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H U Schnitzler

Publications and source records attributed to H U Schnitzler.

At least 37 records · Page 2Linked to original sources

Lesions of the central gray block conditioned fear as measured with the potentiated startle paradigm.

The amplitude of the acoustic startle response (ASR) in rats is increased in the presence of a cue which has previously been paired with an electric footshock. This phenomenon is termed fear-potentiated startle and is a useful model to investigate the neural systems underlying fear and anxiety. A series of studies have shown, that the amygdaloid complex is necessary for the acquisition and the expression of conditioned fear. Further experiments have delineated an efferent amygdalofugal pathway to the primary startle circuit, at the level of the caudal pontine reticular formation, which mediates the expression of conditioned fear [10]. Yet it was unclear, whether this amygdaloreticular pathway directly transfers the effects of conditioned fear from the amygdala to the primary startle circuit or whether there exist one or more relay nuclei within this pathway or even additional parallel circuits. Based on our previous finding that the midbrain central gray (CG) is involved in the mediation of the facilitatory effects on the ASR of unconditioned aversive events, the present study tested the hypothesis that the CG is important for the potentiation of the ASR by conditioned fear. Therefore, we lesioned the CG before and after fear-conditioning and examined the effects of these lesions on fear-potentiated startle. Pre- and post-training lesions of the CG totally blocked the potentiation of the ASR amplitude by conditioned fear, which was seen in sham-lesioned rats, indicating that CG lesions affected the expression of conditioned fear. The baseline ASR amplitude was not influenced by CG lesions. We discuss possible pathways and mechanisms underlying the expression of conditioned and unconditioned fear in rats.

Acoustic Stimulation↗

Lesions of the amygdala do not affect the enhancement of the acoustic startle response by background noise.

The acoustic startle response (ASR) is enhanced in the presence of loud background noise. We examined whether or not this increase of response strength is mediated by the amygdala, which is known to be involved in various phenomena of enhancement of the ASR. To achieve this aim, we tested whether or not amygdaloid lesions with the excitotoxin N-methyl-D-aspartate (NMDA) would abolish the enhancement of the ASR by background noise in 13 Wistar rats. Loss of foot-shock sensitization in these rats, as well as histological evaluation, proved the successful destruction of the amygdala. However, the enhancement by background noise of the ASR, which was observed in sham-operated controls, was not affected in amygdala-lesioned rats. Therefore, we conclude that the background noise facilitation does not involve emotional components that are mediated by the amygdala. On the basis of these findings, we differentiate between the startle-enhancing effect of background noise and the amygdala-mediated effect of foot shocks on the ASR.

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Cholecystokinin enhances the acoustic startle response in rats.

The present study examined the effects of the neuropeptide cholecystokinin (CCK) on neurones of the caudal pontine reticular nucleus (PnC), which mediates the acoustic startle response (ASR) in rats. Electrophysiological experiments revealed an excitatory effect of CCK on acoustically responsive neurones in the PnC. On the behavioural level, CCK also enhanced the ASR. Since the PnC is not only an obligatory relay station of the brain circuit mediating the ASR, but also receives modulatory input from brain areas involved in the expression of fear and anxiety, the enhancement of the ASR by CCK could be interpreted as an anxiogenic-like effect of this peptide.

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Conditioned pleasure attenuates the startle response in rats.

The acoustic startle response of rats was found to be attenuated if elicited in the presence of a conditioned stimulus predicting reward. During conditioning, animals received a total of 21 pairings of light with palatable food and sucrose solution, whereas controls received food and sucrose in the absence of light. The amplitude of the acoustic startle response was significantly reduced in the presence of light in conditioned animals, but not in controls. It is assumed that a conditioned response to light is the activation of a central state of pleasure. We therefore suggest that "pleasure-attenuated startle" reflects a mechanism by which a defensive or aversive response is attenuated during a pleasant, hedonic state.

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Lesions of the central gray block the sensitization of the acoustic startle response in rats.

