Block of glucocorticoid synthesis during re-activation inhibits extinction of an established fear memory

BackgroundThe pharmacology of traumatic memory extinction has not been fully characterized despite its potential as a therapeutic target for established, acquired anxiety disorders, including post-traumatic stress disorder (PTSD). Here we examine the role of endogenous glucocorticoids in traumatic memory extinction.MethodsMale C57BL/6J mice were injected with corticosterone (10 mg/kg, i.p.) or metyrapone (50 mg/kg, s.c.) during re-activation of a contextual fear memory, and compared to vehicle groups (N = 10–12 per group). To ensure that metyrapone was blocking corticosterone synthesis, we measured corticosterone levels following re-activation of a fear memory in metyrapone- and vehicle-treated animals.ResultsCorticosterone administration following extinction trials caused a long-lasting inhibition of the original fear memory trace. In contrast, blockade of corticosteroid synthesis with metyrapone prior to extinction trials enhanced retrieval and prevented extinction of context-dependent fear responses in mice. Further behavioral analysis suggested that the metyrapone enhancement of retrieval and prevention of extinction were not due to non-specific alterations in locomotor or anxiety-like behavior. In addition, the inhibition of extinction by metyrapone was rescued by exogenous administration of corticosterone following extinction trials. Finally, we confirmed that the rise in corticosterone during re-activation of a contextual fear memory was blocked by metyrapone.ConclusionsWe demonstrate that extinction of a classical contextual fear memory is dependent on endogenous glucocorticoid synthesis during re-activation of a fear memory. Our data suggest that decreased glucocorticoids during fear memory re-activation may contribute to the inability to extinguish a fear memory, thus contributing to one of the core symptoms of PTSD.     

The hippocampus and prefrontal cortex are differentially involved in serial memory retrieval in non-stress and stress conditions

We previously showed that 24 h after learning, mice significantly remembered the first (D1) but not the second (D2) discrimination in a serial spatial task and that an acute stress delivered 5 min before the test phase reversed this memory retrieval pattern.A first experiment evaluated the effects of dorsal hippocampus (HPC) or prefrontal cortex (PFC) lesions, these two brain areas being well-known for their involvement in serial and spatial memory processes. For this purpose, six independent groups of mice were used: non-lesioned (controls), PFC or HPC-lesioned animals, submitted or not to an acute stress (electric footshocks; 0.9 mA). Results show that (i) non-stressed controls as well as PFC-lesioned mice (stressed or not) remembered D1 but not D2; (ii) stressed controls and HPC-lesioned mice (stressed or not) remembered D2 but not D1; (iii) stress significantly increased plasma corticosterone in controls and PFC-lesioned mice, but not in HPC-lesioned mice which already showed a significant plasma corticosterone increase in non-stressed condition.Since data from this first experiment showed that stress inhibited the hippocampal-dependent D1 memory retrieval, a second experiment evaluated the behavioral effect of intrahippocampal corticosterone injection in non-stressed mice. Results show that intrahippocampal corticosterone injection induced a reversal of serial memory retrieval pattern similar to that induced by acute stress.Overall, our study shows that (i) in non-stress condition, the emergence of D1 is HPC-dependent; (ii) in stress condition, the emergence of D2 requires the PFC integrity; moreover, intrahippocampal corticosterone injection mimicked the effects of stress in the CSD task.     

Involvement of dorsal hippocampal α-adrenergic receptors in the effect of scopolamine on memory retrieval in inhibitory avoidance task

The present study evaluated the possible role of α-adrenergic receptors of the dorsal hippocampus on scopolamine-induced amnesia and scopolamine state-dependent memory in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulae in the CA1 regions of the dorsal hippocampus, trained in a step-through type inhibitory avoidance task, and tested 24 h after training to measure step-through latency. Results indicate that post-training or pre-test intra-CA1 administration of scopolamine (1 and 2 μg/rat) dose-dependently reduced the step-through latency, showing an amnestic response. Amnesia produced by post-training scopolamine (2 μg/rat) was reversed by pre-test administration of the scopolamine that is due to a state-dependent effect. Interestingly, pre-test intra-CA1 microinjection of α1-adrenergic agonist, phenylephrine (1 and 2 μg/rat) or α2-adrenergic agonist, clonidine improved post-training scopolamine (2 μg/rat)-induced retrieval impairment. Furthermore, pre-test intra-CA1 microinjection of phenylephrine (0.25, 0.5 and 1 μg/rat) or clonidine (0.25, 0.5 and 1 μg/rat) with an ineffective dose of scopolamine (0.25 μg/rat), synergistically improved memory performance impaired by post-training scopolamine. On the other hand, pre-test injection of α1-receptors antagonist prazosin (1 and 2 μg/rat) or α2-receptors antagonist yohimbine (1 and 2 μg/rat) prevented the restoration of memory by pre-test scopolamine. It is important to note that pre-test intra-CA1 administration of the same doses of prazosin or yohimbine, alone did not affect memory retrieval. These results suggest that α1- and α2-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state-dependent memory.     

