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PubMed2005

Temporary inactivation of the rostral perirhinal cortex induces an anxiolytic-like effect on the elevated plus-maze and on the yohimbine-enhanced startle response.

The present study investigated whether the rostral perirhinal cortex is involved in aversive information processing, particularly in unconditioned fear (anxiety). We temporarily inactivated the rostral perirhinal cortex by local injections of the GABA(A) agonist muscimol (0.0, 1.1, and 4.4 nmol/0.5 microl) and tested whether these injections affected the behavior of rats in the elevated plus-maze and in the yohimbine-enhanced startle test. Temporary inactivation of the rostral perirhinal cortex increased the number of open arm entries and the open arm ratio in the elevated plus-maze. In addition, startle response enhancement caused by the anxiogenic drug yohimbine was reduced by perirhinal cortex inactivation. Taken together, these data clearly show that the rostral perirhinal cortex is involved in the processing of emotional stimuli and is critical for the expression of unconditioned fear (anxiety).

Adrenergic alpha-Antagonists↗
PubMed1989

Prepulse inhibition of the acoustic startle response is disrupted by N-ethyl-3,4-methylenedioxyamphetamine (MDEA) in the rat.

N-Ethyl-3,4-methylenedioxyamphetamine (MDEA) is a derivative of methylenedioxyamphetamine (MDA), a substituted amphetamine with demonstrated abuse liability. MDA, MDEA and a third substituted amphetamine, methylenedioxymethamphetamine (MDMA), all produce a destructive action on central serotonin neurons and appear to induce some similar behavioral effects. The present study investigated the effects of racemic MDEA and its stereoisomers on prepulse inhibition of the acoustic startle response, a behavioral model of sensorimotor gating that is sensitive to psychostimulant drugs. Rats were subjected to 122 dB[A] acoustic noises, some of which were preceded by a weak 80 dB[A] prepulse noise. In vehicle-injected control rats, the prepulse induced a significant decrease in startle amplitude when compared to trials in which startle stimuli were not preceded by prepulses. Administration of racemic MDEA (0.3-10.0 mg/kg) and (+) MDEA (0.1-3.0 mg/kg) induced a significant attenuation in prepulse inhibition, while (-) MDEA (0.3-10.0 mg/kg) did not. Racemic MDMA (0.3-10.0 mg/kg) produced similar though not significant effects. These results confirm a stimulant-like behavioral effect of MDEA despite its relatively modest effects on dopamine markers, and support findings that the (+) stereoisomers of substituted amphetamines are more potent than tha (-) stereoisomers in producing psychostimulant-like biochemical and behavioral effects.

3,4-Methylenedioxyamphetamine↗
PubMed2005

Brief intermittent access to sucrose differentially modulates prepulse inhibition and acoustic startle response in obese CCK-1 receptor deficient rats.

Otsuka Long-Evans Tokushima Fatty (OLETF) rats lack the CCK-1 receptor and are hyperphagic and obese. CCK-1 receptors play a role in prepulse inhibition (PPI) by modulating mesolimbic dopamine transmission, a modulator of sensorimotor gating. Therefore, the present study assessed the effects of brief, daily sucrose access on PPI and acoustic startle response (ASR) in OLETF rat and age-matched non-mutant Long-Evans Tokushima Otsuka (LETO) rats. The results revealed that OLETF rats with sucrose access showed an increased ASR [F(1,16) = 6.84; P < 0.01)], relative to sucrose receiving LETO rats. No significant sucrose effect (P = 0.283) on PPI was noted in OLETF rats, whereas sucrose receiving LETO rats had a significantly lower (P < 0.05) PPI percentage than non-sucrose controls. In contrast, sucrose-receiving OLETF rats expressed significantly higher PPI percentage than LETO rats with identical sucrose presentation (P < 0.01). Taken together, these results suggest that sucrose access alters PPI and ASR in general, and the CCK-1 receptors play a modulatory role in facilitating or inhibiting these responses, respectively. A similar effect may be contributory to the hyperphagic behavioral phenotype of obese animal models with altered central dopamine regulation.

Acoustic Stimulation↗
PubMed2005

Association between violent behaviour and impaired prepulse inhibition of the startle response in antisocial personality disorder and schizophrenia.

