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J Vetulani

Publications and source records attributed to J Vetulani.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Comparison of effectiveness of two schedules of rapid transcranial magnetic stimulation on enhancement of responsiveness to apomorphine.

Locomotor response to apomorphine (0.5 mg/kg s.c.) was tested in rats pre-treated with multiple rapid transcranial magnetic stimulation (rTMS) or electroconvulsive shock (ECS). rTMS (B = 1.6T, f = 20 Hz, t = 300 s) was delivered 9 times during 18 days (group rTMS1, total number of stimulations 54,000) or 18 times during 18 days (group rTMS2, total number of stimulations 108,000); ECS (I = 150 mA, f = 50 Hz, t = 500 ms) was delivered 9 times at 48 h intervals. Apomorphine given 24 h after the last treatment induced hyperactivity that was significantly more pronounced in rats receiving ECS and rTMS. The effect was most pronounced for electroconvulsive treatment, the least in the rTMS1 group. The results indicate that an increase in the total number of impulses during the rTMS may increase the responsiveness of rats to dopaminergic stimulation to the level comparable with that induced by ECS.

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Haloperidol treatment selectively affects expression of Galpha(i)3 subunit mRNA in specific regions of the rat brain.

Relative abundance of GTP binding protein mRNA coding for subunits alpha(i)1, alpha(i)2 and alpha(i)3, and their changes induced with chronic blockade of D2 receptor by haloperidol were compared in the frontal cortex, striatum, hippocampus and cerebellar cortex of the rat using a specific method based on multiplex RT-PCR. Galpha(i) subtype 2 mRNA was the most abundant, followed by subtype 1 and subtype 3. The haloperidol treatment produced an area specific increase in Galpha(i)3 mRNA in the frontal cortex and a decrease of Galpha(i)3 in the striatum. After 8-day withdrawal period, haloperidol-induced,changes disappeared in the striatum but became accentuated in the frontal cortex. Changes in the relative expression of Galpha(i) subtypes may significantly influence long-lasting effects of chronic D2 receptor blockade.

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Adrenergic receptors' responsiveness after acute and chronic treatment with haloperidol in the presence of calcium channel blockade.

The effects of acute and chronic (14 days) treatment with haloperidol (0.5 mg/kg ip) given alone or 15 min after nifedipine (5 mg/kg ip) on responsiveness of the alpha1- and beta-adrenergic receptors was investigated ex vivo by measuring of the second messenger responses. The accumulation of inositol phosphate (IP) or cyclic AMP were measured in brain cortical slices challenged with noradrenaline or isoproterenol. The facilitatory effect of a single dose of haloperidol on IP accumulation (an increase by approximately 50%) was abolished by nifedipine pretreatment. After chronic treatment with haloperidol alone its facilitatory effect disappeared, but a treatment with haloperidol after nifedipine caused a significant increase in IP accumulation. No treatment affected the responses from beta-adrenoceptors. These data show that the action of chronically administered haloperidol may be changed by the concomitant calcium channel blockade that prevents development of adaptation to persistent presence of the drug.

Adrenergic alpha-Agonists↗
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[The behavioral effects of the transcranial magnetic brain stimulation in rat: the comparison with electroshock].

The few experimental studies suggest that repetitive rapid-rate transcranial magnetic stimulation (TMS) evokes in the brain functional and structural changes similar to those evoked by electroconvulsive therapy (ECT). The aim of the present work was to compare the influence of the repetitive TMS (B = 1.6 T; f = 20 and 30 Hz; t = 5 and 5.5 minutes; N = 9 and 18 days) and that of ECT (I = 150 mA; f = 50 Hz; t = 0.5 s; N = 9 days) on rats' behaviour in the tests of free field, tail flick, motor hyperactivity after administration of apomorphine and in forced swimming. None of the rats subjected to TMS suffered from convulsive attack, which followed every electroconvulsive shock. In the free field test it was detected that neither TMS nor ECT applied individually or repetitively disturbed general motor activity of rats. Repetitive electroconvulsive shocks caused analgesia, prolonging the latency of tail flick by 46% (p < 0.001). Moreover, the tail flick test revealed hyperalgesia in the rats subjected to TMS (24 and 21% of control values respectively; p = 0.05). Motor hyperactivity of rats stimulated with administration of apomorphine was intensified both by TMS (by 58% at maximum in the 30th minute of the experiment; p = 0.001) and, all the more, by ECT (by 92% at maximum at the end of the test; p = 0.01). In the forced swimming test, the greatest decrease of inertia period was observed ECT--up to 50% of control values (p = 0.001). TMS had weaker effects--the decrease amounted to 29% of control values (p = 0.01). The shortening effect depended on the parameters of TSM. The obtained results seem to confirm that TMS, like ECT, evokes in rats certain reactions suggesting its antidepressive action, but causes less undesirable effects.