Post-training administration of corticosterone enhances consolidation of contextual fear memory and hippocampal long-term potentiation in rats

This study was designed to examine the effect of corticosterone on consolidation of contextual fear memory and hippocampal long-term potentiation (LTP) in rats. In Experiment 1, dose–response effects of corticosterone on consolidation of contextual fear memory were determined. Immediately after training in contextual fear conditioning task, rats received different doses of corticosterone. Testing 24 h later, it revealed that corticosterone enhanced memory consolidation in an inverted U shape as evidenced in increased freezing behavior of corticosterone-treated animals. The most effective dose was 3 mg/kg. In Experiment 2, LTP was examined in rats whose memory consolidation has been enhanced with corticosterone. The rats were trained as the above and received corticosterone (3 mg/kg) immediately after training. Immediately or up to one day after retention test, rats were anesthetized with urethane for LTP experiments. For LTP induction, three episodes of high frequency stimuli, 30 s apart, were delivered to the perforant path, each consisting of 10 stimuli at 250 Hz. LTP was assessed by measuring the increase in the initial slope of the population excitatory post-synaptic potentials and the amplitude of the population spikes. Data indicated that animals whose memory has been enhanced by corticosterone, also displayed enhanced hippocampal LTP. The above findings suggest that glucocorticoids may enhance contextual fear memory consolidation via enhancing hippocampal LTP.     

Memory-enhancing corticosterone treatment increases amygdala norepinephrine and Arc protein expression in hippocampal synaptic fractions

Considerable evidence indicates that glucocorticoid hormones enhance the consolidation of memory for emotionally arousing events through interactions with the noradrenergic system of the basolateral complex of the amygdala (BLA). We previously reported that intra-BLA administration of a β-adrenoceptor agonist immediately after inhibitory avoidance training enhanced memory consolidation and increased hippocampal expression of the protein product of the immediate early gene activity-regulated cytoskeletal-associated protein (Arc). In the present experiments corticosterone (3 mg/kg, i.p.) was administered to male Sprague-Dawley rats immediately after inhibitory avoidance training to examine effects on long-term memory, amygdala norepinephrine levels, and hippocampal Arc expression. Corticosterone increased amygdala norepinephrine levels 15 min after inhibitory avoidance training, as assessed by in vivo microdialysis, and enhanced memory tested at 48 h. Corticosterone treatment also increased expression of Arc protein in hippocampal synaptic tissue. The elevation in BLA norepinephrine appears to participate in corticosterone-influenced modulation of hippocampal Arc expression as intra-BLA blockade of β-adrenoceptors with propranolol (0.5 μg/0.2 μL) attenuated the corticosterone-induced synaptic Arc expression in the hippocampus. These findings indicate that noradrenergic activity at BLA β-adrenoceptors is involved in corticosterone-induced enhancement of memory consolidation and expression of the synaptic-plasticity-related protein Arc in the hippocampus.     

Effects of acute stress and GluN2B-containing NMDA receptor antagonism on object and object–place recognition memory

The mechanisms underlying the complex effects of acute stress on memory are incompletely understood. Previous work suggests that the activation of N-methyl-d-aspartate (NMDA) receptors specifically containing GluN2B subunits may underlie the disruptions in spatial memory retrieval caused by acute stress (Wong et al., 2007 PNAS 104:11471). The present experiments were designed to assess whether a similar mechanism is involved in recognition memory. Recognition memory retrieval was assessed in Sprague–Dawley rats using an object recognition test and an object–place recognition test, both of which rely on patterns of spontaneous exploration. Exposure to acute stress for 30 min immediately before the test phase of either test disrupted memory retrieval. Administration of the GluN2B-selective antagonist Ro25-6981 (6 mg/kg; i.p.) enhanced memory in the object recognition test regardless of whether animals were exposed to acute stress. In the object–place test, Ro25-6981 had no effect on memory retrieval in the absence of stress but promoted memory following acute stress. These data highlight the specific contributions made by GluN2B-containing NMDA receptors to recognition memory for different types of stimuli.     