Violent behaviour has a strong association with antisocial personality disorder (APD) and schizophrenia. Although developments in the understanding of socio-environmental factors associated with violence should not be ignored, advances in prevention and treatment of violent behaviour would benefit by improved understanding of its neurobiological and cognitive basis. The authors, therefore, investigated prepulse inhibition (PPI) of the startle response in APD and schizophrenia in relation to a history of serious violence. The neural substrates of PPI, especially the hippocampus, amygdala, thalamus and basal ganglia, are implicated in violence as well as in APD and schizophrenia. The study included four groups: (i) patients with APD and a history of violence, (ii) patients with schizophrenia and a history of violence, (iii) patients with schizophrenia without a history of violence, and (iv) healthy subjects with no history of violence or a mental disorder. All subjects were assessed identically on acoustic PPI. Compared to healthy subjects, significantly reduced PPI occurred in APD, violent schizophrenia and non-violent schizophrenia patients. Although PPI did not significantly differentiate the three clinical groups, high ratings of violence were modestly associated with reduced PPI across the entire study sample. Violent patients with impulsive and premeditated violence showed comparable PPI. The association between violent behaviour and impaired PPI suggests that neural structures and functions underlying PPI are implicated in (inhibition of) violence.

Acoustic Stimulation↗
PubMed1996

Amygdala kindling does not change emotional responding as measured by the acoustic startle response in the rat.

Human patients with limbic epilepsy are often prone to anxiety and depression. The present study investigated the effect of seizures on emotional responding in the kindling model of complex-partial seizures. Male Wistar rats received electrodes into the right basolateral amygdala and were subsequently kindled until fully generalized seizures could be elicited. These rats did not show a change in the magnitude of the acoustic startle response (ASR) compared to the response amplitude before kindling, or compared to unimplanted controls and to only partially kindled rats. Since the ASR amplitude is a sensitive measure for anxiety or fear, these findings suggest that amygdala kindling does not induce a state of anxiety or fear. However, when analyzing the time course of the ASR within a session, the normally occurring habituation of the ASR was absent in electrode-implanted rats suggesting that the physiological changes induced by electrode implantation interfere with response habituation. Kindling even tended to sensitize the ASR in electrode-implanted rats. Finally, the effect of carbamazepine which is both anticonvulsant and antipsychotic was tested. Carbamazepine significantly reduced the ASR in control and partially kindled rats while this effect was less pronounced in fully kindled rats. It is concluded that amygdala kindling does not change emotional responding as measured by the ASR in rats.

Acoustic Stimulation↗
PubMed2003

Baclofen reverses the reduction in prepulse inhibition of the acoustic startle response induced by dizocilpine, but not by apomorphine.

RATIONALE: Since baclofen, the prototypical GABA(B) receptor agonist, is known to reduce the activity of dopaminergic mesolimbic neurons, a putative antipsychotic property of this compound has been suggested, but the evidence for this is still controversial. OBJECTIVES: The aim of the present study was to elucidate the effects of baclofen on the prepulse inhibition (PPI) of the acoustic startle response (ASR), a behavioral paradigm considered to be one of the most powerful tools for the evaluation of sensorimotor gating and for the screening of antipsychotics. METHODS: We tested the effects of baclofen (1.25, 2.5, 5 and 10 mg/kg IP) in rats, per se and in co-treatment with some of the substances known to induce a robust reduction of PPI, such as apomorphine (0.25 mg/kg SC) and dizocilpine (0.1 mg/kg SC). Finally, in order to ascertain whether the effects of baclofen could be ascribed to its activity on GABA(B) receptors, we analyzed whether its action could be prevented by pretreatment with SCH 50911, a selective GABA(B) receptor antagonist (20 mg/kg IP). All the experiments were carried out using standard procedures for the assessment of PPI of the ASR. RESULTS: Baclofen per se produced no significant change in PPI parameters. Moreover, while no effect on apomorphine-mediated alterations in PPI parameters was observed, baclofen proved able to reverse dizocilpine-induced PPI disruption, and this effect was significantly prevented by SCH 50911. On the other hand, this last compound exhibited no effects per se at the same dose. CONCLUSIONS: These results indicate that GABA(B) receptors are implicated in the neurobiological circuitry accounting for glutamatergic action in sensorimotor gating, and therefore can be proposed as putative new targets in the pharmacological therapy of psychotic disorders. Further studies should be addressed to evaluate more closely the clinical efficacy of baclofen in this respect.

Acoustic Stimulation↗
PubMed2006

Intrahippocampal injections of Tat: effects on prepulse inhibition of the auditory startle response in adult male rats.

