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PubMed2001

Dorsolateral and ventral regions of the periaqueductal gray matter are involved in distinct types of fear.

Stepwise increases in the electrical stimulation of the dorsolateral periaqueductal gray (dlPAG) produces alertness, then freezing and finally escape. This paper examines whether this freezing is (i) caused by Pavlovian fear conditioning to the contextual cues present during stimulation and (ii) the result of the stimulation of neurons located inside the dlPAG or elsewhere. To this end, freezing behavior was assessed in rats exposed either to the same or a different environment (context shift test) following the application of either footshocks or stimulation of the dlPAG at the freezing threshold. Rats submitted to footshocks presented freezing to the context 24h later whereas rats submitted to the dlPAG stimulation showed freezing only immediately after the stimulation, regardless of the context. In the second experiment, aversive states generated by activation of the dlPAG were assessed either by measuring the thresholds for freezing and escape responses or the duration of these responses following microinjections of semicarbazide inside the dlPAG. The duration of freezing behavior was also measured in rats submitted to a contextual fear-conditioning paradigm using footshocks as unconditioned stimulus. Lesions of the ventral periaqueductal gray (vPAG) disrupted conditioned freezing to contextual cues associated to footshocks but vPAG lesions did not change the threshold of either freezing or escape responses elicited by electrical stimulation of the dlPAG. Lesions of the vPAG did not change the amount of freezing or escape responses produced by microinjections of semicarbazide into the dlPAG. These results indicate that stimulation of dlPAG neurons produce freezing behavior independent of any contextual fear conditioning and add to previously reported evidence showing that the vPAG is a critical structure for the expression of conditioned fear. In contrast, the neural substrate of unconditioned dlPAG stimulation-induced freezing is likely to elaborate unconditioned fear responses to impending danger, which have been implicated in panic disorder.

Animals↗
PubMed2006

Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.

The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.

Amygdala↗
PubMed2004

Perirhinal and postrhinal contributions to remote memory for context.

The perirhinal (PER) and postrhinal (POR) cortices, two components of the medial temporal lobe memory system, are reciprocally connected with the hippocampus both directly and via the entorhinal cortex. Damage to PER or POR before or shortly after training on a contextual fear conditioning task causes deficits in the subsequent expression of contextual fear, implicating these regions in the acquisition or expression of contextual memory. Here, we examined the contribution of PER and POR to the processing of remotely learned contextual information. Male Long-Evans rats were trained in an unsignaled contextual fear conditioning paradigm. After training, rats received bilateral neurotoxic lesions to PER or POR or sham control surgeries at three different training-to-lesion intervals: 1, 28, or 100 d after training. Two weeks after surgery, lesioned and control rats were returned to the training context to assess contextual fear as measured by freezing. Rats with PER or POR damage froze significantly less in the training context than control rats but were not different from each other. The severity of the deficit did not differ across training-to-lesion intervals for any group. This pattern of deficits differs from that of posttraining hippocampal lesions, for which longer training-to-lesion intervals produce significantly more fear-conditioned contextual freezing than shorter training-to-lesion intervals. In the absence of such a retrograde gradient in the present study, our interpretation is that PER and POR have an ongoing role in the storage or retrieval of representations for context. Alternatively, these regions may be involved in a more extended consolidation process that becomes apparent beyond 100 d after learning.

Animals↗
PubMed2001

Amygdala, hippocampus, and unconditioned fear.

Embedded within contemporary views of emotional learning is a well-founded agreement that the amygdala plays a pivotal role in the formation and consolidation of aversive memories formed during fear conditioning. However, it is important to determine whether observed deficits are reflective of a memory impairment or whether they are simply attributable to a deficit in the performance of unconditioned fear responses such as freezing. Within the neurobiology of learning and memory literature, there is an ongoing debate concerning the potential role of the amygdala in the performance of unconditioned fear responses. A view put forth by Vazdarjanova and McGaugh (1998) suggests that the amygdala is not required for the formation and consolidation of the aversive memories formed during fear conditioning, but is essential in the performance of unconditioned fear responses. Data provided by Maren (1999) counter this view by positing that the amygdala is not required for the performance of fear responses, but its role is of a mnemonic nature in the conditioning of fear to neutral cues. To clarify the amygdala's participation in these two processes, a useful approach would involve a situation where animals with amygdala damage were examined for their unconditioned fear responses in reaction to footshock as well as the conditioning of these reactions to previously neutral cues paired with the aversive event. We have previously reported that rats with amygdala or hippocampal damage are impaired in discriminative fear conditioning to context. In the present experiment, we report the initial unconditioned fear responses to footshock by these same animals as well as the conditioned responses during testing. In both groups, the fear responses assessed (freezing, urination, defecation, and locomotion) were not impaired and did not differ from those expressed by the sham animals. The impairment of discriminative fear conditioning to context, in combination with the present experiment, represents a dissociation where damage to specific memory structures (amygdala or hippocampus) debilitates the mnemonic processes involved in fear conditioning, but not the performance of the fear responses per se.

Amygdala↗
PubMed2001

Selective responding of nucleus accumbens core and shell dopamine to aversively conditioned contextual and discrete stimuli.

