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Biomedical subjects

F Petty

Publications and source records attributed to F Petty.

At least 91 records · Page 5Linked to original sources
PubMed1994

A preliminary neuroendocrine study with buspirone in major depression.

We administered the serotonin-1a agonist buspirone (0.4 mg/kg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III-R major depressive disorder (MDD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = 8). Our findings support a role for the serotonin-1a receptor in the etiology of MDD, specifically at the postsynaptic site.

Adult↗
PubMed1994

Plasma concentrations of gamma-aminobutyric acid (GABA) and mood disorders: a blood test for manic depressive disease?

gamma-Aminobutyric acid (GABA), an inhibitory neurotransmitter that serves about one-third of brain neurons, is involved in the development of depression and in the treatment of depression and mania with pharmacological therapy. Brain activity of GABA may be conveniently measured in plasma, and changes in plasma concentrations of GABA reflect brain GABA activity. Plasma concentrations of GABA are significantly lower than control values in about one-third of patients with major depressive disorder; concentrations are also low in patients with mania and in bipolar patients who are depressed. These low concentrations of GABA appear to persist after recovery from depression and are not increased by treatments that improve depressive symptoms. Follow-up studies suggest that GABA concentrations remain relatively constant over at least 4 years. Additionally, preliminary data suggest that low plasma GABA is a familial marker of mood disorders in a subset of patients. Despite the difficulty of demonstrating that a particular biochemical measure is a true genetic trait marker for vulnerability for development of an illness, the accumulated data suggest that low plasma GABA may represent a biological marker of vulnerability for development of various mood disorders.

Affective Disorders, Psychotic↗
PubMed1993

Intravenous sodium lactate decreases plasma GABA levels in man.

Gamma aminobutyric acid (GABA), an inhibitory neurotransmitter, may play an important role in anxiety. We studied changes in plasma GABA levels in nine healthy subjects before and after infusions of sodium lactate and dextrose. Plasma GABA significantly decreased during infusions of sodium lactate (109.3 +/- 4.4 versus 91.6 +/- 5.1 pmol/ml; P = 0.0001) but not during infusions of dextrose.

Adult↗
PubMed1993

Learned helplessness and in vivo hippocampal norepinephrine release.

Hippocampal norepinephrine release was measured using in vivo microdialysis in rats before and after exposure to inescapable tail shock stress and after testing for learned helplessness. Rats that did not develop learned helplessness after stress had higher basal norepinephrine release after stress than rats developing learned helplessness or than control rats. After the shuttlebox test for learned helplessness, K(+)-stimulated norepinephrine release was lower in learned helpless than in nonhelpless or control rats. These results confirm an important role for the hippocampal noradrenergic system in differential behavioral responses to stress.

Animals↗
PubMed1993

Desipramine does not alter plasma GABA in patients with major depression.

Low plasma GABA is a biological marker for depression in a subset of patients tested. Plasma GABA has been shown to reflect brain GABA activity. This marker has many characteristics of a trait marker for depression, including stability with time, and lack of influence by coincident factors such as gender, season, time, activity or diet. We here report that plasma GABA remained stable after 4 weeks of treatment with desipramine in patients with major depression. Since the levels of plasma GABA did not change with time, nor with clinical improvement, plasma GABA is not a state marker of depression.

Adult↗
PubMed1993

Tridimensional Personality Questionnaire and serotonin in bulimia nervosa.

To determine the relationship between Tridimensional Personality Questionnaire (TPQ) scales and bulimia nervosa, TPQ scores of 27 bulimic women, age range 21-59, were compared with values for an age-matched sample of 128 normal control women drawn from the national norming sample by Przybeck. Scores for Novelty Seeking and Harm Avoidance were significantly higher, while scores for Reward Dependence were significantly lower for the bulimic women. A stepwise regression model of severity of purging on TPQ selected Novelty Seeking and a composite depression score, with Novelty Seeking being the stronger of the two predictors. Whole blood serotonin levels did not relate to TPQ scores or to purging frequency.

Adult↗
PubMed1993

Low plasma GABA is a trait-like marker for bipolar illness.