The presence of human immunodeficiency virus (HIV-1) in the brain mediates the pathogenesis of HIV-associated dementia complex (HAD), partially through the viral toxins gp120 and Tat. This study characterized potential deficits in sensorimotor gating, as measured by prepulse inhibition (PPI), following hippocampal administration of Tat. Adult, male Sprague-Dawley rats were bilaterally injected with 50 microg Tat or saline (1 microl volume), into the hippocampus. Following 7 weeks of recovery, all animals were tested using the auditory startle response (ASR) with habituation, control, and PPI trials. Assessment of ASR habituation [100dB(A) white noise stimulus, 70dB(A) background, 5-min acclimation period, 36 habituation trials with fixed interstimulus interval (ISI) of 10 s] demonstrated a significant approximately 50% reduction in the overall peak ASR amplitude, but no change in peak ASR latency, nor an effect on the rate of habituation. PPI measures demonstrated robust alterations in sensorimotor gating. The PPI test (ISI of 0, 8, 40, 80, 120, or 4000 ms, 6-trial blocks, Latin-square) showed an attenuated response on peak ASR amplitude during the control trials (0 and 4000 ms ISI), but not on the PPI trials (8-120 ms ISI). Most striking was the rightward shift in ISI for maximal inhibition of the response (chi2(1)=4.7, p<or=0.03). There was no significant peak ASR latency effect during the control trials (<1 ms) of the PPI test, although there was the suggestion of a slowing of the response (4 ms, approximately 15%) across PPI trials. Collectively, the present data suggest that intrahippocampal injections of Tat have adverse effects on cognitive processing, as indexed by sensorimotor gating.

Acoustic Stimulation↗
PubMed1999

Effect of nonaversive and aversive stimulations in infancy on the acoustic startle response in adult rats.

Two groups, each consisting of 8 three-week-old rat pups, were exposed to different behavioral treatments with the aim to determine how the experimental manipulation influenced their adult emotional reactivity. Every day for two weeks the pups from the first group received 15 min of handling whereas the animals from the second group were exposed to various aversive stimuli, differing each day. Following these manipulations, after a 5-day break the acoustic startle response (ASR) was measured in all animals and the testing was repeated after another four weeks. Statistical analysis of the data revealed significant differences between groups in the ASR parameters. Surprisingly, in the test which directly followed the treatment the mean ASR amplitudes were similar in both groups. Highly significant differences, however, were observed in the ASR amplitude four weeks later. The rats from the handling group responded with greater amplitudes. The latency of the ASR was significantly shorter in the nonaversive group compared with the second group exposed to aversive stimuli. The results suggest that early exposure to aversive stimulation significantly decreases rats emotional reactivity whereas nonaversive and impoverished stimulation clearly elevates arousal levels when the animal is placed in a novel situation.

Acoustic Stimulation↗
PubMed2006

Acoustic startle response is disrupted in iron-deficient rats.

Diurnal effects on motor control are evident in the human disease of Restless Leg Syndrome (RLS), which is purported to be linked to brain iron deficiency as well as alterations in dopaminergic systems. Thus, we explored the relationship between daily rhythms, the onset of motor dysregulation and brain iron deficiency in an animal model of iron deficiency. Male and female weanling Sprague-Dawley rats consuming control (CN) or iron-deficient (ID) diets were examined weekly for acoustic startle response (ASR) and prepulse inhibition (PPI) for a 5-week period. Iron deficiency reduced the magnitude, but not timing, of the ASR at specific time points. ASR was elevated 60% at the onset of the dark cycle relative to the median of the light cycle in male CN and ID rats. The respective elevation was 400% and 150% in female CN and ID rats during the first 2 weeks of testing. The diurnal cycle of ASR response was attenuated by 3 weeks of testing in both dietary treatment groups. PPI was not affected by iron deficiency, sex, diurnal cycle or the interaction between these factors. These results thus demonstrate that iron deficiency moderately alters ASR signaling although the inhibitory pathways of ASR do not appear to be affected.

Acoustic Stimulation↗
PubMed1996

The behavioral salience of tones as indicated by prepulse inhibition of the startle response: relationship to hearing loss and central neural plasticity in C57BL/6J mice.

