Startle Threshold Research Articles

The sounds of silence: cessation of singing and song pausing are ultrasound-induced acoustic startle behaviors in the katydid Neoconocephalus ensiger (Orthoptera; Tettigoniidae)

Previous studies of acoustic startle in insects have dealt with behavioral and/or neural mechanisms employed in evading aerially hawking, echolocating bats; however, insects also face terrestrial predators. Here we describe an acoustic startle response of the nocturnal katydid, Neoconocephalus ensiger. Stridulating males disturbed in the field perform obvious antipredatory behaviors--cessation of singing, freezing, jumping, and evasive flight. Under controlled laboratory conditions we found that cessation of singing and song pausing are ultrasound-specific behaviors: when stimulated with pulsed ultrasound (20-100 kHz), but not audio-sound (< 20 kHz), males cease mate calling or insert pauses in their song. A second factor influencing acoustic startle is the phase of stimulation: an acoustic startle response occurs only when the pulse of ultrasound arrives during the window of silence between stridulatory syllables. The average startle threshold and response latency was 70 +/- 5 dB SPL and 34.2 +/- 6.0 ms, respectively. N. ensiger is particularly useful for examining acoustic startle responses of nonflying insects because (1) its calling song is broadband and contains ultrasound, thus the possibility exists of confusion over the biological meaning of ultrasound, and (2) this species shows the classic bat-avoidance response while flying, so a direct comparison between two types of acoustic startle is possible within the same species.

Two-tone suppression of the ultrasound induced startle response in a cricket

For the ground cricket, Eunemobius carolinus, frequencies &amp;gt;20 kHz elicit an acoustic startle response during flight. No startle responses are elicited by single pulses of low-frequency stimuli. However, simultaneous presentation of a low-frequency signal with ultrasound can suppress the startle response. The effect of frequency on suppression was measured for seven frequencies (3–9 kHz) at four intensities of the startle stimulus (40 kHz): 5, 8, 10, and 12 dB above startle threshold. Suppression was tuned to frequencies near 5 kHz. This effect of frequency on suppression diminished slightly at the higher ultrasound intensities, however. Because suppressor growth (change in suppression dB versus change in 40-kHz dB) was &amp;gt;1 for 5–7 kHz and &amp;gt;1 for 3 to 4, 8 to 9 kHz, equal suppression curves flattened at the highest ultrasound levels. Startle threshold decreases with increases in ultrasound duration, and temporal integration time constants were estimated to be 32 ms. In nonsimultaneous presentations, however, no suppression occurs when the suppressing tone is &amp;gt;2 ms after and &amp;gt;5 ms before the ultrasound stimulus. These times suggest that across-channel integration time is shorter than within-channel integration. [Supported by NIMH.]

Habituation and Sensitization of the Acoustic Startle Response in Rats: Amplitude, Threshold, and Latency Measures

The amplitude of the acoustic startle response habituates to repetitive stimulation. The input and output of the startle system were measured to determine if the decrease in startle amplitude during repetitive stimulation is due to an increase in the startle threshold. Two experimental approaches were used in 35 Sprague–Dawley rats to probe the relationship between the input (the sound pressure level of the stimulus) and the behavioral output (startle amplitude). The results show that the minimum threshold for a response does not change during habituation; rather, the slope of the dependence of startle amplitude on stimulus level decreases. Because habituation does not influence startle threshold we propose that the site for habituation is located in the neural circuitry downstream from the site for startle threshold. Besides amplitude and threshold, as an additional parameter we measured startle latency. In general, the latency of the acoustic startle response is negatively correlated with the response amplitude. This correlation has been repeatedly shown, therefore one would expect a latency increase during the amplitude decrease caused by habituation. However, the latency of the startle reaction also decreased during the course of repetitive stimulation. According to the dual process theory of habituation, a stimulus has both a response-decreasing, i.e., habituating, as well as a response-increasing, i.e., sensitizing, influence on a behavior (Groves & Thompson, 1970). Our explanation of the present results is that startle amplitude is reduced following repetitive stimulation because it is mainly influenced by habituation; latency, however, is shortened because it is mainly influenced by sensitization.