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Janusz Supniewski as a researcher of psychotrophic drugs (on his 100th birthday).

On October 17, 1999, late Professor Janusz Supniewski's disciples celebrated the 100th anniversary of his birthday, and on June 3, 2000, they gathered to commemorate the 36th anniversary of his death. In our article we present one of the areas of Professor Supniewski's scientific activity, which is fruitfully pursued at the Institute of Pharmacology of the Polish Academy of Sciences, the successor of the Department of Pharmacology created by Supniewski in 1954.

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[Transcranial magnetic stimulation versus electroconvulsive shocks: neuroanatomical investigations in rats].

Since the time of introducing ECT to the clinical practice, the method always raised questions regarding possibility that the current running through structures of a brain may evoke structural changes and, as a result, evoke convulsive attacks. Pathological changes (swelling, gliosis, atrophy, necrosis) were observed most often after "mega"--schemes including series of several to several hundred ECT treatments. Regime used nowadays including only 8-12 ECT sessions seems to be entirely safe. There are, however, only a few experimental works dealing with this problem. In 1992 research started on a new neurophysiological technique--transcranial magnetic stimulation (TMS) in depression. The advantage of this method is that is does not seem to evoke convulsive attacks. Prolonged rapid rate TMS (rTMS) seems to be particularly efficient in treatment of depression. Despite thousands of works describing various functional effects of TMS, there are obviously no researches on structural effects of the technique. In the case of experimental research on animals a few works were published and their results seem to be ambiguous. We have examined the influence of prolonged repetitive rTMS (B = 1.4 T, t = 5.5 min, f = 30 Hz), and standard ECT (I = 150 mA, t = 0.5 s, f = 50 Hz) on the structure of brain tissue in rats. Both groups of animals (n = 10) received 12 stimulation sessions. After the treatment the animals were routinely processed for electron microscopy (EM) and for light microscopy (LM). Our investigations suggest that the technique of ECT shows a considerable neurotoxic potential. In comparison to ECT--the rTMS method seems to be more safe.

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Drug addiction. Part I. Psychoactive substances in the past and presence.

Substances capable of changing the functions of the central nervous system are widely distributed in plant kingdom, and many of them were discovered by ancient food-gatherers at the dawn of humanity. In the Old World only a few substances producing euphoria or altered states of consciousness and having habit-forming properties are still widely used. They are the products of poppy (opium, morphine), hemp (hashish, marijuana), and of fermentation of various organic materials alkohol. This list has recently been joined by the psilocybin-containing mushrooms. The addiction-forming compounds originated in the New World and widely spread are tobacco (nicotine) and cocaine. In the 19th and 20th, century the development of medicinal chemistry resulted in several synthetic compounds, originally proposed as therapeutics, such as barbiturates, benzodiazepines and amphetamines. Due to legal problems, to avoid production of the substances already prohibited, many designer drugs were manufactured. In addition, several compounds were synthesized as recreational drugs. Also some compounds that were not regarded as drugs, such as aromatic hydrocarbons and other cleansing agents, as well as steroids were found to have properties of dangerous, habit-forming agents. The attitude of society and the pattern of use of psychoactive substances have changed with time, particularly in the last decades. The active principles are now more addictive because of concentration, purification, chemical modifications and the way of ingestion, which now favors most rapid transport to the central nervous system. The substance abuse approaches the level of global epidemics, and the recent usage of drugs of addition is also reviewed.

Anabolic Agents↗
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[Biological basis of psychiatry].

