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Biomedical subjects

Y D Lapierre

Publications and source records attributed to Y D Lapierre.

At least 109 records · Page 6Linked to original sources
PubMed1983

New concepts in the management of depression--possibilities with a non-sedative antidepressant.

Classification of depression is important, as it may provide a valuable indication of which types of treatment are likely to be effective. Most traditional classification systems follow a dichotomous approach (e.g. endogenous versus exogenous, agitated versus retarded), and consideration of such systems has led to increased understanding of depression. Treatment should be tailored to individual requirements, taking into account the type of depression and the stage at which it is being treated, the patient's personality and idiosyncrasies, and the pharmacological profile of the drug. Group trials show many antidepressants to be of approximately equivalent efficacy; however, side-effect profiles differ. The advent of the second generation antidepressants provides clinicians with non-sedating drugs, often with fewer anticholinergic side-effects. Thus, improved patient compliance and better overall functioning can be expected, as sedation often hinders recovery by producing flattening and monotony of affect, and blunting of emotional involvement and responsiveness, while cholinergic blockade increases confusional states.

Antidepressive Agents↗
PubMed1982

Comparative effects of short- and long-term treatment with neuroleptics on behavioural activity as well as dopamine turnover in striatum.

1. Single injection of haloperidol (2 mg/kg, i.p.) or chlorpromazine (10 mg/kg, i.p.) produced an activation of dopamine synthesis and turnover as evidenced by increased activity of tyrosine hydroxylase and higher levels of homovanillic acid in the striatum of rats. 2. The endogenous concentration of dopamine remained unchanged in striatum and other brain regions examined, except in hippocampus where it was slightly (20%), but significantly decreased by acute haloperidol treatment. 3. In contrast, long-term treatment with neuroleptics over a period of 21 days decreased the synthesis and turnover of dopamine in the striatum. Whereas short-term treatment with chlorpromazine and haloperidol produced marked sedation, chronic treatment enhanced spontaneous locomotor activity by 20 and 26% and sniffing frequency by 19 and 24%, respectively. 4. Our data demonstrate that tolerance develops to the stimulating effect of haloperidol and chlorpromazine on striatal dopamine turnover. This adaptive change might be responsible for the emergence of clinical effects. 5. It is suggested that after repeated treatment, "chemical denervation" occurs as a result of chronic blockade of dopaminergic transmission in the striatum and that the proliferation of dopamine receptors (i.e. supersensitivity) is probably responsible for hyperactivity and overt sniffing behaviour.

Animals↗
PubMed1982

Bromocriptine-induced changes in dopamine and gamma aminobutyric acid in haloperidol withdrawn rats.

1. Daily administration of haloperidol (2 mg/kg, i.p.) for 35 days significantly decreased tyrosine hydroxylase activity as well as homovanillic acid in the corpus striatum of rats. 2. Long-term treatment with haloperidol significantly elevated (17%) glutamic acid decarboxylase activity as well as gamma-aminobutyric acid level in the corpus striatum. 3. Withdrawal of rats for 3 and 5 days after 32 and 30 days of haloperidol treatment increased the locomotor activity to 279% and to 211%, respectively, of control values. While haloperidol withdrawal decreased tyrosine hydroxylase activity, it produced no further change in glutamic acid decarboxylase activity and gamma-aminobutyric acid. 4. Daily injection of bromocriptine (2 mg/kg, i.p.) for 5 days in haloperidol-withdrawn rats decreased locomotor activity and dopamine release as evidenced by increased endogenous levels of dopamine and decreased homovanillic acid in striatum of rats. No further increase in striatal glutamic acid decarboxylase activity and GABA levels were reported after bromocriptine treatment. 5. Our data suggest that bromocriptine may elicit its beneficial effect in tardive dyskinesia patients by modifying dopamine turnover in the striatum.

Animals↗
PubMed1982

Cortical slow potential shifts in tardive dyskinesia.

1. Slow cortical potential shifts such as the late terminal E-wave component of the CNV appear to be determined mainly by the level of motor preparation and as such it was employed to investigate the degree of cortical involvement in schizophrenics exhibiting abnormal motor phenomena induced by prolonged treatment with neuroleptics. 2. The basic experimental task was a constant foreperiod warned reaction time task consisting of a brief warning tone (S1) followed 4 sec later by a light, the imperative stimulus (S2), upon which the subject was instructed to release a response key. The task was presented twice, in a randomized order, under neutral and fast set instructions, to tardive (TD) and non-tardive dyskinesia (NTD) groups. 3. Computer EEG analysis identified and analysed on early O-wave measured as the average amplitude 500-1000 msec post S1, and the latter E-wave measured as the average amplitude 500 msec prior to S2. Two additional epochs of PINV activity were also analysed. 4. The results indicated that the TD group exhibited significantly larger PINV activity, but unlike NTD patients, the TD group failed to exhibit any significant increases in E-wave amplitude concommitant with improved behavioral reaction times. The results are discussed in relation to a disinhibitory theory of tardive dyskinesia.

Adult↗
PubMed1982

Neurotransmitter functions in depression.

1. Subgroups of depressions may be identified and treated based on MHPG execution. 2. HVA correlates more with activity than with mood. 3. CSF-5HIAA may be helpful in categorising some depressions. 4. Acetylcholine has some effect on mood most probably through indirect action on other neurotransmitters. 5. GABA is still not adequately investigated. 6. Desensitization of presynaptic adrenergic autoreceptors may explain some of the mechanisms of antidepressant action of drugs. 7. Decreased post-synaptic adrenergic activity is a common effect of most antidepressants and of ECT.

