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PubMedDate not supplied

Reward craving and withdrawal relief craving: assessment of different motivational pathways to alcohol intake.

AIMS: Craving for the rewarding effects of alcohol may be evoked by conditioned alcohol-like effects whereas conditioned compensatory responses may induce withdrawal relief craving. We tested the hypothesis that drinking in positive emotional states is associated with appetitive reactions to alcohol-associated cues and contributes to reward craving, while conditioned withdrawal is associated with drinking in negative situations and distressful, obsessive preoccupations with alcohol. METHODS: In 38 detoxified alcoholics, the Obsessive Compulsive Drinking Scale was used to assess the craving factors 'impaired control', 'interference with social functioning' and 'obsession'. Affective responses to alcohol-associated visual stimuli were measured with the affect-modulated eyeblink startle reflex, positive and negative drinking situations with the Inventory of Drinking Situations (IDS) and withdrawal-like symptoms preceding alcohol intake with the revised Clinical Institute Assessment for Alcohol Scale (CIWA-Ar). RESULTS: Appetitive reactions to alcohol-associated cues correlated positively with drinking in positive situations and contributed significantly to the craving factor 'interference' with social and work functioning. The severity of withdrawal-like symptoms preceding alcohol intake contributed to the craving factor 'obsession'; however, contrary to our hypothesis, this measure of conditioned withdrawal correlated with drinking not only in negative but also in positive situations. CONCLUSIONS: Drinking in positive and negative situations, appetitive reactions to alcohol and withdrawal-like symptoms contributed differentially to the craving factors 'obsession' and 'interference', supporting the notion of different craving factors with separate underlying mechanisms.

Adult↗

PubMed2003

Affective blindsight: intact fear conditioning to a visual cue in a cortically blind patient.

Blindsight refers to remarkable residual visual abilities of patients with damage to the primary visual cortex (V1). Recent studies revealed that such residual abilities do not apply only to relatively simple object discriminations, but that these patients can also differentially categorize and respond to emotionally salient stimuli. The current study reports on a case of intact fear conditioning to a visual cue in a male patient with complete bilateral cortical blindness. The patient was admitted to the stroke unit of the neurological department because of complete loss of vision. Both CT and structural MRI scans confirmed lesions in both territories of the posterior cerebral artery. No visual evoked potentials could be detected confirming complete cortical blindness. During fear conditioning, a visual cue predicted the occurrence of an aversive electric shock. Acoustic startle probes were presented during and between the conditioned stimuli. Relative to the control condition, startle reflexes were substantially potentiated when elicited in the presence of the conditioned stimuli. No such potentiation was observed prior to conditioning. These data suggest that fear learning to visual cues does not require a cortical representation of the conditioned stimulus in the primary sensory cortex and that subcortical pathways are sufficient to activate the fear module in humans.

Aged↗

PubMed2003

Auditory cortex lesions in the rat impair both temporal acuity and noise increment thresholds, revealing a common neural substrate.

Temporal acuity for acoustic transients in rats with bilateral auditory cortex lesions (n = 6) was compared with that of sham-surgery control rats (n = 4), using a standard gap-detection method. A comparison of sensitivity to quiet gaps in noise and dark gaps in light tested for a cross-modal effect of the lesion. The groups were compared also in their sensitivity to noise offset, to noise increments, and to noise pulses presented in quiet. Stimulus detection was assessed with the startle reflex modification procedure, which uses changes in reflex expression caused by stimuli presented immediately before reflex elicitation as the objective evidence for their detection. There were no group differences in sensitivity to noise offset, noise pulses, or dark gaps in light. In contrast, the lesion reduced sensitivity to noise increments and eliminated gap detection. These deficits were maintained for 1 month and only partially recovered 2 months after surgery. The data indicate that the auditory cortex is critically important for temporal acuity in hearing, and suggest that its contribution to gap detection is to enhance the salience of noise increments at the end of the gap.

Acoustic Stimulation↗

PubMed2006

Neurophysiological endophenotypes of schizophrenia: the viability of selected candidate measures.