Blockade of nucleus basalis magnocellularis or activation of insular cortex histamine receptors disrupts formation but not retrieval of aversive taste memory

Recent research, using several experimental models, demonstrated that the histaminergic system is clearly involved in memory formation. This evidence suggested that during different associative learning tasks, histamine receptor subtypes have opposite functions, related to the regulation of cortical cholinergic activity. Given that cortical cholinergic activity and nucleus basalis magnocellularis (NBM) integrity are needed during taste memory formation, the aim of this study was to determine the role of histamine receptors during conditioned taste aversion (CTA). We evaluated the effects of bilateral infusions of 0.5 μl of pyrilamine (100 mM), an H₁ receptor antagonist, into the NBM, or of R-α-methylhistamine (RAMH) (10 mM), an H₃ receptor agonist, into the insular cortex of male Sprague-Dawley rats 20 min before acquisition and/or retrieval of conditioned taste aversion. The results showed that blockade of H₁ receptors in NBM or activation of H₃ receptors in the insular cortex impairs formation but not retrieval of aversive taste memory. These results demonstrated differential roles for histamine receptors in two important areas for taste memory formation and suggest that these effects could be related with the cortical cholinergic activity modulation during CTA acquisition.     

Nociceptin and its metabolite attenuate U0126-induced memory impairment through a nociceptin opioid peptide (NOP) receptor-independent mechanism

Nociceptin binds to nociceptin opioid peptide (NOP) receptors. We reported that although high doses of nociceptin impaired memory function and that these effects were mediated via NOP receptors, low doses of nociceptin attenuated the memory impairment, and these attenuating effects were not mediated via NOP receptors. Even very low doses of nociceptin were biologically active and suggested a certain binding site for this peptide, but the mechanism underlying this attenuating effect has not yet been elucidated. In the present study, we investigated the effect of an intrahippocampal injection (i.h.) of nociceptin on memory impairment induced by U0126, a MEK inhibitor, and Rp-cAMPS, a PKA inhibitor in a step-down type passive avoidance test. U0126 (2.63 nmol/mouse, i.h.) impaired memory formation and training-dependent phosphorylation of ERK2 in the hippocampus. Co-administration of nociceptin (10 fmol/mouse) significantly attenuated memory impairment, while it did not attenuate the inhibition of training-dependent phosphorylation of ERK2 induced by U0126. On the other hand, nociceptin did not attenuate memory impairment induced by Rp-cAMPS (0.448 nmol/mouse, i.h.). Nociceptin (1 fmol/mouse) also attenuated U0126 (5.26 nmol/mouse)-induced memory impairment in NOP receptor knockout mice. Nociceptin was reported to metabolize into fragments (1–13) and (14–17) in vivo, which showed pharmacological activities without affecting NOP receptors. Our findings showed that nociceptin (14–17) (1 fmol/mouse) also attenuated U0126-induced memory impairment, while nociceptin (1–13) (0.1–10 fmol/mouse) did not attenuate memory impairment. These results suggest a novel action site or mechanism for the attenuating effects of nociceptin and its metabolite, and the sequence of nociceptin (14–17) is a critical structure.     

Nonbelieved memories in middle-aged and older people

Previous studies have reported that young participants typically date events that they remember, but no longer believe they experienced, to the period of childhood. The present study investigated whether participants aged between 40 and 79 years dated events related to relinquished memories to the period of childhood, as do younger people, or whether they dated such events to a period later in life. The study also compared believed and nonbelieved memories with respect to memory perspective (1st vs 3rd person perspective). Results indicated that the majority of middle-aged and older people dated nonbelieved memories to the period of childhood (median age = 8 years). No correlation was found between the participants’ current age and their age at the time the nonbelieved event occurred. In addition, results showed that believed memories were more likely to be retrieved from a 1st person perspective than were nonbelieved memories.     

