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Biomedical subjects

N Sitaram

Publications and source records attributed to N Sitaram.

At least 55 records · Page 3Linked to original sources
PubMed1986

Interface of panic and depression: clinical and sleep EEG correlates.

Four groups of subjects were compared with respect to their clinical and demographic status and electroencephalographic (EEG) characteristics, namely: primary major depressive disorder (PRI MDD); panic disorder (Panic); "Mixed" group comprising patients meeting full syndromal criteria for MDD and panic occurring concomitantly; and normal controls. The "Mixed" (MDD + Panic) patients were characterized by earlier age of onset of psychiatric illness, longer duration of current episode, greater intensity of symptoms, higher impairment of functioning, increased miscellaneous psychopathology, and greater objective stress and anger. With respect to sleep EEG variables, PRI MDD patients were clearly different from the other three groups. The sleep profile of the "Mixed" group occupies an intermediate position between the "pure" Panic and MDD groups. Classification of the "Mixed" patients based on the discriminant function coefficients of the Schedule for Affective Disorders and Schizophrenia and sleep analysis of the "pure" groups (PRI MDD and Panic) reveals that some patients are classified as true PRI MDD while others are classified as falling somewhere along the PRI-MDD/Panic spectrum. The separation of the PRI MDD from Panic and Normals, however, is clear, suggesting that sleep can be successfully used as a physiological marker in the separation of these conditions.

Adult↗
PubMed1985

Interaction of bovine seminalplasmin with Escherichia coli RNA polymerase in the presence of rifampicin.

The interaction of bovine seminalplasmin and rifampicin with E. coli RNA polymerase was studied using fluorescence spectroscopy. Both seminalplasmin and rifampicin are known to be the inhibitors for the initiation of RNA synthesis in E. coli. Rifampicin quenced the intrinsic fluorescence of RNA polymerase and seminalplasmin when excited at 280 nm. However, excess of seminalplasmin reversed the quenching of RNA polymerase fluorescence by rifampicin. Upon addition of rifampicin to the seminalplasmin-RNA polymerase complex, no change in fluorescence spectrum was observed. It appeared that although rifampicin could form complexes with RNA polymerase and seminalplasmin alone, no binding domain was available for rifampicin in the RNA polymerase-seminalplasmin complex. These observations are discussed in the light of the 'initiation site' of E. coli RNA polymerase.

Animals↗
PubMed1985

Cholinergic REM induction response: separation of anxiety and depression.

Five groups of subjects underwent EEG sleep recordings, arecoline rapid eye movement (REM) induction response testing, and Schedule for Affective Disorders and Schizophrenia (SADS) interview. Group I: 20 patients with primary major depressive disorder (MDD) (endogenous) without any coexisting anxiety disorder; Group II: 19 primary MDD (endogenous) patients with secondary panic, GAD, or phobic disorders; Group III: 18 patients with primary anxiety disorder without coexisting MDD; Group IV: 14 patients with primary anxiety plus secondary MDD; Group V: 26 normal controls. Modified Research Diagnostic Criteria (RDC) were used for diagnosis, based on the SADS interview. There was considerable overlap of SADS scaled scores between patient groups, which is consistent with a heterogeneous clinical presentation of depressive and anxiety states. REM latency was significantly shorter in patients with primary MDD (without anxiety) as compared with that in patients with primary anxiety (no MDD) and normals. Arecoline REM induction response time was significantly shorter in both primary affective groups (I and II) as compared with primary anxiety (no MDD) patients and normal controls. REM latency and arecoline REM induction time was not significantly different between the primary anxiety groups (III and IV) and normals. The study highlights the use of biological markers in differentiating between clinical syndromes confounded by mixed or overlapping phenomenology.

Adult↗
PubMed1985

Cholinergic REM sleep induction response correlation with endogenous major depressive subtype.

We compared central cholinergic responsiveness (using the latency to induction of rapid eye movement sleep after arecoline challenge as a response marker) in 90 subjects: patients with major depressive disorder (MDD) (n = 53), nonaffective psychiatric controls (n = 17), and normal controls (n = 20). MDD patients as a whole showed a supersensitive cholinergic response compared to nonaffective patients and normal subjects. Further analysis indicated a strong association between cholinergic supersensitivity and endogenous subtype of MDD, including a significant correlation with specific endogenous features such as distinct quality of mood, anhedonia, lack of reactivity, and agitation. Unlike rapid eye movement (REM) latency (a more conventional physiological marker), cholinergic sensitivity did not correlate with age or severity of illness but only with the presence of endogenous features. Previously described sleep physiological correlates such as REM latency and REM density of the first REM period also distinguished between endogenous and nonendogenous MDD. There was a statistically significant correlation between REM latency and arecoline REM induction response.