In an effort to reveal susceptibility genes, schizophrenia research has turned to the endophenotype strategy. Endophenotypes are characteristics that reflect the actions of genes predisposing an individual to a disorder, even in the absence of diagnosable pathology. Individual endophenotypes are presumably determined by fewer genes than the more complex phenotype of schizophrenia and would, therefore, reduce the complexity of genetic analyses. Unfortunately, despite there being rational criteria to define a viable endophenotype, the term is sometimes applied indiscriminately to characteristics that are deviant in affected individuals. Schizophrenia patients exhibit deficits in several neurophysiological measures of information processing that have been proposed as candidate endophenotypes. Successful processing of sensory inputs requires the ability to inhibit intrinsic responses to redundant stimuli and, reciprocally, to facilitate responses to less frequent salient stimuli. There is evidence to suggest that both these processes are "impaired" in schizophrenia. Measures of inhibitory failure include prepulse inhibition of the startle reflex, P50 auditory evoked potential suppression, and antisaccade eye movements. Measures of impaired deviance detection include mismatch negativity and the P300 event-related potential. The purpose of this review is to systematically evaluate the endophenotype candidacy of these key neurophysiological abilities. For each candidate, we describe typical experimental procedures, the current understanding of the underlying neurobiology, the nature of the abnormality in schizophrenia, the reliability, stability and heritability of the measure, and any reported gene associations. We conclude with a discussion of the few studies thus far that have employed a multivariate approach with these candidates.

Arousal↗

PubMed1994

Hyperekplexia: report of a nonfamilial adult onset case associated with obstructive sleep apnea and abnormal brain nuclear tomography.

We report the unique occurrence of hyperekplexia and obstructive sleep apnea (OSA) in a 48-year-old male. Polysomnography and multiple sleep latency testing excluded cataplexy, which can be confused with startle attacks. A new imaging finding was a nuclear tomography abnormality in the left frontal lobe. We postulate that this finding may represent a functional cortical lesion of a descending pathway that normally inhibits the startle reflex. Serious complications of pharmacotherapy with clonazepam, the drug of choice for hyperekplexia, can be avoided by first evaluating for OSA.

Brain↗

PubMed1998

Ethanol concentrations approaching minimum alveolar anesthetic concentration are required to suppress learning in a fear-potentiated startle paradigm in rats.

UNLABELLED: We previously demonstrated that desflurane and two nonimmobilizers dose-dependently decrease learning and memory in rats. This suggests that although they do not suppress movement in response to noxious stimuli, nonimmobilizers act like inhaled anesthetics in their effects on learning and memory. Like most conventional anesthetics, nonimmobilizers have a greater affinity for lipid than for aqueous phases. In the present study, we examined the effect of ethanol on learning and memory to test the hypothesis that a large part of the capacity of anesthetics to affect learning depends on an action on a lipid (nonpolar) phase. Unlike volatile anesthetics and nonimmobilizers, ethanol has a greater affinity for water than for lipids. Thus, if our hypothesis is correct, ethanol should be relatively less potent in its suppression of memory. Rats receiving various doses of ethanol were conditioned to fear a light followed by a footshock. Fear conditioning to the light was subsequently assessed by measurement of potentiation of the acoustic startle reflex in the presence, compared with the absence, of light. Ethanol up to 0.54 minimum alveolar anesthetic concentration (MAC) did not abolish fear, but 0.82 MAC ethanol did abolish learning. Expressed as a fraction of MAC or predicted MAC, ethanol is less potent than desflurane or the nonimmobilizer 1,2-dichlorohexafluorocyclobutane in suppressing learning. This finding is consistent with the hypothesis that the capacity of anesthetics and nonimmobilizers to impair learning and memory depends mostly on an action at a nonpolar site. IMPLICATIONS: Abolition of learning and memory is an important property of inhaled anesthetics. This effect primarily results from an action at a lipid (nonpolar) site, rather than a polar site or a water-lipid interface.

Anesthetics, Inhalation↗

PubMed1999

Effects of an auditory startle stimulus on blood pressure and heart rate in humans.