Effects of anesthetic agents on socially transmitted olfactory memories in mice

Mice can learn a food preference from odor cues transmitted on the breath of a conspecific, even if the “demonstrator” is anesthetized. To our knowledge there are no studies examining the effect of anesthetizing the “observer” on development of memory for socially transmitted food preferences (STFP). In Experiment 1 we found that 2–4 month-old F2 C57Bl/6x129sv male and female mice demonstrated a STFP after a 5 min exposure to an anesthetized demonstrator mouse when tested 24 h later. In Experiment 2, observer mice anesthetized with Sagatal (60 mg/kg) prior to the “social interaction” preferentially avoided the cued food when tested 24 h later. This aversion was not due to any overt aversive effects of this dose of Sagatal because mice that ate the food and were then anesthetized, or could only smell the food for 5 min while anesthetized, showed no preference or aversion. In a third experiment we found that the Sagatal-induced aversion was not a general property of anesthesia because there were varied results produced by observer mice treated with anesthetic drugs with different mechanisms of action. Vetalar (200 mg/kg) and Rompun (10 mg/kg) treated animals ate similar amounts of cued and non-cued food at test, indicating an absence of learning. Hypnorm (0.5 ml/kg) treated animals showed a preference for the cued food whereas those treated with Hypnovel (2.5 ml/kg) showed an aversion to the cued food. These results show that the food aversion observed with Sagatal is not a general property of anesthetic agents, but appears to be restricted to those acting primarily on the GABAergic system. Thus, we have shown that under certain conditions it is possible for an anesthetized observer mouse to learn a preference or aversion of a socially-linked olfactory cue.     

Postural stability with exhaustive repetitive sit-to-stand exercise in young adults

Previous research has indicated that muscle fatigue due to repeated bouts of physical activity can have negative residual effects on balance; however investigations using multi-joint forms of exercise involved in everyday settings and determination of how control of posture is altered during the physical activity itself are limited. The purpose of this investigation was to evaluate alterations in postural stability before, during, and after prolonged multi-joint STS exercise in healthy young adults. Center of pressure (COP) acquisitions were collected during repetitive STS exercise, while voluntary limits of stability (LOS) testing was performed before, immediately after, and 10 min after STS exercise. By 50% total STS exercise time, fatigue resulted in increased anterio-posterior (y) and medio-lateral (x) COP path lengths (p = 0.003 and p = 0.018 respectively) and an anterior shift of COP at seat-off towards the mid-foot (p = 0.010). No significant change in LOS mean amplitude was found after STS exercise; however a significant fatigue effect resulted in increased COPy sway velocity at maximal lean positions (p = 0.006), but returned to PRE values after 10 min of rest. Declines in postural stability during repetitive STS exercise was associated with reduced control of COP, as well as a reduced ability to stably control COP at extreme postural limits; however, 10 min was adequate in young adults for recovery. These results may have important implications for monitoring fall risk due to acute bouts of exercise induced muscle fatigue from repetitive multi-joint activities such as the STS.     

Cyclophosphamide impairs hippocampus-dependent learning and memory in adult mice: Possible involvement of hippocampal neurogenesis in chemotherapy-induced memory deficits

Cyclophosphamide (CYP) is an anti-neoplastic agent as well as an immunosuppressive agent. In order to elucidate the alteration in adult hippocampal function following acute CYP treatment, hippocampus-related behavioral dysfunction and changes in adult hippocampal neurogenesis in CYP-treated (intraperitoneally, 40 mg/kg) mice (8–10-week-old ICR) were analyzed using hippocampus-dependent learning and memory tasks (passive avoidance and object recognition memory test) and immunohistochemical markers of neurogenesis (Ki-67 and doublecortin (DCX)). Compared to the vehicle-treated controls, mice trained at 12 h after CYP injection showed significant memory deficits in passive avoidance and the object recognition memory test. The number of Ki-67- and DCX-positive cells began to decrease significantly at 12 h post-injection, reaching the lowest level at 24 h after CYP injection; however, this reverted gradually to the vehicle-treated control level between 2 and 10 days. We suggest that the administration of a chemotherapeutic agent in adult mice interrupts hippocampal functions, including learning and memory, possibly through the suppression of hippocampal neurogenesis.     

Intensive video gaming improves encoding speed to visual short-term memory in young male adults

The purpose of this study was to measure the effect of action video gaming on central elements of visual attention using Bundesen's (1990) Theory of Visual Attention.To examine the cognitive impact of action video gaming, we tested basic functions of visual attention in 42 young male adults. Participants were divided into three groups depending on the amount of time spent playing action video games: non-players (< 2 h/month, N = 12), casual players (4–8 h/month, N = 10), and experienced players (> 15 h/month, N = 20). All participants were tested in three tasks which tap central functions of visual attention and short-term memory: a test based on the Theory of Visual Attention (TVA), an enumeration test and finally the Attentional Network Test (ANT). The results show that action video gaming does not seem to impact the capacity of visual short-term memory. However, playing action video games does seem to improve the encoding speed of visual information into visual short-term memory and the improvement does seem to depend on the time devoted to gaming. This suggests that intense action video gaming improves basic attentional functioning and that this improvement generalizes into other activities. The implications of these findings for cognitive rehabilitation training are discussed.     

