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Biomedical subjects

A Sattin

Publications and source records attributed to A Sattin.

At least 37 records · Page 2Linked to original sources
PubMed1989

Tetrahydroaminoacridine (THA) as a pharmacological probe in Alzheimer's disease (AD) and other neurodegenerative disorders.

Unlike other potent enhancers of cholinergic function in the central nervous system (CNS), THA appears to sustain improved function in many moderately impaired AD patients when the Summers procedure is followed. THA has a complex pharmacology. In addition to its enhancement of cholinergic transmission a hydroxylated metabolite might chelate aluminum (A1), thereby removing multiple toxicological constraints on CNS function. This mobilized THA metabolite-A1 complex might either be re-distributed to less sensitive sites or removed from the CNS across the blood-brain barrier (BBB). Since the known presence of A1 in AD brain is not necessarily causal, a positivistic approach to research and treatment with THA and its metabolites might serve to clarify this difficult and challenging problem.

Aluminum↗
PubMed1987

Effects of ECT given two vs. three times weekly.

The benefits and side effects of electroconvulsive therapy (ECT) given two vs. three times per week were examined in depressed inpatients. Twenty subjects were randomly assigned to one of two treatment conditions (unilateral ECT two or three times weekly). Examiners without knowledge of treatment condition rated depression and psychiatric status and administered tests of memory and visual-motor problem solving; subjects also provided self-ratings of depression. Measures were collected before treatment and 2 and 4 weeks after treatment began. Both schedules of treatment produced significant and equivalent improvements in psychiatric symptomatology, but visual memory impairment was significantly lower in the twice-weekly group.

Depressive Disorder↗
PubMed1987

The prolonged increase in thyrotropin-releasing hormone in rat limbic forebrain regions following electroconvulsive shock.

We have previously demonstrated substantial increases in thyrotropin-releasing hormone (TRH) in specific regions of rat forebrain two days after single or repeated alternate-day electroconvulsive shock (ECS). To determine longer term effects of ECS-induced seizures on forebrain TRH content, we extended the time of the post-ECS observations to 6 and 12 days following 1 (ECS x 1) or 3 (ECS x 3) alternate-day ECS. Previous observations at 2 days post-ECS were confirmed except that hippocampal content of TRH was higher after ECS x 1. In pyriform cortex TRH remained elevated for 6 days after ECS x 1 and 3, and for 12 days after ECS x 3. In hippocampus TRH was elevated for 6 days after ECS x 1 and tended to remain elevated beyond 2 days after ECS x 3. In anterior cortex the increase persisted 6 days after ECS x 1 and 12 days after ECS x 3. These data show that convulsive seizures can induce sustained elevations of TRH beyond 48 h. This finding may be especially important in pyriform cortex and hippocampus where TRH may function as an endogenous anti-epileptic. Our data are also consistent with a possible role for TRH in affective regulation in the hippocampus, amygdala, pyriform and other cortical regions. Moreover, the present results further advance the analogy of the time-course of the TRH changes in rat to the course of the antidepressant response to electroconvulsive treatment in humans.

Animals↗
PubMed1987

Tetrahydroaminoacridine blocks potassium channels and inhibits sodium inactivation in Myxicola.

In voltage-clamped Myxicola giant axons internally and externally applied tetrahydroaminoacridine (THA) blocked K+ channels with a dissociation constant of 100 microM and slowed their rate of activation. At a concentration of 10 microM, internal THA primarily slowed inactivation of conducting Na+ channels. At 100 microM the decline of the Na+ current during depolarizing pulses was biphasic, with an initial phase 2 to 3 times faster than in control axons. In the presence of THA there was a steady-state inward current accompanied by an increase in amplitude and time constant of Na+ tail currents, as if THA blocked Na+ channels by first entering them and then rendered THA-occluded channels resistant to fast inactivation. THA did not alter activation, prepulse-induced fast inactivation or slow inactivation. The effects of THA on voltage-dependent axonal ion channels might account for central nervous system hyperexcitability seen in some patients treated with THA. Because THA is a potent, centrally active anticholinesterase, even subtle ion channel-directed effects might contribute to its putative antidementia action in clinical states involving a central nervous system deficiency of acetylcholine by selective augmentation of acetylcholine release and/or negation of autoreceptor effects of endogeneous acetylcholine.

