced duration of the tonic-clonic seizures up to the epileptic status on the 9th postpartum day. The findings suggest the PACAP involvement in mechanisms of experimental febrile seizures through its effect upon arginine-vasopressin neurosecretion.

The seizure susceptibility of amygdaloid complex in rat was investigated. In piriform cortex and cortical nucleus of amygdaloid complex the structural and electrophysiological rostro-caudal differences were found (using relative spectral densities EEG, seizure thresholds, electrical kindling rate). The fundamental dependence of severity of motor seizures from structural (nuclear or cortical) organization of stimulating area was shown. There were more of limbic stages while stimulating anterior and posterior cortical nuclei, and there were more generalized stages while stimulating piriform and periamygdaloid cortex. Using the model of electrical kindling anticonvulsant effects of Sacricin were demonstrated. Sacricin is one of the compounds of polycarbonic acid. Sacricin has fully coped the process of secondary generalization of epileptic seizures.

Generation of nitric oxide and the content of lipid peroxidation products in the brain are increased in rat pups during febrile convulsions. NO-synthase inhibitor N-nitro-L-arginine in a dose of 250 mg/kg prevented hyperthermia-induced accumulation of nitric oxide, increased the latency febrile convulsions, and had no effect on the content of lipid peroxidation products.

Behavior of nonlinear rats and animals from Wistar and WAG/Rij (with inborn generalized absence epilepsy) strains was examined in the elevated plus-maze and the hole board. WAG/Rij rats demonstrated low exploratory behavior in both tests. In the elevated plus-maze, WAG/Rij rats were more balanced and more anxious than Wistar and nonlinear rats. Administration of ethosuximide completely eliminated spike-wave discharges but did not change behavioral interstrain differences. Since the spike-wave patterns develop in WAG/Rij at the age of 3 months, the behavior of young (2-moth-old) pups from different strains was compared and significant differences were revealed. Correlation between the genetically defined features (spike-wave discharges) and behavioral peculiarities in WAG/Rij rats is supposed.

The effects of a 5-day heparin treatment (10 kD, 64 IU/kg, intraperitoneally) on food-procuring behavior and spatial memory in a 12-arm radial maze were studies on Wistar rats. The maximum reinforcement scores in heparinized rats were attained by day 7 and in control rats only by day 16. In total, 75% heparinized and 45% control rats successfully learned the task for 24 days. On day 25 the contents of major transmitters and their metabolites in various brain structures and in the small intestine of control and experimental rats were determined. The rats treated with heparin showed increased concentrations of norepinephrine in the hypothalamus, homovanillic acid in the striatum, and serotonin in the small intestine. Our findings indicate that heparin exhibits a wide range of activities in addition to its anticoagulant effect.

Modern data of molecular and biological properties and physiological role of new pituitary adenylate cyclase activating polypeptide--PACAP--review. PACAP play key role in the embryogenesis of brain, in the protection of brain nerve cells from ischemia-induced death, injuring and apoptosis. New data are discussed concerned with molecular cloning and tissue distribution of receptors for PACAP, gene proPACAP expression in gastrointestinal tract, reproductive organs and nervous system. PACAP increase cytosolic free calcium and modifies the calcium-sensitive K(+)-channels, PACAP protects cultures cortical and hippocampal neurons from glutamate-induced cytotoxicity. The sleep modulation and modification of seizures activity of brain through the secretion of vasopressin or/and through NMDA receptors directly should be include in the program of PACAP "physiological continuum" of functions.

The basics of neurophysiological, neurochemical and molecular mechanisms of epileptogenesis in early ontogeny are discussed. The role of developmental neuropathology, synaptogenesis; the role of glutamatergic and GABA-ergic transmitter systems are summarized. The candidates of genes in the childhood epilepsies, developmental changes in the expression of genes of voltage-gated ionic channels and receptor genes are reviewed.

In this work polyfunctional peripheral (pancreas) and central effects of galanin 1-29 (gal.) were reviewed. In hypothalamus gal. exerts neuroendocrine effects through modulation of secretion of principal hormones of hypophysis, co-localized with acetylcholine in some brain structures including hippocampus. Gal. influences behaviour and memory. Newest hypotheses of T. Hokfelt and J. N. Crawely [correction of G. Crowly] on the involvement of gal. to pathogenesis of in Alzheimer disease and possibilities of its clinical antiamnestic utility are discussed. Our own data indicates antiseizure effect of gal. in the model of febrile convulsions in children--hyperthermia induced seizures in neonatal rats in the age from 5 to 13 days. Systemic intraperitoneal administration of gal. was effective in certain age--7-11 days of postnatal period--in preventing hyperthermia induced seizures: in increased by 2-3 times latency of minimal seizures and clonic-tonic generalized seizures. In adults rats gal. showed antiseizure action when administered intranasal in the model of pentilenetetrazol seizures (modified test with repeated administration of subthreshold doses). Modern data on structure and function of galanin, its chimeric analogs and galanin receptors receptors are discussed.