The amplitude of the acoustic startle response (ASR) in rats is increased after administration of footshocks, a phenomenon termed sensitization. The neural circuitry underlying this kind of modulation of the ASR is only partly understood. It has been shown that the central nucleus of the amygdala (cA) and its efferent pathway to the caudal pontine reticular nucleus (PnC), an essential part of the primary startle circuit, is important for the sensitization of the ASR. It was unclear, however, whether the amygdaloreticular pathway directly transfers the effects of footshocks onto the PnC, or whether there exists a relay nucleus within this pathway. The present study tested the hypothesis that the midbrain central gray (CG) is important for the sensitization of the ASR. Neuroanatomical tracing experiments indicate that a descending projection from the medial part of the cA might form synapses in the region of the midbrain CG, where a descending projection to the PnC takes its origin. We lesioned the dorsal and lateral part of the CG with the neurotoxin quinolinic acid and measured the effects of this lesion on the sensitization of the ASR by footshocks. Lesions confined to the dorsal and lateral parts of the CG totally blocked the sensitization of the ASR, without affecting the ASR amplitude in the absence of sensitizing stimuli. These findings suggest a crucial role of the CG for the sensitization of the ASR. The present data are reconciled with other findings from our laboratory and from the literature and we discuss possible mechanisms underlying the mediation of the sensitization of the ASR in rats.

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Sensorimotor gating deficit after lesions of the superior colliculus.

The superior colliculus (SC) is important for the processing of sensory information of different modalities and for the mediation of adequate motor responses in mammals. The present study investigated the effects of excitotoxic lesions of the SC on two different modulations of the acoustic startle response (ASR) in rats. Modulations of the ASR (i.e. increase or decrease of the response strength) represent useful models for the study of sensorimotor integration phenomena. Lesions of the SC decreased the prepulse inhibition of the ASR without affecting the baseline startle amplitude or the enhancement of the ASR by footshock sensitization. These results suggest a crucial role of the SC in the prepulse inhibition of the ASR, a model of sensorimotor gating.

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Substance P is involved in the sensitization of the acoustic startle response by footshocks in rats.

The acoustic startle response (ASR) can be enhanced by administration of footshocks (sensitization). The neural mechanisms underlying this effect are largely unknown. A previous electrophysiological study (Kungel et al., Brain Res., 643 (1994) 29-39) has shown that the neuropeptide substance P (SP) increases the responsiveness to acoustic stimuli of neurons in the caudal pontine reticular nucleus (PnC). Since the PnC is an important part of the primary acoustic startle circuit, we hypothesized that SP is involved in the enhancement of the ASR by electric footshocks. We tested this hypothesis in different experiments by locally injecting SP and SP-antagonists into the PnC of freely moving rats. The present data show that SP (0.5 pmol-1 nmol) locally injected into the PnC dose-dependently increases the amplitude of the ASR in rats. This effect was antagonized by pretreatment with the SP-antagonist CP-96,345. Furthermore, we show that the sensitization of the ASR by 0.6 mA-footshocks can be blocked by local microinjections of the SP-antagonists CP-96,345 (5 pmol-10 nmol) or CP-99,994 (0.5 nmol-100 nmol) into the PnC. Possible pathways relevant for the sensitization of the ASR are discussed.

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Echo SPL influences the ranging performance of the big brown bat, Eptesicus fuscus.

Four bats of the species Eptesicus fuscus were trained in a two-alternative forced-choice procedure to discriminate between two phantom targets that differed in range. The rewarded stimulus was located at a distance of 52.7 cm, while the other unrewarded stimulus was further away. Only one target was presented at a time. In the first experiment we measured the range discrimination performance at an echo SPL of -28 dB relative to the bat's sonar transmission. A 75% correct performance level was arbitrarily defined as threshold and was obtained at a delay difference of 80 microseconds, corresponding to a range difference of 13.8 mm. In the second experiment the delay difference was fixed at 150 microseconds and the echo SPL varied between -8 and -48 dB relative to sonar emissions. The performance of the bats depended on the relative echo SPL. AT -28 dB the bats showed the best performance. It deteriorated at an increase of the relative echo SPL to -18 dB and -8 dB. The performance also deteriorated when the relative echo SPL was reduced to -38 dB and -48 dB. Only at low relative echo SPLs did the bats partially compensate for the reduction in echo SPL and increased the SPL of their emitted signals by a few dB. Our results support the hypothesis that neurons exhibiting paradoxical latency shift may be involved in encoding target range. This hypothesis predicts a decrease in performance at high echo SPLs as we found it in our experiments. The observed reduction in performance at very low echo SPLs may be due to a decrease in S/N ratio.

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Amygdaloid noradrenaline is involved in the sensitization of the acoustic startle response in rats.

