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Biomedical subjects

Henry Szechtman

Publications and source records attributed to Henry Szechtman.

23 records · Page 2Linked to original sources

How can brain activity and hypnosis inform each other?

Applying P. Teitelbaum's conception of the method of physiological psychology as interlocking stages of analysis and synthesis, the authors examine how studies of brain function can advance the understanding of hypnosis as a psychological process. They consider the exploration of animal analogues of human hypnosis, the study of brain injury in humans as a window on mechanisms underlying hypnosis, the distinct questions that brain-imaging studies of hypnosis can address, and the potential for comparative and developmental approaches to hypnosis as close allies to psychophysiological approaches. They conclude both that hypnosis is a powerful technique for studying the brain mechanisms of conscious experience and that underlying brain mechanisms may shed new light on longstanding theoretical debates about hypnosis.

Animals↗

Enhanced salience and emotion recognition in Autism: a PET study.

OBJECTIVE: This study examined neural activation of facial stimuli in autism when the salience of emotional cues was increased by prosodic information. METHOD: Regional cerebral blood flow (rCBF) was measured while eight high-functioning men with autism and eight men without autism performed an emotion-recognition task in which facial emotion stimuli were matched with prosodic voices and a baseline gender-recognition task. RESULTS: Emotion processing in autistic subjects, compared to that in comparison subjects, resulted in lower rCBF in the inferior frontal and fusiform areas and higher rCBF in the right anterior temporal pole, the anterior cingulate, and the thalamus. CONCLUSIONS: Even with the enhanced emotional salience of facial stimuli, adults with autism showed lower activity in the fusiform cortex and differed from the comparison subjects in activation of other brain regions. The authors suggested that the recognition of emotion by adults with autism is achieved through recruitment of brain regions concerned with allocation of attention, sensory gating, the referencing of perceptual knowledge, and categorization.

Adult↗

D2 receptor blockade in the dorsal raphe increases quinpirole-induced locomotor excitation.

The D2/D3 dopamine receptor agonist quinpirole (QNP) produces biphasic effects on locomotion and can induce oral behaviour. To determine whether or not these behaviours result from actions of QNP at D2 receptors located in the dorsal raphe, nucleus (DRN), rats were pretreated intra-DRN with the selective dopamine D2 receptor antagonist, raclopride (0, 1 or 2 microg) prior to an acute peripheral injection of QNP (0 or 0.5 mg/kg, s.c.). Intra-DRN raclopride did not affect QNP-induced oral activity or QNP-induced locomotor inhibition. However, the high dose of raclopride potentiated QNP-induced locomotor excitation. These data suggest that D2 receptor activation in the DRN suppresses QNP-induced locomotor excitation, an effect that may be related to D2 receptor-mediated alterations in serotonin transmission.

Animals↗

Effect of nicotine on quinpirole-induced checking behavior in rats: implications for obsessive-compulsive disorder.

BACKGROUND: Rats treated chronically in a large, open field with the dopamine D2/D3 receptor agonist quinpirole (QNP) develop compulsive checking behavior as defined by a set of behavioral criteria. This paradigm has been suggested as an animal model of obsessive-compulsive disorder (OCD). Because nicotine blocks various behaviors induced by ontogenetic QNP administration, we asked whether nicotine could attenuate QNP-induced compulsive checking. METHODS: Adult male Long-Evans rats (n = 14/group) were treated twice weekly with saline (control), or with QNP (0.5 mg/kg) for 14-16 injections. On the last two injections, rats were pretreated in random order with an acute dose of nicotine (0.3 mg/kg base) or saline 10 min before administration of QNP or saline; and the effects on checking behavior was examined. The effects of chronic QNP treatment on nicotinic receptors in discrete brain regions were also determined. RESULTS: Chronic QNP resulted in compulsive checking and increases in cerebellar alpha4beta2 and alpha7 nicotinic receptor densities. Nicotine pretreatment significantly reduced one of the three measures of compulsive checking behavior. CONCLUSIONS: Nicotine attenuates some symptoms of compulsive checking in a rat model of OCD; however, the mechanisms of this effect and therapeutic efficacy of nicotinic agonists in OCD require further study.

Animals↗

Altered neurotransmission in brains of autoimmune mice: pharmacological and neurochemical evidence.

Depressive-like behavior is the most profound manifestation of autoimmunity-associated behavioral syndrome in lupus-prone MRL-lpr mice. This led to the hypothesis that chronic autoimmunity and inflammation alter the activity of central serotonergic and dopaminergic systems. Three drugs with a selective mode of action were used to probe the functional status of these two systems in vivo. The behavioral effects of single and repeated intraperitoneal (i.p.) injections of sertraline, quinpirole (QNP) and risperidone were measured in the forced swim and brief sucrose preference tests. In comparison to MRL +/+ controls, autoimmune MRL-lpr mice did not show a reduction in sucrose intake after the administration of sertraline. Acute injection of quinpirole increased floating more in the MRL-lpr than in the control group, while intermittent administration induced self-injurious behavior in both groups. Acute injection of risperidone significantly increased floating in MRL-lpr mice, while repeated administration abolished the difference between the substrains in sucrose intake. These discrepancies in responsiveness implied that the central neurotransmitter activity is dissimilar in the two MRL substrains. This notion was confirmed in a cohort of untreated MRL-lpr and MRL +/+ mice by comparing their neurotransmitter/metabolite levels in several brain regions. In particular, MRL-lpr brains showed increased dopamine (DA) levels in the paraventricular nucleus (PVN) and median eminence (ME), decreased concentrations of serotonin in the PVN and enhanced levels in the hippocampus, as well as decreased norepinephrine (NE) levels in the prefrontal cortex. Behavioral deficits correlated with the changes in PVN and median eminence. These results are consistent with the hypothesis that imbalanced neurotransmitter regulation of the hypothalamus-pituitary axis plays an important role in the etiology of behavioral dysfunction induced by systemic autoimmune disease.

Aging↗