Effects of support surface and optic flow on step-like movements in pre-crawling and crawling infants

Step-like movements were examined in pre-crawling (n = 9) and crawling (n = 9) 6–13 month-old infants in the air and on a surface in response to a static pattern or optic flows that moved toward or away from the infant. Infants completed six 60-s trials. A significant interaction between locomotor status and support condition revealed that pre-crawling infants made more step-like movements in the air than on a rigid surface. In contrast, crawling infants made an equivalent number of step-like movements in the air and on the surface. Optic flow did not influence the number of step-like movements made by infants. The pre-crawling infant finding is consistent with a finding in a previous study in which two month-old infants were shown to step more in the air than on the ground. This finding is discussed relative to the idea that the infant stepping pattern disappears because the legs become too heavy to lift.     

Propranolol reduces emotional distraction in working memory: A partial mediating role of propranolol-induced cortisol increases?

Noradrenalin modulates prefrontal function, such as working memory (WM), and is associated with enhanced distractibility, and enhanced memory for emotional events and stimuli. The beta-blocker propranolol has been shown to reduce memory for emotional stimuli. Herein we describe investigations aimed at assessing whether the administration of propranolol would reduce the interference by emotional distractions during WM performance. In a between-subjects design, 48 young, healthy men received 80 mg propranolol (n = 25) or placebo (n = 23), before performing an “emotional Sternberg task” with neutral and negatively arousing distracters. Compared to placebo, propranolol impaired WM at low load, however, it also reduced the interference by emotional distracters at high load. Furthermore, an explorative moderated-mediation analysis indicated that the observed propranolol effects on emotional distraction were partially mediated by cortisol. In future non-clinical and clinical memory studies using propranolol administration, cortisol elevations should be monitored to further investigate the potential mediating role of cortisol.     

Gap junctions and memory: An investigation using a single trial discrimination avoidance task for the neonate chick

Gap junctions are important to how the brain functions but are relatively under-investigated with respect to their contribution towards behaviour. In the present study a single trial discrimination avoidance task was used to investigate the effect of the gap junction inhibitor 18-α-glycyrrhetinic acid (αGA) on retention. Past studies within our research group have implied a potential role for gap junctions during the short-term memory (STM) stage which decays by 15 min post-training. A retention function study comparing 10 μM αGA and vehicle given immediately post-training demonstrated a significant main effect for drug with retention loss at all times of test (10–180 min post-training). Given that the most common gap junction in the brain is that forming the astrocytic network it is reasonable to conclude that αGA was acting upon these. To confirm this finding and interpretation two additional investigations were undertaken using endothelin-1 (ET-1) and ET-1 + tolbutamide. Importantly, a retention function study using 10 nM ET-1 replicated the retention loss observed for αGA. In order to confirm that ET-1 was acting on astrocytic gap junctions the amnestic action of ET-1 was effectively challenged with increasing concentrations of tolbutamide. The present findings suggest that astrocytic gap junctions are important for memory processing.     

Sensory memory consolidation observed: Increased specificity of detail over days

Memories are usually multidimensional, including contents such as sensory details, motivational state and emotional overtones. Memory contents generally change over time, most often reported as a loss in the specificity of detail. To study the temporal changes in the sensory contents of associative memory without motivational and emotional contents, we induced memory for acoustic frequency by pairing a tone with stimulation of the cholinergic nucleus basalis. Adult male rats were first tested for behavioral responses (disruption of ongoing respiration) to tones (1–15 kHz), yielding pre-training behavioral frequency generalization gradients (BFGG). They next received three days of training consisting of a conditioned stimulus (CS) tone (8.00 kHz, 70 dB, 2 s) either Paired (n = 5) or Unpaired (n = 5) with weak electrical stimulation (～48 μA) of the nucleus basalis (100 Hz, 0.2 s, co-terminating with CS offset). Testing for behavioral memory was performed by obtaining post-training BFGGs at two intervals, 24 and 96 h after training. At 24 h post-training, the Paired group exhibited associative behavioral memory manifested by significantly larger responses to tone than the Unpaired group. However, they exhibited no specificity in memory for the frequency of the tonal CS, as indexed by a flat BFGG. In contrast, after 96 h post-training the Paired group did exhibit specificity of memory as revealed by tuned BFGGs with a peak at the CS-band of frequencies. This increased detail of memory developed due to a loss of response to lower and higher frequency side-bands, without any change in the absolute magnitude of response to CS-band frequencies. These findings indicate that the sensory contents of associative memory can be revealed to become more specific, through temporal consolidation in the absence of non-sensory factors such as motivation and emotion.     