The present study examined the role of noradrenaline (NA) in the central nucleus of the amygdala (cA) in the sensitization of the acoustic startle response (ASR) in rats. In the first experiment, local microinjections of 0, 0.5, 1, 2 nmol of the alpha 2-adrenergic antagonist yohimbine into the cA increased the magnitude of the ASR in a dose-dependent way. In the second experiment, foot shocks were applied to increase the ASR amplitude (sensitization). Local microinjections of 0, 4, 8, 16 nmol of the alpha 2-adrenergic agonist ST-91 into the cA dose dependently decreased the sensitizing effects of foot shocks on the amplitude of the ASR. It is conjectured that yohimbine increases and ST-91 decreases local NA release by acting at presynaptic autoreceptors. The present data suggest that the release of NA in the cA is involved in the mediation of the sensitizing effects of foot shocks on the ASR.

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Discrimination of two-wavefront echoes by the big brown bat, Eptesicus fuscus: behavioral experiments and receiver simulations.

1. Echolocating bats (Eptesicus fuscus) were trained to discriminate between simulated targets consisting of one or two echo-wavefronts with internal time delays of up to 100 microseconds. Spectral and temporal properties and total signal energy of the targets were evaluated and predictions for performances of bats derived from receiver models were compared with measured performances. 2. Eptesicus fuscus was able to discriminate a one-wavefront target from two-wavefront targets with distinct internal time delays (12 microseconds, 32-40 microseconds and 52-100 microseconds). Performance was not affected by changes in total signal energy. Bats also successfully discriminated between two-wavefront targets with different internal time delays. 3. Performance predicted from differences in total energy between targets did not match the measured performance, indicating that bats did not rely on total echo energy. This finding is also supported by the behavioral data. Performance predicted from spectral and temporal receiver models both matched the measured performance and, therefore, neither one of these models can be favored over the other. 4. The behavioral data suggest that Eptesicus fuscus did not transform echo information into estimates of target range separation and, therefore, did not perceive the two wavefronts of each simulated two-wavefront echo as two separate targets.

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Acoustic startle response and habituation in freezing and nonfreezing rats.

Rats can be divided according to their responses to startle-eliciting stimuli into 2 groups with different emotional states. About half of the 54 female Sprague-Dawley rats showed long-lasting freezing behavior after 1-8 stimuli (10 kHz, 110 dB spl). In freezing rats the startle amplitude was higher than in nonfreezing rats, even on the very first startle response. This finding demonstrates that the anxiety state of these animals before the first startle-eliciting stimulus, and not just the aversiveness of the stimulus, contributes to freezing behavior. In addition, in freezing rats there was no influence of spontaneous motor activity or of adaptation time on startle amplitude. Only in nonfreezing rats were high motor activities correlated with lowered startle amplitudes, and only in these rats did the course of startle habituation depend on adaptation time.

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Glutamate antagonists in the reticular formation reduce the acoustic startle response.

A previous study has shown that the acoustic responsiveness of reticulospinal neurones in the caudal pontine reticular nucleus (PnC) is reduced by glutamate antagonists. It was postulated that the acoustic startle response is mediated by glutamate receptors on PnC-neurones. In the present study, we tested this hypothesis by local microinjections of different glutamate antagonists into the PnC of unrestrained awake rats. In order to differentiate the drug effects on the head and body startle responses, we measured the head startle response electromyographically, and the body startle response in a ballistic chamber. Both the AMPA/kainate and the NMDA receptor antagonists reduced both components of the startle response dose-dependently. We conclude that both subtypes of ionotropic glutamate receptors in the PnC are relevant for the acoustic startle response in rats.

2-Amino-5-phosphonovalerate↗

Range resolution and the possible use of spectral information in the echolocating bat, Eptesicus fuscus.

Individuals of the echolocating bat Eptesicus fuscus were trained to discriminate simulated two-wave-front targets with internal time delays of 0 to 100 microns between the wave fronts from a one-wave-front target. The ability of bats to discriminate between such targets can be referred to as range resolution. In Eptesicus fuscus, this ability is limited to distinct internal time delays (12, 32-40, and 52-100 microns) between the two wave fronts of a double-wave-front target. Analysis of the simulated two-wave-front echoes reveals periodic frequency minima in the spectrum. Position and separation of these spectral minima depend on the time delay between the two wave fronts. The occurrence of spectral minima within the frequency range of the first harmonic in the echo of the bats' echolocation call correlates to the bats' ability to discriminate a one-wave-front echo from two-wave-front echoes, suggesting that Eptesicus fuscus uses spectral differences within the first harmonic in echoes for range resolution.

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Effects of a change in tone frequency on the habituated orienting response of the sleeping rat.