Flinders resistant hypocholinergic rats exhibit startle sensitization and reduced startle thresholds

Based on the hypothesis that depression involves a cholinergic-adrenergic neurotransmitter imbalance, a putative genetic animal model of depression has been developed by selectively breeding rats to exhibit hypocholinergia (Flinders Resistant Line — FRL), or hypercholinergia (Flinders Sensitive Line — FSL). The present experiments were designed to test the behavioral reactivity of these rats to external stimuli by measuring acoustic startle responses. The FRL rats exhibited lower startle thresholds compared to both FSL and control rats, while the FSL rats' startle thresholds were between those of controls and FRL rats. Despite the differences in thresholds, the three groups demonstrated similar levels of maximal startle reactivity to a high-intensity acoustic stimulus. With repeated stimulus presentations, FRL rats developed startle sensitization, a rarely observed phenomenon, while FSL and cotrol rats exhibited habituation. There were no differences between the three groups in prepulse inhibition of startle. These results indicated that FRL rats exhibited interesting startle phenomena that are characteristic of certain psychiatric disorders, such as schizophrenia, post-traumatic stress disorder, and, potentially, depression.

Collision-like interactions between acoustic and electrical signals that produce startle reflexes in reticular formation sites

A startle-like response can be evoked at low currents by one-pulse electrical stimulation of reticular formation sites from the rostrolateral pons to the caudomedial medulla. To test whether this response is mediated by the same reticular formation neurons as those that mediate the acoustic startle, we delivered a brief, subthreshold acoustic stimulus followed by an 0.1-ms electrical pulse to one side of the reticular formation of rats. The current thresholds for electrical startle were usually powerfully reduced (50–80%) whenever the acoustic stimulation was presented within 5 ms of the electrical pulse. This summation was, however, interrupted by brief (0.2–1.0 ms) spike-like increases in threshold when the electrical pulse was delivered 4.0–4.6 ms after the offset of the acoustic stimulus. The timing of the spike-like increase in threshold shifted to longer intervals in more caudal sites, consistent with the conduction of action potentials in the startle pathway. For example, the increase occurred at an interval of 4.1 ms near the ventral lateral lemniscus (VLL) and at intervals of 4.4–4.6 ms for sites in the pontine or medullary reticular formation The increases in startle threshold are attributed to collisions between antidromic action potentials evoked by the electrical pulses and orthodromic action potentials evoked by the acoustic stimuli. These results suggest that the neurons in reticular formation that produce the acoustic startle reflex overlap greatly with the neurons that mediate electrically evoked startle-like responses. Also, the acoustic signals mediating the startle reflex must be, in large part, a synchronous volley of action potentials conducted by longitudinal bundles of reticular formation axons.

Cholinergic mechanisms in startle and prepulse inhibition: effects of the false cholinergic precursor N-aminodeanol.

We examined the effects of cholinergic deficiency on prepulse inhibition (PPI) of the acoustic startle. Rats treated with a choline-free diet that contained the false cholinergic precursor N-aminodeanol showed great deficit in PPI. This deficit does not appear to be secondary to an increase of stereotyped behaviors. Startle threshold was also greatly reduced, as these rats startled to the 70-dB prepulse and the baseline startle amplitude was increased by 60% over the control rats. Arecoline (4 mg/kg) partially reversed the deficit in PPI. This improvement persisted beyond the period of drug treatment. On the other hand, scopolamine (1 mg/kg) reduced PPI in the control rats. These results suggest that cholinergic systems play a major role in both the elicitation and prepulse inhibition of startle.

Low current electrostimulation produces naloxone-reversible analgesia in rats.

A new form of transcranial electrostimulation (TE) has been shown to induce analgesia in rats, as measured by the wet tail flick test. Charge-balanced rectangular current pulses of very low amplitude were delivered bilaterally into low impedance regions of the rat pinnae. The resultant analgesia was studied as a function of systematic variations in stimulus frequency, amplitude and duration. The optimal current for inducing analgesia was found to be 10 microA, well below the startle threshold, and several orders of magnitude below effective stimulus current levels required for other treatment modalities. The optimal stimulation duration was 30 min, during which time a slow onset of analgesia was noted. Significant analgesia persisted for at least 200 min after stimulation ended, and no evidence was found of tolerance developing in the course of 5 daily stimulation sessions. Consistent with findings for other forms of electrostimulation, the analgesic effect of TE was abolished by subcutaneous injection of 3 mg/kg naloxone, suggesting that the mechanism of TE analgesia has an endogenous opioid component.