Hippocampal structure and human cognition: Key role of spatial processing and evidence supporting the efficiency hypothesis in females

Here we apply a method for automated segmentation of the hippocampus in 3D high-resolution structural brain MRI scans. One hundred and four healthy young adults completed twenty one tasks measuring abstract, verbal, and spatial intelligence, along with working memory, executive control, attention, and processing speed. After permutation tests corrected for multiple comparisons across vertices (p < .05), significant relationships were found for spatial intelligence, spatial working memory, and spatial executive control. Interactions with sex revealed significant relationships with the general factor of intelligence (g), along with abstract and spatial intelligence. These correlations were mainly positive for males but negative for females, which might support the efficiency hypothesis in women. Verbal intelligence, attention, and processing speed were not related to hippocampal structural differences.     

The effects of foot cooling on postural muscle responses to an unexpected loss of balance

The purpose of this study was to examine the role of foot sole somatosensory information during reactive postural control. Twenty young adults (22.0 ± 1.4 y) participated in this study. Baseline skin sensitivity from the foot sole was assessed using Semmes-Weinstein monofilaments. Postural muscle responses, in the form of electromyographic (EMG) onset latencies and amplitudes, were then obtained while participants recovered their balance while standing on a moveable platform that could translate in either the forward or backward direction. Following these baseline measures, the participant’s foot soles were immersed in a 0–2 °C ice-water bath for 12 min followed by a 3 min re-immersion period. At the completion of foot cooling, foot sole sensitivity and postural muscle responses to the balance perturbations were re-assessed. Results indicated that the foot cooling protocol reduced foot sole sensitivity and remained reduced throughout the duration of the experiment (p < 0.001). The reduction in foot sole somatosensation resulted in the soleus EMG onset latency being delayed by 3 ms (p = 0.041) and the soleus and medial gastrocnemius EMG amplitudes increasing by 14–23% (p = 0.002–0.036) during the balance perturbation trials. While the magnitude of these results may suggest that foot cooling has a minor functional consequence on reactive postural control, it is likely that the results also reflect the ability of the central nervous system to rapidly adapt to situations with altered somatosensory feedback.     

Comparison of fetal and maternal heart rate measures using electrocardiographic and cardiotocographic methods

PurposeTo determine the reliability at term of: (1) two methods of measuring fetal heart rate (HR), electrocardiographic (ECG, the ‘gold standard’) and cardiotocographic (CTG) and (2) two ECG methods of measuring maternal HR variability over relatively brief periods of time (s–min).MethodsDuring 20 min of rest (N = 39) and during 2 min of auditory stimulation (mother's recorded voice, n = 19), fetal HR data were collected using an ECG (Monica AN24) and a Hewlett-Packard Model 1351A CTG. Simultaneously, maternal HR data (n = 37) were collected using the same ECG device (Monica AN24) and a second stand-alone cardiac monitor (Spacelab 514T cardiac monitor with a QRS detector).ResultsDuring 20 min of maternal rest, correlations of individual fetal CTG with ECG measures of HR at each second were moderate to high (r = .57–.97) for 77% of fetuses. Correlations of HR averaged over fetuses and over each of the 20 min were high (r = .93–.97); fetal HR averaged over 20 min varied between devices from 0.0 to 0.8 bpm. During 2 min of maternal voice presentation, correlations of fetal HR over each second were moderate to high (r = .54–.99) for 95% of fetuses and high (all rs = .99) when averaged across fetuses in 30 s or 2 min epochs. Average fetal HR between devices over the 2 min voice varied from 0.0 to 0.6 bpm. Correlations and/or % agreement between the two ECG methods of measuring maternal HR were high. Average maternal HR over 10 min showed 81% of pairs with a difference of ≤1 bpm; correlations for HR variability measures varied from r = .89 to .97.ConclusionsGood reliability was demonstrated between individual spontaneous and auditory induced fetal CTG and ECG with high correlations when HR data were averaged over fetuses or in 30–120 s epochs. High reliability of maternal HR measures was obtained using two ECG devices.