Adult C57BL/6J mice exhibit high-frequency, sensorineural hearing loss accompanied by physiological changes in the upper auditory brainstem and cortex, referred to as hearing-loss induced (HLI) plasticity: as high-frequency sensitivity declines, many neurons come to respond better to still-audible, middle-frequency tones (especially 12-16 kHz). We used prepulse inhibition (PPI) to assess the relationship between the behavioral salience of tones and HLI plasticity. The ability of a tone 'prepulse' (S1), presented 100 ms before a startle-eliciting tone (S2), to 'inhibit' startle responses was measured in normal-hearing 1-month-olds and 5-month-olds with high-frequency hearing loss. Tone bursts of 4, 8, 12, 16, and 24 kHz were used as S1s and S2s in all possible combinations. PPI was significantly improved (more inhibition) in 5-month-olds with 12 or 16 kHz S1s. This effect was not influenced by S2 frequency or the size of the startle evoked by S2-only stimuli (smaller for high-frequency S2s in older mice). The increased salience of 12-16 kHz S1s in 5-month-old C57 mice parallels changes in the central representation of tone frequency and implies a behavioral effect of HLI plasticity.

Acoustic Stimulation↗
PubMed2000

Enhancement of the acoustic startle response by dopamine agonists after 6-hydroxydopamine lesions of the substantia nigra pars compacta: corresponding changes in c-Fos expression in the caudate-putamen.

Rats with 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal pathway show enhanced locomotor and stereotyped behaviors when challenged with direct and indirect dopamine (DA) agonists due to the development of postsynaptic supersensitivity. To determine if this phenomenon generalizes to other motor behaviors, we have used this rat model of Parkinson's disease to examine the effects of the direct dopamine D(1) receptor agonist SKF 82958 and the indirect DA agonist L-3,4-dihydroxyphenylalanine (L-DOPA) on the acoustic startle response. In addition, we used the expression of c-Fos protein as a marker of neuronal activity to assess any corresponding drug-induced changes in the caudate-putamen (CPu) after L-DOPA administration. Male Sprague-Dawley rats received bilateral injections of 6-OHDA into the substantia nigra pars compacta and 1 week later were tested for startle after systemic administration of SKF 82958 (0.05 mg/kg) or L-DOPA (1, 5, 10 mg/kg). SKF 82958 produced a marked enhancement of startle with a rapid onset in 6-OHDA-lesioned but not SHAM animals. L-DOPA produced a dose- and time-dependent enhancement of startle in 6-OHDA-lesioned rats that had no effect in SHAM animals even at the highest dose (10 mg/kg). Furthermore, L-DOPA produced a dramatic induction of c-Fos in the CPu in 6-OHDA-lesioned animals. Consistent with other literature, these data suggest that neurons in the CPu become supersensitive to the effects of DA agonists after 6-OHDA-induced denervation of the nigrostriatal pathway and that supersensitive dopamine D(1) receptors may mediate the enhancement of startle seen in the present study.

Acoustic Stimulation↗
PubMed2001

Effects of alpha 4/beta 2- and alpha 7-nicotine acetylcholine receptor agonists on prepulse inhibition of the acoustic startle response in rats and mice.

RATIONALE: Nicotine and agonists at subtypes of the nicotine acetylcholine receptor (nAChR) affect auditory gating, but the magnitude and direction of such effects appear highly variable. This variability may be due to differences in the tested dose range, selectivity of the test compound, species and strain, and suggests that nAChR subtypes are differentially involved in the control of auditory gating. OBJECTIVES AND METHODS: This study aimed to characterise the effects of nicotine and agonists with preferential activity at alpha4/beta2- and alpha7-nAChRs on auditory sensorimotor gating using a prepulse inhibition (PPI) paradigm. Similar experimental conditions were employed in rats and two strains of mice. The paradigm used startle stimuli of 120 dB and prepulse intensities of 3, 6 and 12 dB above a background of 70 dB. RESULTS: In Sprague-Dawley rats, nicotine disrupted PPI [minimal effective dose (MED): 1 mg/kg, SC] and this effect was mimicked by the potent nAChR agonist, epibatidine, (MED: < or = 0.001 mg/kg, IP) and the potent, and relatively selective, alpha4/beta2-nAChR agonist A-85380 (MED: < or = 0.1 mg/kg, IP). The effects of epibatidine, A-85380 and, to a lesser extent, nicotine were blocked by the non-selective nAChR antagonist mecamylamine. The relatively selective alpha7-nAChR agonists, GTS-21 and AR-R-17779, did not affect PPI in a consistent manner, both in rats and in DBA/2 mice, a strain expressing a disrupted gating phenotype, presumably due to altered activity of hippocampal alpha7-nAChRs. In BALB/c mice, a strain expressing a normal gating phenotype, nicotine (MED: 10 mg/kg, SC), epibatidine (MED: 0.03 mg/kg, IP) and A-85380 (MED: 0.3 mg/kg, IP) predominantly augmented PPI and mecamylamine attenuated these effects. CONCLUSIONS: The present results confirm that the effects of nAChR agonists on PPI are species dependent and suggest that stimulation of heteromeric nAChRs containing both alpha and beta subunits, and possibly of the alpha4/beta2 type, affect sensorimotor gating. Evidence supporting a role for alpha7-nAChRs in the control of PPI of the acoustic startle response was not obtained.