A new approach was applied to evaluation the errors in the course of learning of rats in 12-arm radial maze (RM). The number of repeated erroneous visits of the last six arms ("late errors") decreased only after a decrease in the number of repeated erroneous visits of the first six arms ("early errors"). This points to insufficiency of using the common index of the mean error for evaluating learning ability in the RM. Change in the character of errors in the operative and space memory was studied in the RM-conditioned rats after disruption of the relations between the intra- and extra-maze markers. This disruption was reached by rotation of the RM by 180 degrees after rat's visiting of 5 arms during its stay in the 6th one. It was found out that rats were able to recognize the changes in the extra-maze markers caused by the RM turn and to relearn within 4-5 days.

Learning abilities of mice selected by the small and large brain weights were studied in Y-maze. Thirsty mice were trained to find water in one of the maze arms. The minimal latency of this reaction reached in the process of learning was shorter in the mice selected by the heavy brain. Benzaldehyde which is commonly supposed to be an aversive olfactory stimulus being presented before drinking sharply increased the latency, nevertheless, it remained shorter in mice with heavy brain. The response to the aversive stimulus varied between the individuals, especially in mice selected by the small brain weight.

Effects of alaptide on self-stimulation of the lateral hypothalamus, rotation behaviour and learning ability were studied in rats growing either in social adaptation or in groups. The effects on self-stimulation were opposite in these rats. Alaptide facilitated the learning process in grouped rats and potentiated the indirect dophamine-mimetic action of amphetamine in isolated rats.

In addition to the well-known activities of TRH (stimulation of respiration, antidepressant action, increase of motility, antishock action, therapeutic effects against ataxia, and so forth), some new properties were established. TRH was found (1) to stimulate the contractility of lymph vessels in ultra-low doses and to be useful in the treatment of acute pancreatitis; (2) to normalize cerebral circulation in rats and neonates after asphyxia; (3) to improve the electrophysiological parameters of the retina and pigmented epithelium in rats and man, to exert a long-term positive influence on the health status of patients suffering from senile retinal macular dystrophy; (4) to potentiate the analgesic effect of low doses of morphine in a definite range of doses (analog PR-546). It is of paramount importance that most of the indicated activities of TRH may hold promise for clinical application.

The integral rat brain temperature was measured by radiothermoscope after intranasal instillation of thyroliberin in a dose 400 mkg. The recording increase of temperature lasted during two hours after instillation. This phenomenon is based both on the direct action of thyroliberin and on its capacity to stimulate the induction of other regulatory peptides.

Synaptic junctions in the rabbit amygdala were studied by electron microscopy. A definite distribution of morphologically different synapses on the neuronal surface was noticed. This distribution changed 3 days after ipsilateral lobectomy. A suggestion is made on transformation of a certain morphological form of synaptic contact into another one during the changed function.

The chemoreactive properties of neurons of the rabbit basal amygdaloid nucleus were investigated at various times after unilateral division of all the direct hypothalamo-amygdaloid pathways (stria terminalis, ventroamygdalofugal pathway) and the anterior commissure. After immobilization with diplacin, the activity of the absolute majority of neurons of the partially deafferented basal nucleus (by contrast with responses of neurons of the intact amygdala) were inhibited by acetylcholine. Sodium glutamate caused facilitation of activity during electrophoresis, followed by inhibition. The results are compared with those obtained on neurons of long-isolated cortical slabs.

Changes in spontaneous activity of 291 neurons in the rabbit amygdala were analyzed during microelectrophoretic application of somatostatin under pentobarbital anesthesia. Somatostatin was found both to enhance and to inhibit the spontaneous activity of these cells, by contrast with the exclusively inhibitory effect on spontaneous activity of hypothalamic neurons described previously. After partial chronic deafferentiation of the amygdala, 76% of 103 neurons responded to somatostatin application; 90% of the responding cells, in which the initial spontaneous firing rate was 6–20 spikes/sec, responded by more rapid firing, and only 10% of neurons (with an initial spontaneous discharge frequency of over 20 spikes/sec) showed a decrease in firing rate. Neuronal responses in the amygdala to somatostatin, glutamate, and noradrenalin are compared. Preliminary application of noradrenalin caused an increase in the number of inhibitory responses on subsequent application of somatostatin to the same cell.

Effects of the ACTH4-7 pro-gly-pro, calcium valproate ("Germed", DDR) and nembutal on kindling preparation and audiogenic epilepsy were investigated. Development of after-discharges in response to repeated amygdaloid electrical stimulation was assessed in normal rats and in rats susceptible to audiogenic epilepsy (KM line of rats). ACTH4-7 pro-gly-pro had an anticonvulsant profile. ACTH4-7 pro-gly-pro decreased seizure threshold in the audiogenic epilepsy test, but did not prevent the motor convulsions.