Adult↗
PubMed1985

A cardioacceleratory response to low-dose arecoline infusion during sleep in patients with major depressive disorder: relationship to REM sleep induction.

We studied the cardiovascular effect of 0.5 mg of arecoline, a centrally active cholinergic muscarinic agonist, infused over a 3-minute period during the second non-REM (rapid-eye-movement) sleep cycle in 23 patients with major depression. A clear-cut cardioacceleratory response, beginning at the second minute of the 3-minute infusion, and reaching a peak about 5-6 minutes from the start of the infusion, was noted. Placebo infusion did not alter heart rate. There was a significant correlation between the magnitude of the heart rate increase and the latency to onset of the second REM period after arecoline infusion (-0.49). Neither baseline nor arecoline-induced heart rate increases were related to age, sex, or sleep stage changes during or following arecoline infusion. Our data suggest the use of the cardioacceleratory response to cholinomimetics as an additional research tool in assessing central cholinergic sensitivity in humans, especially in neuropsychiatric and stress-related states where cholinergic alterations may occur.

Adult↗
PubMed1984

Acetylcholine and alpha 1-adrenergic sensitivity in the separation of depression and anxiety.

Three relatively clear-cut diagnostic groups, namely primary major depressive disorder-endogenous subtype (PRI MDD-E), primary anxiety disorder with no depression (PRI ANX), and normal controls as well as two additional patient groups with mixed or coexisting anxious/depressive diagnoses were studied. Clinical assessment was made by routine psychiatric interview, Schedule of Affective Disorder and Schizophrenia (SADS) research interview, and obtaining family history of MDD. Subjects underwent both routine 'baseline' sleep EEG polygraphic arecoline, a muscarinic, cholinergic agonist infused during sleep. Cholinergic sensitivity was assessed by measuring the time to induction of REM sleep after arecoline infusion. In addition, a subgroup of MDD patients underwent pupillographic testing. Peripheral alpha-adrenergic responsivity was measured by the magnitude of pupillary mydriatic response after local ocular instillation of phenylephrine. Successful separation (83% correct classification) of the 'pure' groups (PRI MDD-E, PRI ANX, and normal) was achieved by discriminant function analysis of sleep EEG variables. Compared to PRI ANX and normal groups, patients with PRI MDD-E had supersensitive cholinergic REM-induction response, shorter REM latency, increased first REM density and REM percent. Separation of the PRI ANX and normal groups was by intermittent awake time, delta sleep percent, and total REM density. Classification of the mixed anxious/depressive groups was next attempted using the discriminant coefficients derived from the above analysis of 'pure' groups. We found that the presence of absence of family history of MDD in patients with mixed diagnosis offered the best prediction of classification into PRI MDD-E and PRI ANX groups, respectively. MDD patients with coexisting panic disorder were significantly subsensitive to phenylephrine-induced mydriasis compared to MDD patients without anxiety.

Acetylcholine↗
PubMed1983

Behavioral, physiological, and neuroendocrine responses to arecoline in normal twins and "well state" bipolar patients.

Cholinergic supersensitivity has been postulated to be an etiologic factor in affective disorder. After several pilot dose-response studies, we administered 8 mg of the cholinergic agonist arecoline subcutaneously to eight pairs of normal volunteer identical twins and eight bipolar patients currently euthymic and unmedicated. During the hour following arecoline administration, the Profile of Mood States (POMS) showed an increase in total mood disturbance in both patient and control groups. Mean systolic blood pressure, pulse, plasma cortisol, prolactin, and growth hormone also increased. Anger and elation scores on the POMS showed significant concordance in identical twins, as did change in prolactin, implying that these are the components of drug response possibly influenced by genetic factors. None of these responses differentiated well state patients from controls. Thus, mood, behavioral, and neurochemical responses to arecoline, which appears to have nonspecific neurochemical effects at the dose employed, are not markers of vulnerability to affective illness.

Arecoline↗
PubMed1983

Monoamine metabolites as predictors of antidepressant response: a critique.