Plasma gamma-aminobutyric acid (pGABA) is an index of brain GABA activity and a peripheral marker of mood disorder. Previous research has indicated that pGABA is abnormally low in approximately 40% of patients symptomatic with primary unipolar depression. We have now measured pGABA in a series of patients with bipolar disorder. Blood samples for GABA determinations were collected soon after admission to hospital or clinic while patients were symptomatic. In both manic and depressed phase bipolar patients, mean levels of pGABA were significantly lower than in healthy control subjects. The distribution of pGABA in bipolar patients, whether manic or depressed, was similar to that in symptomatic unipolar depression, with 30% to 40% having pGABA levels lower than the control range. These data indicate that low pGABA is not specific to the depressed state, as it is also found in the manic phase of bipolar disorder. Low pGABA may represent a shared biologic correlate between bipolar and unipolar illness.

Adult↗
PubMed1993

Plasma gamma-aminobutyric acid (GABA) is low in alcoholics.

Plasma levels of gamma-aminobutyric acid (GABA) were measured in male alcoholics on admission to inpatient treatment and at discharge after 3 to 4 weeks of abstinence. Free plasma GABA at discharge was significantly lower in alcoholics than in control subjects and specifically identified a subset of 35 percent of the alcoholic patients with levels below the normal range. However, levels of free plasma GABA in recently detoxified alcoholics on admission were not different from those of controls and had a significant positive correlation with liver enzymes and mean corpuscular volume. These data are compatible with a GABA deficit theory of alcoholism in a subset of alcoholics.

Adult↗
PubMed1992

Low plasma gamma-aminobutyric acid levels in male patients with depression.

Plasma levels of gamma-aminobutyric acid (GABA) were significantly lower in males with primary unipolar major depressive disorder than in healthy controls. Although the difference in means between control and symptomatic depressed patient groups was small, the distribution of plasma GABA in the depressed patients was markedly different from controls. Forty percent of depressed patients had plasma GABA levels below those of controls. Plasma GABA levels correlated positively with duration of illness, and negatively with age at onset of the mood disorder and the total Endogenomorphic Symptom Score on the Hamilton Rating Scale. Plasma GABA levels may be a biochemical marker of vulnerability to depression, as opposed to a consequence of the illness. A low GABA condition in depression fits and complements the prevailing biogenic amine hypotheses of depression.

Adult↗
PubMed1992

Effect of acute and chronic benzodiazepines on plasma GABA in anxious patients and controls.

The acute effects of diazepam on plasma GABA were determined in 18 patients with panic disorder, 13 patients with generalized anxiety disorder and 20 healthy controls. All subjects were benzodiazepine-naive. Four logarithmically increasing doses of diazepam/placebo were administered intravenously at 15-min intervals on 2 separate days. Plasma GABA was measured at baseline and 3 min after the highest dose of diazepam/placebo. There was an overall decrease in plasma GABA that was significantly greater following diazepam compared with placebo, but no group differences in response. In a separate group of 18 panic disorder patients receiving chronic benzodiazepine treatment with alprazolam, the same diazepam infusion procedure (no placebo day) produced decreases in plasma GABA similar to those seen in the untreated panic disorder patients. The clinical and physiologic implications of these findings are discussed.

Adult↗
PubMed1992

Prevention of learned helplessness: in vivo correlation with cortical serotonin.

Learned helplessness (LH) is prevented by pretreatment with acute benzodiazepines (BDZs), subchronic tricyclic antidepressants (TCAs), or escapable stress (ES). We have investigated the role of serotonin (5-HT) in LH prevention by these three prevention paradigms, using microdialysis to measure in vivo 5-HT release in frontal cortex (FC) after LH testing. Rats receiving pretreatment before inescapable stress with any of the three methods of prevention--BDZs, TCAs, or ES--showed escape behavior in the shuttle-box test for LH comparable to naive unstressed controls. K(+)-stimulated 5-HT release in all three groups receiving pretreatment was also similar to naive unstressed controls. Rats receiving saline before inescapable stress showed significantly more LH behavior in the shuttle-box task and had significantly lower 5-HT release as well. This suggests that LH correlates with a significant decrease in intracellular releasable 5-HT in FC, and that three different techniques for LH prevention, acute BDZs, subchronic TCAs, and ES all similarly prevent this 5-HT depletion.

Animals↗
PubMed1992

The depressed alcoholic. Clinical features and medical management.