Psychiatry had retained the status of art rather than science for longer than other branches of medicine. However, the views that psychiatric disorders have material basis, existing since antiquity, had eventually been accepted by modern medicine, in spite of troubles connected with the rise of analytical psychiatry. Presently, there are no doubts that structural and functional integration of the brain is a prerequisite of psychical health. The psychical processes are presently regarded as neurobiological phenomena, and the technical progress, particularly brain imaging techniques, allow to investigate, with objective methods, even phenomena such as consciousness, that for long remained in the domain of philosophy. The applied success of biological psychiatry is the introduction of effective psychotropic drugs. It cannot be forgotten, however, that psychotherapeutic methods (which also have neurobiological roots), are as indispensable as psychopharmacotherapy in a modern psychiatric clinic.

Brain↗
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Conditions of application of repeated transcranial magnetic stimulation to rats may mask the effects of the treatment.

Rats of sham repeated transcranial magnetic stimulation (rTMS) group, kept in noisy room and transiently immobilized (5 min) for 12 consecutive days, showed similar inhibition of body weight gain, increase in exploratory locomotor activity, and elevation of motor response to apomorphine as rats undergoing magnetic stimulation of the brain, and had only slightly lower response in apomorphine stereotypy. Some of the responses ascribed to antidepressant action of rTMS in animal experiment may be due to environmental conditions, and not alternating magnetic field passing the brain.

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Drug addiction. Part III. Pharmacotherapy of addiction.

The last decade brought a considerable progress in pharmacotherapy of addiction. Basing on recently gained knowledge of mechanisms of development of addiction and the physiology of the brain reward system, several therapeutic strategies have evolved. The strategies aimed at targeting the basic mechanisms of addiction rely on the premises that addiction is caused by adaptive changes in the central nervous system and that craving, which is the main cause of relapse, depends on dopaminergic mechanisms and requires high general excitability. The pharmacological approach involves drugs that reduce neuronal adaptability by inhibiting the calcium entry to neurons both through voltage-gated channels (e.g. nimodipine) and NMDA receptors (e.g. memantine), and drugs that stimulate the inhibitory GABAergic system (gamma-vinyl-GABA, baclofen), Particular attention is paid to the compounds that may attenuate dopaminergic hyperactivity, without considerable suppression of tonic activity of dopaminergic neurons (e.g. BP 897, a partial dopamine D3 receptor antagonist). Specific strategies are aimed at interference with the action of particular drugs of addiction. An important group includes the agonistic therapies (known also as substitution or maintenance therapies) in which a long-acting agonist is used in order to reduce the action of the drugs of high addictive potential (e.g. methadone against heroin addiction or vanoxerine (GBR 12909) against psychostimulants). Other specific strategies aimed at reduction of the transport of molecules of addictive substances into the brain: the approaches involve preparation of antibodies that form complexes unable to cross blood-brain barrier or enzymes accelerating the metabolism of the compounds in the blood (e.g. variants of butyrylcholinesterase). A considerable progress has been made in combating the abuse of legal addictive substances, alcohol (naltrexone, acamprosate) and tobacco (bupropion). The prospects for developing effective pharmacotherapies against addiction are bright. Unfortunately, ideological and social implications, as well as the conflict of interest with illegal narcotic manufacturers and distributors, may considerably hamper the progress in combating addiction (e.g. difficulties in introduction of methadone).

4-Aminobutyrate Transaminase↗
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Drug addiction. Part II. Neurobiology of addiction.

The drug addiction may be regarded as the disease of the brain reward system. This system, closely related to the system of emotional arousal, is located predominantly in the limbic structures of the brain. Its existence was proved by demonstration of the "pleasure centers," that were discovered as location from which electrical self-stimulation is readily evoked. The main neurotransmitter involved in the reward is dopamine, but other monoamines and acetylcholine may also participate. The anatomical core of the reward system are dopaminergic neurons of the ventral tegmentum that project to the nucleus accumbens, amygdala, prefrontal cortex and other forebrain structures. Several of those structures may be specifically involved in the reward produced by different substances, when anticipating the reward. The recent discovery of CART peptides may importantly expand our knowledge about the neurochemistry of reward. Natural rewarding activities and artificial chemical rewarding stimuli act at the same locations, but while natural activities are controlled by feedback mechanisms that activate aversive centers, no such restrictions bind the responses to artificial stimuli. There are several groups of substances that activate the reward system and they may produce addiction, which in humans is a chronic, recurrent disease, characterized by absolute dominance of drug-seeking behavior. The craving induced by substances of addiction inhibits other behaviors. The adaptation of an organism to a chronic intake of drugs involves development of adaptive changes, sensitization or tolerance. It is thought that the gap between sensitization developing for the incentive value of the drug and tolerance to the reward induced by its consumption underlies the vicious circle of events leading to drug dependence. The vulnerability to addiction is dependent not only on the environment, but also on genetic factors.