Acoustic Stimulation↗
PubMed2004

Acoustic startle response, prepulse inhibition, and spontaneous locomotor activity in MPTP-treated mice.

Parkinson's disease (PD) is marked by characterised motor deficits and is accompanied by a severe degeneration of the nigrostriatal dopamine (DA) pathway. It has also been reported that PD patients exhibited additional behavioural deficits, including a deficiency in sensorimotor gating mechanisms. We therefore examined whether the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD in mice could lead to a sensorimotor gating deficit in the prepulse inhibition (PPI) of the acoustic startle response (ASR) paradigm. Two MPTP treatment schedules were separately examined here in male C57BL/6 mice. Post-mortem HPLC analysis confirmed that they were effective in depleting DA in the dorsal striatum (75-88%). PPI was evaluated on days 2, 9 and 16 after the last MPTP treatment; spontaneous locomotor activity was assessed 24 h before each PPI test. No significant change in the expression of PPI was detected across the three time points. On the other hand, the MPTP treatment reduced activity on post-treatment day 1. This effect subsided on post-treatment day 8, and was reversed on day 15. The possibility remains therefore that the reported sensorimotor gating deficits in PD patients might stem from structural or neurochemical aberrations beyond those induced by MPTP treatment.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

Prepulse inhibition and habituation of acoustic startle response in male MDMA ('ecstasy') users, cannabis users, and healthy controls.

Chronic administration of 3,4-methylenedioxymethamphetamine (MDMA) is associated with long-term depletion of serotonin (5-HT) and loss of 5-HT axons in the brains of rodents and nonhuman primates. Despite the broad database concerning the selective serotonergic neurotoxicity of recreational MDMA consumption by humans, controversy still exists with respect to the question of whether the well-known functional consequences of these neurotoxic effects, such as memory impairment, were caused by chronic 5-HT deficiency. Habituation and prepulse inhibition (PPI) of the acoustic startle response (ASR) can be used as a marker of central serotonergic functioning in rodents and humans. Thus, we investigated the functional status of the central serotonergic system in chronic but abstinent MDMA users by measuring PPI and habituation of ASR. PPI and habituation of ASR were measured in three groups. The first group (MDMA group) included 20 male drug-free chronic users of MDMA; the second group (cannabis group) consisted of 20 male drug-free chronic users of cannabis; and the third group (healthy controls) comprised 20 male participants with no history of illicit drug use. Analysis revealed significantly increased PPI of MDMA users compared to those of cannabis users and healthy controls. Cannabis users and healthy controls showed comparable patterns of PPI. There were no differences in habituation among the three groups. These results suggest that the functional consequences of chronic MDMA use may be explained by 5-HT receptor changes rather than by a chronic 5-HT deficiency condition. Use of cannabis does not lead to alterations of amplitude, habituation, or PPI of ASR.

Acoustic Stimulation↗
PubMed2004

Extinction of the acoustic startle response in moths endemic to a bat-free habitat.

Most moths use ears solely to detect the echolocation calls of hunting, insectivorous bats and evoke evasive flight manoeuvres. This singularity of purpose predicts that this sensoribehavioural network will regress if the selective force that originally maintained it is removed. We tested this with noctuid moths from the islands of Tahiti and Moorea, sites where bats have never existed and where an earlier study demonstrated that the ears of endemic species resemble those of adventives although partially reduced in sensitivity. To determine if these moths still express the anti-bat defensive behaviour of acoustic startle response (ASR) we compared the nocturnal flight times of six endemic to six adventive species in the presence and absence of artificial bat echolocation sounds. Whereas all of the adventive species reduced their flight times when exposed to ultrasound, only one of the six endemic species did so. These differences were significant when tested using a phylogenetically based pairwise comparison and when comparing effect sizes. We conclude that the absence of bats in this habitat has caused the neural circuitry that normally controls the ASR behaviour in bat-exposed moths to become decoupled from the functionally vestigial ears of endemic Tahitian moths.