OBJECTIVE: To describe the effects of an auditory startle stimulus on blood pressure (BP) and heart rate (HR) in humans. DESIGN AND METHODS: Twenty-five volunteers, including nine untreated hypertensive subjects, were studied in the supine position. Polygraphic recordings were obtained for finger BP, R-R interval using ECG, respiratory movements using a thoracoabdominal belt and for electrooculomyogram using adhesive electrodes. Haemodynamic estimations were derived by modelling flow from the noninvasive BP signal. A background noise of 55 dB was administered through headphones and two acoustic startle stimuli (110 dB, 1-20 kHz, 0.15 s) were generated at 5-min intervals during the tele-expiratory phase. The sham stimulation (0 dB, event marker) was compared with the effects of the noise stimulus (one-way ANOVA with repeated measures followed by a protected t test for multiple comparisons). RESULTS: A biphasic cardiovascular profile was observed in response to noise stimulation. Blood pressure and HR increases were combined in the early response (0-10 s) observed after the immediate motor contraction (blink). The average systolic BP rise was 18.7+/-2.7 mmHg (peak at 5.1 s) and the average HR increase was 10.8+/-1.1 bpm (peak at 3.4 s) for the first stimulus. These effects were highly significant compared with the sham response (P < 0.01). The second stimulus elicited BP and HR rises of a lesser amplitude (P < 0.01). The delayed response (10-30 s) corresponded with a moderate BP decrease. The haemodynamic indexes suggest that the early rise in blood pressure reflects a rise in total peripheral resistance. CONCLUSION: This is the first description of the BP response to an acute loud noise in humans. The early (within 10 s) BP and HR rises may depend upon the autonomic component of the startle reflex. One application of this test could be the discrimination of the different classes of antihypertensive drugs according to their sites of action.

Acoustic Stimulation↗

PubMed1998

Towards a cross-species pharmacology of sensorimotor gating: effects of amantadine, bromocriptine, pergolide and ropinirole on prepulse inhibition of acoustic startle in rats.

Animal models in behavioral pharmacology can be evaluated based on their face, predictive and construct validity. A further level of validity may be achieved if a model is reproduced precisely across species--from laboratory animal to human--using identical conditions and manipulations to elicit identical behavioral changes. Under circumstances in which a model achieves 'homologous' validity, it should be possible to demonstrate that the same pharmacological agents produce parallel changes in the same behavior (as distinct from the clinical condition that the animal behaviors are hypothesized to model), when studied in laboratory animals and in humans. Studies have demonstrated that the disruption of sensorimotor gating of the startle reflex, measured by prepulse inhibition (PPI), in rats by dopamine agonists exhibits face, predictive and construct validity for the relative loss of PPI in schizophrenia patients. To assess the homologous validity of this model, and to expand its utility in understanding the pathophysiology of sensorimotor gating deficits and in developing novel antipsychotic agents to reverse these deficits, it will be important to study PPI across species, comparing response profiles to identical pharmacological manipulations. In the present studies, we report that PPI in rats is reduced in a dose-dependent manner by four dopamine agonists that can be administered with relative ease to humans. We also report that the PPI-disruptive effects of the clinically useful dopamine agonist pergolide are reversed by both typical and atypical antipsychotics. These studies establish a foundation for pursuing human pharmacological studies of PPI, and for extrapolating the substantial neurochemical and neurophysiological information from animal studies of PPI, towards understanding the neural basis for deficient sensorimotor gating in specific neuropsychiatric disorders.

Acoustic Stimulation↗

PubMedDate not supplied

Exaggerated electrodermal startle responses after intracardiac shock discharges in patients with implanted cardioverter defibrillators.