Responses of 291 neurons to microelectrophoretically injected somatostatin were studied in the amygdala of rabbits under nembutal anesthesia. Both excitatory and inhibitory effects were found in contrast to earlier data on the only inhibitory reactions in hypothalamic neurons. After partial chronical deafferentation of the amygdala responses to somatostatin application were observed in 76% of the registered neurons, 90% of these neurons with background discharge frequency from 6 to 20 imp/s, responded by an increase in their activity, while inhibitory reactions were recorded in neurons with average background discharge frequency above 20 imp/s. Since amygdaloid neurons exert a regulating effect on the secretion of the growth hormone through somatostatin, it is suggested that the observed responses reflect one of their feedback mechanisms.

The individual peculiarities of functional changes in motor asymmetry determined by behavioral test in T-maze have been shown in experiments with rats (nonpedigree and line LATI). The application of thyroliberin (10 mkg/kg) causes and increases the left-side lateralization which introduces alteration in the individual strategy of the successive round of 12 rays of radial maze with food during solution of spatial orientation task.

Effects of the ACTH4-7 pro-gly-pro, calcium valproate ("Germed", DDR) and nembutal on kindling preparation and audiogenic epilepsy were investigated. Development of after-discharges in response to repeated amygdaloid electrical stimulation was assessed in normal rats and in rats susceptible to audiogenic epilepsy (KM line of rats). ACTH4-7 pro-gly-pro had an anticonvulsant profile. ACTH4-7 pro-gly-pro decreased seizure threshold in the audiogenic epilepsy test, but did not prevent the motor convulsions.

The effects of intraventricular administration of melanostatin (MIF--I, Pro--Ley--Gly--NH2) on the behaviour and electrical activity in neocortex, amygdala, hippocampus and hypothalamus involved an enhancement of electrical activity: MIF enhanced the 3--7/sec high--voltage activity of neocortex, amygdala, hippocampus and the 7--12/sec one of neocortex. Morphine facilitated the effects of MIF whereas preliminary administration of MIF blocked the effect of threshold doses of morphine. After lesion of the central nucleus of amygdala the responsiveness of ipsilateral neocortex disappeared whereas that of hippocampus preserved.

The influence of TRH (100 micrograms/kg) and ACTH4-7 Pro-Gly-Pro (15 micrograms/kg and 25 micrograms/kg) involved an acceleration of the spatial learning on the 12-arm radial maze and on T-maze in rats; an increase in the number of correct choice after short (5-10 min) retention interval; and affected the working and reference spatial memory in the test of reinforced place performance. The effects of the TRH and ACTH4-7 Pro-Gly-Pro did not interfere with one another.

The EPs in the rabbit Amygdala were recorded after chronic (5 weeks) deafferentation following section of stria terminalis, commissura anterior and the ipsilateral frontal lobe cortex. Stimulation of the bulbar olfactory regions caused some facilitation of the EPs in non-olfactory nucleus of amygdala. Following ventromedial hypothalamic stimulation, the EPs remained unchanged in the caudal parts, diminished in the rostral parts of basolateral amygdala and disappeared in the medial nucleus of amygdala.

The effect of melanostatin (MIF), L-DOPA and morphine on the behaviour and electrical activity in the neocortex and lymbic structures in rats has been strudied. All substances were administered intraventricularly. There was a recorded increase of the energy of the delta and theta slow waves in the hypothalamus, amygdala and neocortex and also of the energy of the alfa waves in the amygdala and neocortex. In addition the administration of L-DOPA and morphine facilitated the effect of MIF while preliminary administration of MIF blocked the effect of morphine given in threshold doses.

The effects of microiontophoretic application of luliberin (LHRH), norepinephrine (NEO) and morphine on activity of the medial preoptic hypothalamic neurons were studied in male rabbits. About 80% of all the neurons responded to LHRH, mainly with facilitation. NEO appeared to have inhibitory influence on the LHRH-induced effects, when LHRH was applied simultaneously with NEO. Since the LHRH effect might be mediated via opiate receptors, it was examined against the background of morphine application. LHRH applied after morphine increased the number of unresponsive units. During simultaneous application of LHRH and morphine the number of unresponsive units increased by 30% and the number of facilitation responses decreased to 30% of the neurons under study. These findings confirm that the opiate receptors and noradrenergic system play a certain role in the central effects of LHRH.

Synaptic junctions in the rabbit amygdala were studied by electron microscopy. A definite distribution of morphologically different synapses on the neuronal surface was noticed. This distribution changed 3 days after ipsilateral lobectomy. A suggestion is made on transformation of a certain morphological form of synaptic contact into another one during the changed function.