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Opiate and alpha 1-adrenergic receptors in mice responding to morphine with sedation or with running fit.

Two subpopulations of Albino Swiss mice were selected on the basis of their response to a dose of 20 mg/kg ip of morphine: individuals in which the drug constantly produced sedation, and those which responded with running fit. Both subpopulations of mice had cerebral opiate delta and mu receptors (defined as [3H]DADLE and [3H]naloxone binding sites) of similar Bmax and KD values but mice responding with sedation showed lower density of alpha 1-adrenoceptors (defined as [3H]prazosin binding sites) as compared both with mice reacting with running fit or randomly selected animals. Chronic administration of imipramine resulted in a significant increase in the density of [3H]prazosin binding sites in the mice responding with sedation, but not in the animals responding with running fit.

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Chronic electroconvulsive treatment counteracts cortical beta-adrenoceptor upregulation induced by morphine abstinence.

Morphine treatment (20 mg/kg for 7 consecutive days) did not affect the density of [3H]dihydroalprenolol ([3H]DHA) binding sites in the cortical membranes of the rat, but during naloxone-precipitated abstinence syndrome the density of these sites increased. Electroconvulsive treatment for 6 days, which by itself decreased the density of [3H]DHA binding sites, prevented the increase.

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Strain differences in changes in some parameters of cerebral cortical adrenergic system following chronic imipramine administration to rats.

The characteristics of [3H]prazosin binding sites in the membranes from cerebral cortex, the basal level of formation of cyclic AMP in cortical slices, and the responsiveness of the cyclic AMP generating system to noradrenaline and isoproterenol in this preparation were measured in Long-Evans, Wistar and Sprague-Dawley rats treated chronically with saline or imipramine. No differences between strains and treatments were observed regarding the Bmax and KD of [3H]prazosin binding sites. The basal levels of cyclic AMP formation were similar in control rats of all strains, but imipramine treatment augmented it significantly in Sprague-Dawley rats. The responses of the cyclic AMP generating system to noradrenaline were significantly lower in Long-Evans than in the remaining strains of rats. Only in Sprague-Dawley rats a significant downregulation of response to noradrenaline was observed after imipramine treatment. All three strains of rats differed significantly among themselves in their responsiveness to isoproterenol; only in Sprague-Dawley rats this response was down-regulated significantly (by 80%) by imipramine treatment.

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Differences in beta-adrenergic regulation of cyclic AMP formation in cerebral cortical slices of the rat and spiny mouse--Acomys cahirinus.

In both the rat and Acomys cahirinus the adrenergic cyclic AMP generating system in the brain is dependent not only on beta-, but also on alpha-adrenoceptors. The relative role of alpha-adrenoceptors is much greater in the Acomys cahirinus. This feature makes the Acomys an interesting animal model for investigating the role of alpha-beta-adrenoceptor coupling in generation of cyclic AMP and the mechanism of action of antidepressant treatment.

Adrenergic alpha-Agonists↗
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Shuttle-box avoidance facilitation by minaprine in mice.

The effects on shuttle-box avoidance acquisition of the new antidepressant minaprine (1, 2.5, 5 or 10 mg/kg) and of the classical antidepressant desipramine (0.5, 1, 2.5 or 5 mg/kg) were tested, without pretreatment or after a 5 day pretreatment, in mice of the CD-1 strain, subjected to five daily 100-trial training sessions. Minaprine, recently proposed as a new nootropic agent, facilitated avoidance performance when given to pretreated animals at a dose of 10 mg/kg, which had no effect on spontaneous locomotor activity. Desipramine did not exert any significant effect on avoidance responses. The results are in agreement with previous findings showing learning improvements by minaprine, but do not clarify the mechanism involved in the avoidance facilitation.

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