Monoamine metabolite measurements are being increasingly used for making nosological, symptomatological and pharmacological profiles of the affective disorders. A number of unresolved methodological issues question the validity of using baseline metabolite levels for predicting treatment response. Some studies show correlations between baseline metabolite levels and response to treatment with specific antidepressant agents. Effects of antidepressant treatment on metabolite levels may be useful in predicting drug response.

Antidepressive Agents↗
PubMed1983

Pharmacology of the human iris: development and use of challenge strategies in the study of antidepression response.

Basic physiological and neurochemical control mechanisms of human iris musculature are reviewed. The advantages and limitations of using pupillary responses to cholinergic and adrenergic drug challenges as peripheral indices of neuronal receptor sensitivity, are examined. A group of 15 depressed patients were tested with ocular instillation of pilocarpine and phenylephrine before and during treatment with Tranylcypromine. No change of pilocarpine sensitivity was found. A significant enhancement of phenylephrine sensitivity during weeks 3-5, but not during the first or second week of treatment was noted. The above potentiation of alpha-adrenergic responsiveness was correlated with clinical recovery.

Depressive Disorder↗
PubMed1983

Clinical strategies for evaluating ECT mechanisms--pharmacological, biochemical and psychophysiological approaches.

Although ECT is a highly effective treatment for severe depression and other psychiatric syndromes, its mode of action is not known. Recent studies have suggested that effects of ECT on central neurotransmitter receptors may underlie its therapeutic action. The effects of chronically administered electroconvulsive shock on receptors for dopamine, serotonin, noradrenaline, acetylcholine and endorphins in rodent brain, are reviewed. Strategies for evaluating the relevance of these animal findings to mechanisms of action of ECT in humans are discussed.

Animals↗
PubMed1983

A twin study of cholinergic REM induction.

Seven monozygotic twin pairs were found to display concordance for sensitivity to REM sleep induction by arecoline (intraclass correlation (ri) of 0.69, F = 5.35, p less than 0.02). The REM1-REM2 interval on the placebo night did not show significant concordance (ri = 0.05, F = 1.11, p = 0.44). Our previous study suggested that increased sensitivity to the muscarinic agonist arecoline, as measured by time to onset of the second REM period during sleep, may be an indicator of vulnerability to affective disorder. The present finding of twin concordance in response to arecoline suggests genetic variation in sensitivity of CNS muscarinic cholinergic receptors. Such increased sensitivity may play an etiologic role in affective disorder.

Adolescent↗
PubMed1982

The effect of naloxone on normal human sleep.

Placebo and naloxone (4, 8, and 12 mg) were infused on separate nights in a double-blind fashion over a 20-min period between the 25th and 45th min of sleep in normal volunteers. Naloxone produced a dose-dependent increase in REM latency (the time from onset of sleep until the first REM period), and duration of the first REM period and second NREM period. The number of REM periods was also reduced.

Dose-Response Relationship, Drug↗
PubMed1982

Free and bound choline blood levels after phosphatidylcholine.

In six normal subjects we investigated the effects of oral phosphatidylcholine (lecithin) on the concentrations of plasma choline, erythrocyte choline, and choline-containing lipids. Plasma choline levels rose 1 hr after treatment and remained elevated for 8 hr, with peaks at 3 and 4 hr after phosphatidylcholine. Erythrocyte choline levels also rose, although the rise was slightly delayed relative to plasma choline. There was no change in the plasma choline-containing lipid concentration. These results demonstrate that, in normal subjects, oral phosphatidylcholine indices prolonged rises in plasma and erythrocyte choline concentrations and is therefore useful when such effects are desired.

Choline↗
PubMed1982

Cholinergic regulation of mood and REM sleep: potential model and marker of vulnerability to affective disorder.

To test the hypothesis that depression and REM sleep share common cholinergic mechanisms the authors administered arecoline 25 min after completion of the first REM period to 14 patients with remitted bipolar affective disorder, 15 normal controls, and 5 subjects with a personal or family history of affective disorder. The second REM period occurred significantly sooner in the remitted patients than in the normal controls. The patients also had a significantly higher density of eye movements during the first REM period and a higher percentage of REM sleep. The authors believe that increased cholinergic sensitivity and REM density may be biological markers of increased vulnerability to bipolar affective illness.

Acetylcholine↗