The startle response to acoustic stimuli near startle threshold: effects of stimulus rise and fall time, duration, and intensity.

ABSTRACTThe present study assessed the interaction of several stimulus parameters in the elicitation of the startle response in humans. Broadband noise stimuli with intensities of 80 and 85 dB(A) and durations of 30 and 50 ms were presented to four groups of 15 college undergraduates. Within subjects, stimulus rise and fall times of 2.5, 10, and 25 ms were presented in a 3 × 3 factorial design. Amplitude, probability, and latency of integrated EMG activity from orbicularis oculi (eyeblink) were assessed. As stimulus rise time increased, response amplitude and probability decreased, and response latency increased, for both durations and both intensities tested. A main effect of stimulus duration on response probability was found, with higher probability for 50‐ms than for 30‐ms stimuli. In conjunction with previous research which found no effect of stimulus rise time on startle responding with more intense stimuli, these results suggest that startle response elicitation is determined by an interaction of stimulus parameters, with manipulation of some parameters being more effective at certain levels of other parameters.

Acoustic startle threshold of the albino rat (Rattus norvegicus).

The startle threshold of the albino Sprague-Dawley rat runs parallel to the curve of the hearing threshold. The difference between the startle and hearing threshold is 87 dB (SPL) at a background noise level of 75 dB (SPL). At 110 dB (SPL), the threshold has a range from 2 kHz to 50 kHz with a minimum at 10 kHz and a second minimum at 40 kHz. Amplitude and latency of the startle response are not only dependent on the sensation level of the acoustic stimulus but also on the frequency. At threshold, only the head movement component of the startle response is elicited.

Sensory-motor function in the aging rat

The purpose of this research was to describe the effects of age on (1) reactivity to auditory and painful stimuli, (2) sensory thresholds for auditory, visual, and painful stimuli, and (3) stimulus processing time. This research is part of a larger effort to develop a behavioral profile which can be used to delineate the effects of age on reflexive, sensory, central, and motor function. The primary behavioral measure used in this research was the startle response and inhibition of that response by weak stimuli presented just prior to the startle-evoking stimulus. Reactivity to painful stimuli, as measured by the magnitude of the startle response to electric shock, did not decline until 30–31 months of age, the oldest age examined. In contrast reactivity to white noise declined steadily with age beginning at least as early as 12–13 months. Sensory thresholds for shock measured by a startle threshold technique did not decline markedly with age. Similarly auditory thresholds for a broad band of white noise, measured by either the startle threshold technique or a lead stimulus inhibition of startle procedure, showed little decline during the first 2 years of life; after that age, however, the loss was quite pronounced. In contrast, sensory thresholds for light, as measured by lead stimulus inhibition of startle, showed a steadier and proportionately greater decline beginning at 10 months of age, the youngest age studied. Sensory information processing time—the time required for a lead stimulus to inhibit the auditory startle response—was remarkably unaffected by age. Peak inhibition occurred at 60 ms and the temporal pattern of inhibition was nearly identical at all ages tested.

The effects of chronic administration of ethanol on startle thresholds in rats.

The thresholds for startle responses to electric shock were measured in adult male Wistar strain rats given ethanol daily in doses rising from 3 to 7 g/kg over a 30-day period, and in controls receiving equicaloric doses of sucrose. Tests made 23, 36, or 47 h after ethanol (i.e., during partial or complete ethanol withdrawal) gave threshold values significantly lower than those obtained with sucrose-treated controls. The difference became greater after longer ethanol treatment and larger doses. However, when threshold measurements were made under the acute influence of ethanol in the experimental group, the mean values were virtually equal to those of the sucrose controls. This normalization, by ethanol, of a disturbance produced by absence of ethanol in a chronically treated animal is indicative of physical dependence. Following termination of ethanol treatment there was a gradual return of startle thresholds almost to control values over a relatively short period, indicating that the changes underlying the hyperexcitability are readily reversible.