Acetylcholine↗
PubMed1985

Effects of subconvulsive and repeated electroconvulsive shock on thyrotropin-releasing hormone in rat brain.

Male Sprague-Dawley rats were given a single electroconvulsive shock (ECS) on alternate days and sacrificed 48 hrs after 1, 3, or 5 seizures. The content of TRH in hippocampus, pyriform cortex and amygdala was increased 2.5-fold, 5.4-fold and 4.3-fold respectively, 48 hrs. after 3 alternate-day electroconvulsive shocks (ECS) and remained unchanged after 2 additional shocks. Pyriform cortex exhibited a significant intermediate increase (1.7-fold) after only 1 ECS. In a second study, rats were sacrificed 48 hrs after a series of 5 alternate-day ECS vs. subconvulsive shocks (SCS). SCS had no significant effect in these same regions, but was seen to alter TRH in striatum. These results provide an interesting parallel to several aspects of clinical electroconvulsive treatment (ECT) of depression. Together with other findings, these data suggest also, that endogenous TRH may play a role in the modulation of convulsive seizures.

Animals↗
PubMed1984

Effect of electroconvulsive shock on the content of thyrotropin-releasing hormone in rat brain.

Five grand-mal seizures were electrically induced in rats on alternate days. Forty-eight hours following the last seizure, TRH was quantitated in extracts of anterior cortex, hippocampus, striatum, thalamus plus midbrain, and hypothalamus. When compared to sham treated controls, TRH was found to be elevated 5-fold in the hippocampus and 2-fold in the striatum with no changes observed in the remaining regions. Since the time chosen for analysis excludes acute post-ictal effects, these results draw attention to a prolonged alteration of TRH levels in specific brain regions in an animal model of electroconvulsive treatment.

Animals↗
PubMed1981

Comparison of MAO, D beta H, and COMT activities in chronic schizophrenics selected on the basis of nailfold capillary pattern.

A group of 17 white male chronic schizophrenic subjects were divided on the basis of plexus visualization score (PVS). High and low PVS subjects were compared to each other and to low PVS controls on measures of platelet monamine oxidase (MAO), rbc catechol-o-methyl transferase (COMT), and plasma dopamine-beta-hydroxylase (D beta H). There were no differences between high and low PVS subjects on any biochemical variable. Schizophrenic subjects had lower platelet MAO activity than controls. Platelet MAO and rbc COMT were significantly correlated in schizophrenic subjects.

Adult↗
PubMed1975

Regulation of cyclic adenosine 3',5'-monophosphate levels in guinea-pig cerebral cortex by interaction of alpha adrenergic and adenosine receptor activity.

Direct assay of adenosine 3',5'-monophosphate (cyclic AMP) in guinea-pig cerebral cortex in vitro has shown that an alpha adrenergic receptor that was previously found to increase tissue content of cyclic AMP requires the co-presence of adenosine. This alpha adrenergic receptor complex was characterized with blocking agents and contrasted with other activities by examining the effect of other biogenic amines on cyclic AMP content in the presence of adenosine. Phentolamine (but not propranolol) reduced the potentiated response to norepinephrine (NE) (or epinephrine) plus adenosine to the level seen with adenosine alone. Theophylline, an adenosine antagonist, blocked the entire effect of NE plus adenosine. The failure of a high Mg++/Ca++ ratio to block the effect of NE plus adenosine argues against indirect mediation of the alpha receptor effect via the release of K+ or via an unknown neurohumoral agent. The complex variety of potentiative interactions between biogenic amines and adenosine is unique to brain. These interactions may be explained by the proposed existence of both independent and dependent receptors. The dependent receptors respond only to the co-presence of two or more neurohumoral agents. An alternative explanation would involve a compartmentally selective impairment of cyclic AMP degradation.

Adenosine↗