OBJECTIVE: We studied whether repetitive intracardiac shock discharges of implantable cardioverter defibrillators (ICDs) provoke an enduring enhancement of startle responses. METHODS: The study population comprised 134 patients with an ICD. Among those, 67 patients had experienced shock delivery. Thirty-five patients had received five or more shocks. We used the startle reflex paradigm, which consisted of 15 acoustic stimuli (95 dB, 1000 Hz, 500 ms duration). Skin conductance response was measured using a constant 0.5 V through 8-mm electrodes placed on each subject's nondominant palm. Response magnitude was calculated by subtracting the baseline response level of the 2 seconds immediately preceding tone onset from the maximum response level within 1 to 4 seconds after tone onset. The left orbicularis oculi electromyogram (EMG) response was calculated by subtracting the mean EMG level during the 2 seconds immediately preceding tone onset from the highest EMG level measured within 40 to 200 ms after tone onset. Habituation was defined by the response slope of the regression equation and by the number of trials required to reach the nonresponse criterion. RESULTS: Although EMG response measures of magnitude and habituation failed to yield differences between study groups, patients who had experienced five or more ICD shocks exhibited a significantly larger skin conductance response magnitude in comparison to the patients who had experienced fewer than five shocks (median, interquartile range: 0.364, 0.209-0.618 vs. 0.512, 0.375-0.791; Mann-Whitney U test, p =.007). Poorer habituation in the group with five or more shocks in comparison with the low shock group was confirmed both by the number of trials needed to reach the nonresponse criterion (median, interquartile range: 10, 5-14 vs. 5, 2-13; p =.003) and by the response slope (median, interquartile range: 0.209, 0.116-0.274 vs. 0.262, 0.181-0.332; p =.008). After controlling for potential confounding factors (age, anxiety, aversiveness of stimuli, time since last shock experience, and use of beta-adrenoceptor antagonists), intracardiac shock discharges had the strongest impact on augmented skin conductance response magnitude (adjusted odds ratio = 3.0, 95% confidence interval = 1.3-7.2, p =.01) and impaired habituation (adjusted odds ratio = 2.8, 95% confidence interval = 1.2-6.3; p =.015). CONCLUSIONS: Intracardiac shock discharges are associated with augmented skin conductance responses and slower habituation, indicating sustained sympathetic arousability, which is presumably centrally mediated.

Defibrillators, Implantable↗

PubMed2004

Behavioural correlates of an altered balance between synaptic and extrasynaptic GABAAergic inhibition in a mouse model.

GABAA receptors mediate fast phasic inhibitory postsynaptic potentials and participate in slower tonic extrasynaptic inhibition. Thy1alpha6 mice with ectopic forebrain expression of GABAA receptor alpha6 subunits exhibit increased extrasynaptic GABAA receptor-mediated background conductance and reduced synaptic GABAA receptor currents in hippocampal CA1 neurons [W. Wisden et al. (2002) Neuropharmacology 43, 530-549]. Here we demonstrate that isolated CA1 neurons of these mice showed furosemide-sensitivity of GABA-evoked currents, confirming the functional expression of alpha6 subunit. In addition, receptor autoradiography of the CA1 region of Thy1alpha6 brain sections revealed pharmacological features that are unique for alpha6betagamma2 and alpha6beta receptors. The existence of atypical alpha6beta receptors was confirmed after completely eliminating GABAA receptors containing gamma1, gamma2, gamma3 or delta subunits using serial immunoaffinity chromatography on subunit-specific GABAA receptor antibodies. Behaviourally, the Thy1alpha6 mice showed normal features with slightly enhanced startle reflex and struggle-escape behaviours. However, they were more sensitive to GABAA antagonists DMCM (shorter latency to writhing clonus) and picrotoxinin (shorter latency to generalized convulsions). Tiagabine, an antiepileptic GABA-uptake inhibitor that increases brain GABA levels, delayed picrotoxinin-induced convulsions at a low dose of 3.2 mg/kg in Thy1alpha6 mice, but not in control mice; however, the overall effect of higher tiagabine doses on the convulsion latency remained smaller in the Thy1alpha6 mice. Altered balance between extrasynaptic and synaptic receptors thus affects seizure sensitivity to GABAergic convulsants. Importantly, the increased extrasynaptic inhibition, even when facilitated in the presence of tiagabine, was not able fully to counteract enhanced seizure induction by GABAA antagonists.

Animals↗

PubMed1994

Emotion and psychopathy: startling new insights.

Abnormal affective response in psychopaths is conceptualized within a broad theory of emotion that emphasizes reciprocal appetitive and defensive motivational systems. The startle response is proposed as a specific measure of the directional component of emotional activation. I review the literature that indicates that criminal psychopaths do not show the expected potentiation of the startle reflex that normally occurs during processing of aversive stimuli such as unpleasant photographs or punishment cues. Evidence is presented to demonstrate that this deviant response pattern is specific to individuals who display the classic affective symptoms of psychopathy. The core emotional deviation in psychopathy could be a deficit in fear response, which is defined as a failure of aversive cues to prime normal defensive actions. This emotional deficit may represent an extreme variant of normal temperament.