Catechol O-Methyltransferase↗
PubMed1982

Current psychopharmacogenetic strategies in primary affective disorders.

1. The evidence is substantial that primary affective disorders are genetically inherited. 2. Using pharmacological probes or strategies, biological markers of the gene(s) should be able to be ascertained or induced during remission of illness. 3. Genetic marker criteria are defined and are applied to the scanty existing data. 4. It is concluded that these strategies have yet to yield a clear marker of primary affective disorder.

Bipolar Disorder↗
PubMed1982

Pharmacokinetics of psychotropic drugs: what can it tell us?

1. Knowledge of basic pharmacokinetic parameters may help the clinician to optimize drug treatment regimen. 2. For some psychotropic drugs (e.g. lithium and some antidepressants) a good correlation exists between plasma levels and therapeutic or toxic effects. 3. "Optimum" steady state levels can now be predicted from single dose blood level data of some drugs (lithium, nortriptyline, desipramine). 4. Altered pharmacokinetics in elderly and children have to be taken into consideration in treatment with psychotropic drugs. 5. With development of suitable drug assays, plasma level control of therapy is becoming a part of a good clinical practice.

Adult↗
PubMed1982

A therapeutic and discontinuation study of clobazam and diazepam in anxiety neurosis.

The efficacy and safety of clobazam and diazepam were compared in 40 patients with generalized anxiety disorder in a 28 day non-placebo-controlled trial followed by a 3-day single-blind placebo washout. The two drugs were equally anxiolytic, and the anxiety symptoms of most patients were brought under control within 1 week. Both drugs were found to be nontoxic. Diazepam had slightly greater sedative properties than clobazam, which was the patients' preferred drug after 28 days of treatment. During placebo washout, anxiety returned to pretreatment levels. Abrupt withdrawal did not result in rebound phenomena.

Adult↗
PubMed1982

Effects of cholinergic and GABAergic drugs on apomorphine-induced gnawing behavior in rats.

The effects of cholinergic and GABAergic agonist and antagonist were studied on the apomorphine-induced gnawing behavior in rats. Physostigmine (0.5 mg/kg) decreased the biting scores, whereas atropine (5 mg/kg) had an opposite effect. Picrotoxin potentiated the physostigmine inhibitory action on gnawing responses. This inhibitory gnawing effect was antagonized by prior treatment with atropine. Pretreatment with amino-oxyacetic acid (25 mg/kg) also potentiated the inhibitory effect of physostigmine on gnawing behavior in animals. Such an additive inhibitory response could be antagonized by simultaneous pretreatment with cholinergic and GABAergic blockers such as atropine and picrotoxin, respectively. These findings indicate that the modulatory action of cholinergic neurons on DA system is probably influenced by changes in the GABAergic system.

Aminooxyacetic Acid↗
PubMed1981

Effects of apomorphine on behavioural activity and brain catecholamine synthesis in normal and L-triiodothyronine-treated rats.

The effect of chronic apomorphine treatment on behavioural activity as well as brain dopamine metabolism was studied in normal and neonatally L-triiodothyronine-treated rats. Neonatal hyperthyroidism was accompanied by an increase in spontaneous locomotor activity as well as by enhanced synthesis and release of dopamine as evidenced by increased catecholamine synthesis in crude synaptosomal preparation (P2 pellet), elevated tyrosine hydroxylase activity and higher concentrations of homovanillic acid and 3, 4-dihydroxyphenylacetic acid in striatum of rats. Repeated apomorphine treatment (1 mg/kg/day s.c) for 15 days, beginning from the 15th day of age, produced hypermobility and stereotyped behavior (consisting of sniffing, gnawing, rearing) which appeared to be more pronounced in neonatally hyperthyroid rats than in normal controls. In addition, apomorphine-treated hyperthyroid animals marched in a row with straub tail, and displayed increased aggressiveness and bizarre social behavior consisting of "mock fighting" when left in pairs. In contrast to normal rats, apomorphine-treated hyperthyroid animals displayed marked hyperactivity which was evident even at 24 hours after the last injection of apomorphine. Administration of apomorphine resulted in significant decreases in striatal tyrosine hydroxylase, catecholamine synthesis in crude synaptosomal preparation (P2 pellet) as well as dopamine metabolite levels in brains of both normal and hyperthyroid animals. Our present data showing that apomorphine potentiates behavioural activity in hyperthyroid rats suggest that L-triiodothyronine and apomorphine probably share certain features common to activating dopaminergic neurons in the brain.

Animals↗
PubMed1981

Thyrotropin releasing hormone potentiates the effects of imipramine on brain serotonergic system.

Daily administration of thyrotropin-releasing hormone (TRH) (20 mg/kg) for 10 days in 2 equally divided doses increased 5-hydroxytryptamine and/or 5-hydroxyindoleacetic acid levels in certain brain areas. Chronic imipramine treatment (10 mg/kg) for 10 days significantly decreased the levels of brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. When TRH was administered concurrently with imipramine (10 mg/kg), this neuropeptide significantly potentiated the effects of imipramine on lowering of endogenous levels of 5-hydroxytryptamine (striatum, hypothalamus) and 5-hydroxyindoleacetic acid (striatum, midbrain, pons-medulla). Our data provide a possible neurochemical basis for the reported potentiation of tricyclic antidepressant action by TRH.

Animals↗