Magnitude Of Startle Response Research Articles

Potentiated startle: Its relation to freezing and shock intensity in rats.

Acoustic startle response and freezing were measured in a potentiated startle paradigm in which a startle stimulus was presented either alone or in the presence of a light conditioned stimulus (CS) which had been paired previously with either 1-mA or 3-mA footshock. During the CS the 1-mA group had higher startle amplitudes and a higher percentage of freezing than the 3-mA group. Startle amplitude was positively correlated with freezing under all conditions. The nonmonotonic relation between potentiated startle and shock intensity replicated Davis and Astrachan's (1978) study. However, rather than suppressing startle, as they suggested, freezing facilitated startle and, like startle amplitude, was nonmonotonically related to shock intensity. Experiment 2 replicated these results and showed a regularly decreasing monotonic extinction function for potentiated startle and shock-associated freezing for both shock-level groups. Brown, Kalish, and Farber (1951) reported that the magnitude of the acoustic startle response was increased when the startle-eliciting stimulus was presented in conjunction with a stimulus previously paired with shock. This phenomenon, now commonly called the potentiated startle effect, has been frequently

Activity, startle magnitude, and prolonged food and water deprivation: Two further failures to duplicate

Studies from one laboratory have shown deprivation-induced attenuation of startle response magnitudes, but another laboratory has reported failures to show any relationship between these variables. In an attempt to locate possible procedural contributions to this discrepancy in outcomes, our Experiment 1 involved 20 massed startle-stimulus presentations (30-sec ISI) to rats that had gone either 43 h or 1 h since eating (80% body weights equated for groups). Experiment 2 entailed spaced presentations (four trials per five bidaily sessions, 20-min ISI) to rats that had gone either 43 h or 1 h since drinking (80% weights also equated). Activity prior to, during, and after startle presentations also was recorded. Although group startle magnitudes differed on some trial blocks of both experiments, these differences were not systematically related to either of the deprivation conditions. Mean activity level was sensitive to startle-stimulus presentations, and showed systematic trial-block rates of decline for periods prior to, during, and following startle presentations that were identical for all groups.

Central noradrenergic involvement in yohimbine excitation of acoustic startle: Effects of DSP4 and 6-OHDA

It was previously shown that i.p. administration of the a 2-adrenergic antagonists yohimbine increased the magnitude of the acoustic startle response in rats 11. The purpose of the present study was to determine possible central noradrenergic involvement in yohimbine's effect on startle. Pretreatment with N-(2-chloroethyl)-N-ethyl-2-bromo-benzylamine (DSP4; 50 mg/kg, i.p.; 1–2 days before testing) completely blocked the excitatory effect of yohimbine on startle. DSP4 reduced forebrain and spinal cord NE levels with the and 56%, respectively, without affecting forebrain or spinal serotonin (5-HT), or forebrain dopamine (DA). Pretreatment with the NE reuptake blocker desmethylimipramine (DMI; 20 mg/kg, i.p.; 30 min before DSP4) prevented the ability of DSP4 to block the yohimbine effect. DMI partially reversed the NE-depleting effects of DSP4. Neither bilateral adrenalectomy nor intravenously administered 6-hydroxydopamine (6-OHDA; 20 mg/kg; 1–2 days before testing) altered the excitatory of yohimbine, indicating that peripheral NE is not involved. 6-OHDA (2 × 200 μg) injected into the lateral ventricles blocked yohimbine's effect, and depleted NE by 95% (spinal cord) adn 86% (forebrain), without affecting 5-HT in either region. 6-OHDA also depleted forebrain DA levels by 49%. Finally, intrathecal administration of 6-OHDA (20 μg; 14 days before testing) into the subarachnoid space of the lumbar spinal cord blocked the excitatory effect of yohimbine, and produced an extensive (94%) depletion of spinal cord NE. Intrathecal 6-OHDA did not alter spinal levels of 5-HT or forebrain levels of NE, 5-HT or DA. In summary, these data indicate that central descending NE neurons are necessary for yohimbine's excitatory effect on startle.

Decreased startle reactivity in the end-to-side portacaval shunted rat

A rat with an end-to-side portacaval anastomosis (PCA) is an extensively used experimental animal for characterization of biochemical alterations following diversion of portal blood flow from the liver; but few behavioral abnormalities have been detected. Biochemical changes observed in rats after PCA include increased plasma and brain levels of the serotonin precursor tryptophan, with increased brain serotonin and its metabolite 5-hydroxyindoleacetic acid. Accumulating evidence indicates that serotonin may be involved in the modulation of the startle response in the rat. In this study, the magnitude of startle responses to both tactile and auditory stimuli were shown to be abnormally decreased in chronic PCA rats. The simplicity of this animal model and the reproducibility of the effect suggest that evaluation of startle responses in rats with PCA may enable assessments of the efficacy of putative therapeutic strategies for the treatment of some of the dysfunctions associated with hepatic encephalopathy.