Adult↗

PubMed1996

Lateralized startle probes in the study of emotion.

Two experiments are reported in which affective modulation of the startle reflex elicited by monaurally presented acoustic probes was further examined. An earlier study in our laboratory obtained significant modulation by affect for probes presented to the left ear, but no significant effect for probes presented to the right ear. Experiment 1 replicated the procedures used in that experiment and obtained the same pattern of effects. Experiment 2 changed the presentation of monaural probes from a blocked to a mixed presentation and again obtained a similar pattern. Modulatory differences in reflex magnitude between pleasant and unpleasant stimuli were consistently large and reliable for reflexes elicited by left ear probes but weak and unreliable for reflexes elicited by right ear probes.

Acoustic Stimulation↗

PubMed2007

Estrous cycle effects on behavior of C57BL/6J and BALB/cByJ female mice: implications for phenotyping strategies.

Systematic behavioral phenotyping of genetically modified mice is a powerful method with which to identify the molecular factors implicated in control of animal behavior, with potential relevance for research into neuropsychiatric disorders. A number of such disorders display sex differences, yet the use of female mice in phenotyping strategies has been a rare practice because of the potential variability related to the estrous cycle. We have now investigated the behavioral effects of the estrous cycle in a battery of behavioral tests in C57BL/6J and BALB/cByJ inbred strains of mice. Whereas the performance of BALB/cByJ female mice varied significantly depending on the phase of the estrous cycle in the open field, tail flick and tail suspension tests, the behavior of C57BL/6J females, with the exception of the tail suspension performance, remained stable across all four phases of the estrous cycle in all of the tests including open field, rotarod, startle reflex and pre-pulse inhibition, tail flick and hot plate. We also found that irrespective of the estrous cycle, the behavior of C57BL/6J females was different from that of BALB/cByJ groups in all of the behavioral paradigms. Such strain differences were previously reported in male comparisons, suggesting that the same inter-group differences can be revealed by studying female or male mice. In addition, strain differences were evident even for behaviors that were susceptible to estrous cycle modulations, although their detection might necessitate the constitution of large experimental groups.

Analysis of Variance↗

PubMed2003

A diminished rate of "physiological decay" at noise offset contributes to age-related changes in temporal acuity in the CBA mouse model of presbycusis.

The persistence of afferent activity at stimulus offset was examined in mice as a function of age (experiment 1) and noise level (experiment 2), using a procedure devised by von Bekesy to study the physiological decay of afferent activity. Noise offset was presented from 1 to 10 ms (the temporal gap) prior to an acoustic startle stimulus, with an abrupt edge or a linear ramp having the duration of the gap. Noise offset inhibited the startle reflex, this effect declining with age. For young (2-3 months old) and "young-old" mice (18-19 months old), the abrupt offset was always more inhibitory than the ramp, even for the one millisecond gap. In "old-old" mice (24-26 months old) abrupt and ramped offsets were not different until the gap exceeded 4 ms. The behavioral difference between abrupt and ramped decay times did not depend on noise level in young mice (4-5 months old), though overall inhibition increased with level. These data indicate that temporal acuity as measured by this gap detection method is limited in very old mice by their reduced ability to follow the abrupt change in noise level at the beginning of the gap.

Acoustic Stimulation↗

PubMed2004

Pharmacologic interactions between the muscarinic cholinergic and dopaminergic systems in the modulation of prepulse inhibition in rats.