A relationship between depression and alcoholism has long been postulated. A review of prior research studies reveals that though patients with depression do not appear to develop alcoholism to any great extent, recently detoxified alcoholics have a depressive syndrome about 20% of the time. This cannot be accounted for readily from data on family studies or genetic studies, which generally suggest that alcoholism and depression are two independent illnesses, albeit both quite common. Clinically, depressed alcoholics resemble alcoholics more than they resemble depressives. The clinical course of depression when it coexists with alcoholism is generally benign and self-limited, with most patients becoming euthymic over the course of 2-4 weeks without specific antidepressant treatment. In some depressed alcoholics, however, a more chronic depression persists, and may predict a worse outcome for the alcoholism. Treatment of depression in alcoholics should be initially conservative. Tricyclic and other antidepressants should be used with extreme care as they may potentiate toxic effects of alcohol.

Alcoholism↗
PubMed1991

Patient factors predicting early alcohol-related readmissions for alcoholics: role of alcoholism severity and psychiatric co-morbidity.

The current study was undertaken primarily to identify whether psychiatric co-morbidity was associated with the rate and time of alcohol-related inpatient readmissions for a group of 255 patients discharged from alcoholism treatment at a midwestern rural medical center. A structured interview obtained information regarding psychiatric disorders, including depression, antisocial personality disorders and polysubstance abuse, as well as alcohol history and sociodemographics. Ninety-eight subjects (38.4% of sample) were readmitted for alcoholism-related diagnoses within 15 months of discharge. Patients with a long history of heavy drinking, high daily alcohol consumption and history of previous alcoholism treatment were most likely to be readmitted with an alcoholism-related primary diagnosis. Once these variables were controlled for, other major psychiatric disorders, polysubstances abuse and sociodemographic variables did not appear to predict time to readmission. However, other potentially more sensitive outcome measures such as return to drinking were not evaluated in the present study.

Alcohol Drinking↗
PubMed1990

Longitudinal characteristics of hospital use before and after alcoholism treatment.

The frequency of inpatient hospital care for three years before and three years after alcoholism treatment was evaluated for a group of 255 patients of predominantly lower socioeconomic status treated for alcoholism at a rural midwestern medical center in 1983. Subjects were interviewed while in treatment to obtain information regarding alcoholism history and demographics. Hospital care was ascertained from an electronic data file of discharges from 172 acute care hospitals throughout the United States and Puerto Rico. One-third of the sample was never hospitalized for an alcohol-related condition in the years prior to or after alcoholism treatment, and 23% of the sample experienced no hospitalizations at all other than the treatment episode when interviewed. The majority of hospital stays before and after treatment were attributed to alcohol abuse. The frequency and total hospital length of stay for alcohol-related admissions increased yearly before treatment, peaked in the year after treatment, and then declined, but not to earliest pretreatment levels. Subjects experienced significantly more hospitalizations and length of stay after alcoholism treatment than before when comparing both the two three-year periods and the immediate 12 months before and after treatment. More frequent hospital care was also significantly associated with higher levels of daily alcohol consumption and drinking duration but not with sociodemographic indicators.

Adult↗
PubMed1990

Plasma GABA in mood disorders.

Plasma levels of gamma-aminobutyric acid (GABA) were determined in 68 healthy controls and in 133 patients with mood disorder. Plasma GABA levels were significantly lower in the patients with mood disorder compared to controls. Levels of plasma GABA were similar among diagnostic groups (primary unipolar depression, bipolar depression, mania, and secondary depression). No differences in plasma GABA were found in patients classified according to family history, nor were any correlations found between plasma GABA levels and severity of depression as determined by the 17-item Hamilton Rating Scale for Depression. These findings support the notion that low plasma GABA may represent a biological marker for mood disorder.

Affective Disorders, Psychotic↗
PubMed1990

Reversal of chronic hepatic encephalopathy by colonic exclusion: poor correlation with blood GABA levels.

Previous studies have suggested that the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is a key factor in the syndrome of portasystemic encephalopathy. We report the case of a patient with medically intractable portasytemic encephalopathy after portacaval shunt who had marked clinical improvement after creation of an end ileostomy. Plasma GABA and serum ammonia levels were measured before and after ileostomy. Although the clinical syndrome and the EEG improved markedly after the ileostomy, the plasma GABA levels remained markedly elevated. Preoperative and postoperative GABA levels were 865 and 633 pmol/ml, respectively (nl = 100-180 pmol/ml). Our findings confirm previous reports of the efficacy of colonic exclusion in patients with intractable portasystemic encephalopathy. However, our results conflict with the hypothesis that GABA itself is the key mediator of the syndrome.

Ammonia↗