Opposite effects of intraventricular serotonin and bufotenin on rat startle responses

Rat startle responses to air puffs were monitored in a stabilimeter during the intraventricular infusion of various doses of 5-hydroxytryptamine (5-HT) or the putative hallucinogenic congener of 5-HT, 5-hydroxy-N, N-dimethyltryptamine (5-HDMT) or saline. Qualitatively opposite effects were observed, with 5-HT producing a dose-dependent decrease in responsivity and 5-HDMT increasing the magnitude of startle responses. No specific effects of either compound could be demonstrated on the presumably separable processes of sensitization and habituation. The results are discussed in the context of a central serotonergic system which facilitates behavioral inhibition and which antagonized by indoleamine hallucinogens.

Induction of rage in rats by central injection of 6-hydroxydopamine

Intracisternal injection of 300 μg of 6-hydroxydopamine in male rats elicited a syndrome of hyperreactivity or hyperemotionality, i.e., rage, similar to that previously reported after septal or ventromedial hypothalamic (VMH) lesions. Specifically, rats showed increased resistance to capture as well as increased number and magnitude of startle responses compared to vehicle injected or normal controls. As with septal but not VMH lesions, this rage subsided with repeated testings (handling). These findings are discussed with regard to the possible importance of brain neurotransmitters in the expression of behaviors.

Parachlorophenylalanine and habituation to repetitive auditory startle stimuli in rats

The relationship between brain serotonin levels and habituation of a skeletal-motor startle response was studied using parachlorophenylalanine (PCPA), a drug which inhibits the formation of serotonin. Depletion of brain serotonin by PCPA slows down, but does not prevent, habituation. PCPA given to rats that were habituated before starting drug treatment causes a transitory increase in startle response magnitude. Whether PCPA is administered before or after habituation, the treated rats exhibit heightened reactivity to startle stimuli following exposure to novel stimuli. These results suggest that brain serotonin plays a role in inhibitory processes.

Startle response circadian rhythm in rats: Lack of correlation with motor activity

Acoustic startle response magnitude in rats exhibits an age related circadian rhythm beginning at sexual maturity rising to a peak between 70 and 100 days followed by a fall. At 90 days the night startle response magnitude is over 90 per cent greater than during the day. Night startle response latency is also significantly shorter at this age. Startle response magnitude did not correlate with motor activity when immature and mature animals were compared during day and night conditions. A dose of amylobarbitone sodium causing 50 per cent reduction in motor activity at night did not affect startle response magnitude, and this was also observed following a dose of dexamphetamine causing a 36 per cent increase in motor activity during the day.

Magnitude of the startle response and drive level.

The hypothesis that greater drive would be reflected in larger magnitude of startle response to an abrupt auditory stimulus was investigated. The first experiment provided direct support of this hypothesis, demonstrating that rats deprived of water for 48 hr. showed a significantly greater startle response than both 0- ( p < .01) and 24-hour ( p < .025) deprived rats, who did not differ from each other. The second experiment showed an increase in startle in the presence of a former SΔ and a decrease in startle in the presence of a former SD. The results were taken to support the hypothesis of a direct relationship between drive level and startle magnitude, although problems associated with differential postural adjustments affecting the data could not be ruled out.

A method for measuring acoustic startle response latency and magnitude in rats: Detection of a single stimulus effect using latency measurements

A method is described for measuring startle response magnitude in terms of acceleration using an accelerometer transducer with suitable frequency characteristics to enable accurate measurements of latency to be made. Cine photography synchronised with the accelerometer trace was used to investigate the body movements accompanying the startle response. Histograms show a normal distribution for startle response magnitude and a skew distribution for startle response latency. Significant reductions in startle response latency occur without change in startle response magnitude when a single large stimulus is followed by a second stimulus 24 hr later. This effect is dependent upon stimulus strength, a weak stimulus resulting in a significant reduction in startle response magnitude without change in startle response latency, indicating habituation.

Conditioned fear and magnitude of startle response: a replication and extension.

Conditioned fear and magnitude of startle response: a replication and extension.

The effect of amobarbital sodium on conditioned fear as measured by the potentiated startle response in rats.

The startle response in rats to a sudden sound was increased when the startle was elicited in the presence of a flashing light (CS) which had previously been paired with electric shock. The magnitude of this potentiated startle was used as a measure of the conditioned fear elicited by the CS. The effects of different doses of amobarbital sodium on the potentiated startle, the startle in the presence of a flashing light which had not been paired with shock, and the startle to electric shock were tested. It was found that the drug reduced the magnitude of the potentiated startle response and reduced even more the startle to electric shock, but apparently had little, if any, effect on the startle to loud sound in the presence of a neutral CS. The effects lasted for at least 90 min after i.p. injections of the drug. The action of amobarbital was interpreted in terms of a selective reduction in the strength of the fear drive, but other interpretations were not ruled out. The fact that this drug produced differential effects on startle responses elicited in different ways, suggests that such responses may be useful measures of differential psychopharmacological effects.

Conditioned fear as revealed by magnitude of startle response to an auditory stimulus.

Conditioned fear as revealed by magnitude of startle response to an auditory stimulus.