EEG arousal and heart rate responses to change in tone frequency following habituation training were studied during slow wave sleep in the rat. Rats were exposed to sequences of 12 tone pulses. Habituation stimuli (trials 1-7) had a frequency of 16 kHz. The frequency of the following (test) trials was changed to either 5, 12, 14, 22, or 40 kHz. Hearing level was held constant for all frequencies. Test trials were repeated five times to study rehabituation. The results indicate that heart rate deceleration is an indicator of the orienting reflex and its magnitude is a positive function of the amount of frequency change of the stimulus. Large frequency changes in either direction relative to the habituation frequency lead to re-evocation of the habituated EEG arousal and heart rate deceleration, with subsequent rehabituation. Small tone-frequency changes do not result in EEG arousal or heart rate deceleration responses that differ from the responses to the habituated frequency. Heart rate acceleration shows neither short-term habituation nor significant reaction to any of the test frequencies.

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Range estimation by echolocation in the bat Eptesicus fuscus: trading of phase versus time cues.

Bats of the species Eptesicus fuscus have been trained to discriminate a stationary simulated target from a target with a virtual distance that jitters from sound to sound. Similar to Simmons [Science 207, 1336-1338 (1979)], a jitter-detection threshold below 1 microsecond was found. However, Simmons' decreased performance at a time delay jitter of 30 microseconds could not be replicated, a critical feature used to postulate the idea that bats employ a coherent cross-correlation receiver for ranging. Such a receiver uses all phase information in the signal for delay estimation and therefore will be biased by phase manipulations. To test for such a bias, a phase jitter of +/- 45 degrees and a time jitter in the echo were overlaid. It was not found that there was a combination of both where their effects canceled. Full phase information is thus not used in delay estimation. However, bats were able to detect a pure phase jitter, e.g., polarity inversion of the signal. Bats could also detect phase jitter in the presence of randomized time jitter and vice versa. Phase jitter and time jitter, therefore, are separable features for a bat. The underlying physiological mechanism is not clear.

Amplifiers, Electronic↗

The echolocation and hunting behavior of the bat, Pipistrellus kuhli.

The echolocation and hunting behavior of Pipistrellus kuhli was studied in the field using multi-exposure photography synchronized with high-speed tape recordings. During the search phase, the bats used 8-12 ms signals with sweeps (sweep width 3-6 kHz) and pulse intervals near 100 ms or less often near 200 ms. The bats seemed to have individual terminal frequencies that could lie between 35 and 40 kHz. The duty cycle of searching signals was about 8%. The flight speed of hunting bats was between 4.0 and 4.5 m/s. The bats reacted to insect prey at distances of about 70 to 120 cm. Given the flight speed, the detection distance was estimated to about 110 to 160 cm. Following detection the bat went into the approach phase where the FM sweep steepened (to about 60 kHz bandwidth) and the repetition rate increased (to about 30 Hz). The terminal phase or 'buzz', which indicates prey capture (or attempted capture), was composed of two sections. The first section contained signals similar to those in the approach phase except that the pulse duration decreased and the repetition rate increased. The second section was characterized by a sharp drop in the terminal frequency (to about 20 kHz) and by very short pulses (0.3 ms) at rates of up to 200 Hz. Near the beginning of the buzz the bat prepared for capturing the prey by extending the wings and forming a tail pouch. A pause of about 100 ms in sound emission after the buzz indicated a successful capture (Fig. 4).(ABSTRACT TRUNCATED AT 250 WORDS)

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The pattern and habituation of the orienting response in man and rats.

Autonomic and central nervous indices of the orienting response (OR) were investigated in awake human subjects and sleeping rats. Ten acoustic stimuli of 60 dB and two stimuli of 80 dB were presented for 10 s each with a constant interstimulus interval of 50 s. Responses were averaged across subjects for each single trial. An exponential fit to scores of each physiological variable was used to compare OR, habituation and dishabituation between samples and variables. An OR to the first stimulus, habituation of response amplitude, and dishabituation in response to the change in stimulus intensity were observed for event-related EEG desynchronization, a negative-positive evoked potential complex in humans and rats, as well as for skin conductance in humans. While heart rate did not show systematic changes across the 60 dB tones in both samples, a deceleration was observed in response to the first 80 dB tone. Results suggest comparable patterns of orienting to acoustic stimuli and habituation of the OR in the awake human and the sleeping rat, suggesting the possibility of OR as a unitary response. Species differed with respect to speed of habituation but not with respect to sensitivity towards stimulus change.

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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.

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