Prepulse inhibition (PPI) of the acoustic startle reflex is a sensorimotor gating process known to be deficient in a number of neurologic and psychiatric conditions, including schizophrenia. Multiple lines of evidence have indicated that the dopaminergic and muscarinic cholinergic systems play an important role in modulating PPI. Moreover, interactions between the dopaminergic and muscarinic cholinergic systems are well known; however, little is known about potential interactions between the two systems in modulating PPI. Therefore, the purpose of the present studies was to determine whether interactions occur between the muscarinic cholinergic and dopaminergic systems in modulating PPI. The efficacy of muscarinic cholinergic receptor agonists in reversing the disruption of PPI induced by apomorphine, a D1/D2 dopamine receptor agonist, was evaluated in male Sprague-Dawley rats. The M1/M4-preferring muscarinic agonist xanomeline and the M2/M4-preferring agonist BuTAC [([5R-[exo]-6-[butylthio]-1,2,5-thiadiazol-3-yl-]-1-azabyciclo-[3.2.1])octane oxalate] reversed the apomorphine-induced disruption of PPI in a manner similar to that produced by the D2-like dopamine receptor antagonists haloperidol and olanzapine. The muscarinic agonists oxotremorine, RS86 [[2-ethyl-8-methyl-2,8-diazaspiro(4.5)decane-1,3-dione] hydrochloride], pilocarpine, milameline, and sabcomeline also reversed the apomorphine-induced disruption of PPI. Moreover, the muscarinic antagonist scopolamine also disrupted PPI, and the D2-like receptor antagonist haloperidol, but not the D1-like receptor antagonist SCH23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine], reversed the scopolamine-induced disruption. In addition, xanomeline produced a significant reversal of the disruption in PPI produced by scopolamine. Collectively, the present findings demonstrate that a functional interaction occurs between the muscarinic cholinergic and dopaminergic systems in modulating PPI and that muscarinic cholinergic agonists may be effective in the treatment of the PPI and other cognitive impairments observed in schizophrenia.

Acoustic Stimulation↗

PubMed1980

Prenatal exposure to diazepam alters behavioral development in rats.

Characteristic potentiation of rat locomotion responses and acoustic startle reflexes that normally appear in the third postnatal week was absent in rats exposed to diazepam during the third week of gestation. Loss of these behaviors suggests a long-term effect that may result from changes in cellular development. Tissue undergoing neuronal differentation may be especially sensitive to drugs that act on the central nervous system, and the period in which differentiation occurs is perhaps critical for the induction of changes that are later expressed as altered behavior.

Animals↗

PubMed1994

Information-processing deficits and thought disorder in schizophrenia.

OBJECTIVE: The goal of this investigation was to study the relationship between information-processing deficits and thought disorder in schizophrenic patients. METHOD: Fifty-two subjects diagnosed with schizophrenia were administered tests of information processing and thought disorder. The information-processing tests included visual backward masking and prepulse inhibition of the startle reflex. Thought disorder was measured with the Magical Ideation Scale, the Scale for the Assessment of Positive Symptoms, the alogia subscale of the Scale for the Assessment of Negative Symptoms, and the Ego Impairment Index-human experience variable and its subcomponents derived from the Rorschach. RESULTS: Elevated poor responses on the Ego Impairment Index-human experience variable were significantly correlated with information-processing deficits. In a simultaneous multiple regression, the auditory prepulse inhibition measure was the best predictor of poor responses on the Ego Impairment Index-human experience variable. CONCLUSIONS: The results suggest a correlative relationship between information-processing deficits and thought disorder. The relationship is most apparent when highly sensitive measures of both information processing and thought disorder are used. Furthermore, the prediction of poor responses on the Ego Impairment Index-human experience variable by auditory prepulse inhibition is important, since the neural circuitry of prepulse inhibition is known and involves the modulatory influences of the cortical-striatal-pallidal-thalamic circuit. These findings lend support to the hypothesis that information-processing failures are associated with cognitive fragmentation and thought disorder. More speculatively, these results allow us to hypothesize that impairments in part of the cortical-striatal-pallidal-thalamic circuit may lead to thought disorder, as well as prepulse inhibition deficits.

Adult↗

PubMed1996

Preliminary evidence of an association between sensorimotor gating and distractibility in psychosis.

Impaired sensory gating and increased distractibility are key information-processing deficits in schizophrenia. This study evaluated the hypothesis that distractibility is related to reduced sensory gating. Performance on vigilance and distractibility tasks was compared to prepulse inhibition (PPI) of the acoustic startle reflex in 28 stable chronic psychotic patients. PPI significantly correlated with distractibility task score on a continuous performance test and lateralized attention on the Posner test. These results suggest that performance on tests of distractibility and lateralized attention are related to a measure of sensory gating.

Acoustic Stimulation↗