Animals↗
PubMed2002

Alterations in the auditory startle response in Fmr1 targeted mutant mouse models of fragile X syndrome.

Fragile X syndrome results from inadequate production of the fragile X mental retardation protein (FMRP). Mice with a mutation targeted to the Fmr1 gene lack FMRP and thus are a valuable animal model for studying the behavioral and neural phenotype of this human disorder. Mice of two genetic backgrounds containing the Fmr1 mutation, C57BL/6J (C57-KO) and an F1 hybrid (C57BL/6J mutant x FVB/NJ; F1-KO) did not differ from control mice in behavior in the elevated plus maze or the open field. Both the C57-KO and F1-KO mice exhibited greater startle responses than normal mice to low intensity (80 dB) white noise bursts and decreased responses to high intensity (120 dB) white noise bursts. These behavioral alterations appear to be specific to the Fmr1 mutation since they are present on both genetic backgrounds. Furthermore, the mice lacking FMRP resemble individuals with fragile X syndrome in their increased sensitivity to low intensity auditory stimuli. These findings should prove useful in determining how the absence of FMRP alters the brain and behavior, and in testing potential treatments for fragile X syndrome.

Acoustic Stimulation↗
PubMed2005

Alterations in diurnal cortisol rhythm and acoustic startle response in nonhuman primates with adverse rearing.

BACKGROUND: Early adverse experiences represent risk factors for the development of anxiety and mood disorders. Studies in nonhuman primates have largely focused on the impact of protracted maternal and social deprivation, but such intense manipulations also result in severe social and emotional deficits very difficult to remediate. This study attempts to model more subtle developmental perturbations that may increase the vulnerability for anxiety/mood disorders but lack the severe deficits associated with motherless rearing. METHODS: We investigated the consequences of repeated maternal separations between 3 to 6 months of age on rhesus monkeys' hypothalamic-pituitary-adrenal (HPA) axis function and acoustic startle reactivity. RESULTS: Repetitive maternal separation led to increased cortisol reactivity to the separation protocol in female infants and alterations in mother-infant interaction. It also resulted in a flattened diurnal rhythm of cortisol secretion and increased acoustic startle reactivity at later ages. CONCLUSIONS: Macaques with adverse rearing exhibited short-term and long-term alterations in HPA axis function and increased acoustic startle response comparable with changes associated with mood/anxiety disorders. The magnitude of HPA axis reactivity to the separations and the alterations in mother-infant relationship detected during the separation protocol predicted some of the alterations in HPA axis and emotionality exhibited later in life.

Acoustic Stimulation↗
PubMed2000

A double-blind, placebo-controlled study on the effects of Gotu Kola (Centella asiatica) on acoustic startle response in healthy subjects.

Investigations of the pharmacologic profile of medicinal plants have revealed that a number of plants with purported anxiolytic activity bind to cholecystokinin (CCK) receptors. This finding is intriguing in view of the proposed involvement of CCK in the pathophysiology of fear and anxiety. This double-blind, placebo-controlled study was undertaken to evaluate the anxiolytic activity of Gotu Kola (Centella asiatica) in healthy subjects. Gotu Kola has been used for centuries in Ayurvedic and traditional Chinese medicine to alleviate symptoms of depression and anxiety. Recent studies in the rat have shown that long-term pretreatment with Gotu Kola decreases locomotor activity, enhances elevated-plus maze performance, and attenuates the acoustic startle response (ASR). In this study, the authors evaluated the effects of Gotu Kola on the ASR in humans. Subjects were randomly assigned to receive either a single 12-g orally administered dose of Gotu Kola (N = 20) or placebo (N = 20). The results revealed that compared with placebo, Gotu Kola significantly attenuated the peak ASR amplitude 30 and 60 minutes after treatment. Gotu Kola had no significant effect on self-rated mood, heart rate, or blood pressure. These preliminary findings suggest that Gotu Kola has anxiolytic activity in humans as revealed by the ASR. It remains to be seen whether this herb has therapeutic efficacy in the treatment of anxiety syndromes.

Acoustic Stimulation↗