Dopamine transmission within the nucleus accumbens has been implicated as a neurochemical substrate of associative learning processes. It has been suggested that the acquisition of classically conditioned fear to a specific environment, or context, differs fundamentally from the development of conditioned fear to a discrete stimulus, such as a light or a tone. In this study, we assessed extracellular dopamine in the rat nucleus accumbens shell and core during the expression of a conditioned fear response. Animals were aversively conditioned to either a context or a tone and extracellular dopamine was measured in the nucleus accumbens shell and core by in vivo microdialysis over the next 2 days as animals were returned first to the conditioning chamber (day 1: context test), and subsequently as animals were again returned to the chamber and presented with the conditioned tone stimulus (day 2: tone test). Dopamine levels in the core were significantly higher in the Context-Shock group compared to the Tone-Shock group during the 30-min exposure to context while dopamine levels in the nucleus accumbens shell did not differ significantly during the context test between groups. In contrast, extracellular dopamine in the shell but not the core of Tone-Shock animals increased significantly during presentation of the tone. Dopamine in both the shell and core remained unchanged during the tone test in the Context-Shock groups.These data suggest distinct roles for shell and core dopamine transmission in the expression of a conditioned emotional response. While dopamine increased in the shell primarily during the presentation of a discrete tone conditioned stimulus, core dopamine responded more to a contextual conditioned stimulus. These results may reflect differences in either the type of information acquired or the salience of the learned associations which are formed to a context vs. a discrete tone cue.

Acoustic Stimulation↗
PubMed2001

The effects of water deprivation on conditioned freezing to contextual cues and to a tone in rats.

In two experiments we used an automated system for quantifying freezing responses in rats to replicate and extend Maren et al. (Maren S, DeCola JP, Fanselow MS. Water deprivation enhances fear conditioning to contextual, but not discrete, conditional stimuli in rats. Behav Neurosci 1994;108:645-9; Maren S, DeCola JP, Swain RA, Fanselow MS, Thompson RF. Parallel augmentation of hippocampal long-term potentiation, theta rhythm and contextual fear conditioning in water deprived rats. Behav Neurosci 1994;108:44-57) who found that water deprivation in rats produced a selective enhancement in conditioning to context, as opposed to conditioning to a tone. In experiment 1 we gave water deprived and non-deprived rats either three or ten pairings of a tone and foot shock. During conditioning water deprivation decreased overall freezing only in rats that received ten pairings. On 2 subsequent days we assessed conditioned freezing (1) to the contextual cues of the conditioning chamber and (2) to the tone when presented in a distinctive, novel environment. We found, in direct contrast to Maren et al. (Maren S, DeCola JP, Fanselow MS. Water deprivation enhances fear conditioning to contextual, but not discrete, conditional stimuli in rats. Behav Neurosci 1994;108:645-9), that (a) water deprived rats did not differ from non-deprived rats in levels of conditioned contextual freezing and that (b) water deprived rats did show reduced levels of freezing to the tone stimulus. In the same experiment we found that the number of tone-shock pairings did not affect levels of conditioned contextual freezing but that rats that had received three pairings did show reduced levels of freezing to the tone stimulus compared with rats that had received ten pairings, thereby demonstrating that the behavioural procedure and analysis system that we used was appropriately sensitive to differences in conditioning. In experiment 2, therefore, we sought to replicate Maren et al. (Maren S, DeCola JP, Fanselow MS. Water deprivation enhances fear conditioning to contextual, but not discrete, conditional stimuli in rats. Behav Neurosci 1994;108:645-9) using, as far as possible, exactly the same procedural parameters. Here we found that water deprivation produced no effects on conditioned freezing to the contextual cues or to the tone. We conclude that there is sufficient reason to doubt the generality of the previously reported findings.

Acoustic Stimulation↗
PubMed2002

Glucocorticoid involvement in memory formation in a rat model for traumatic memory.

Contextual fear conditioning under training conditions involving high stressor intensities has been proposed as an animal model for traumatic memories. The strength of memory for this task has been related to the intensity of the conditioning stressor and post-training corticosterone values. However, administration of a glucocorticoid receptor (GR) antagonist only attenuated memory for this task in rats conditioned at a moderate shock intensity (0.4 mA), but failed to influence conditioning in rats trained at a high shock intensity (1 mA). Here, we further questioned whether interfering with glucocorticoid action at the time of training might be effective in influencing contextual fear conditioning in rats trained under different shock intensities. Rats were subcutaneously injected with the glucocorticoid synthesis inhibitor metyrapone (50, 100 mg/kg) 90 min before being trained in the contextual fear conditioning task, at either 0.4 or 1 mA shock intensities. The results showed that metyrapone, in a dose-dependent manner: (i) attenuated long-term expression of contextual fear conditioning, both in 0.4- and 1 mA-trained rats; and (ii) efficiently prevented increased plasma corticosterone concentration. In addition to further supporting a facilitating role of glucocorticoids in memory consolidation, these findings suggest a critical involvement of these hormones in the formation of traumatic memories.

Animals↗
PubMed2005

Theta activity in neurons and networks of the amygdala related to long-term fear memory.

With a combined in vitro/in vivo electrophysiological and behavioral approach, we have correlated conditioned fear behavior to electrophysiological activities in the lateral amygdala and the hippocampal formation in rodents. Data indicate that projection neurons in the lateral amygdala display a continuum of spike patterns including accommodating patterns, regular firing, and oscillatory activity at theta frequencies. The firing pattern is controlled to an important part by the intracellular cAMP system, in that an increase in intracellular cAMP concentration facilitates regular firing and theta oscillations. Oscillatory electrical activity, in turn, provides an important cellular element of synchronized theta activity at 4-8 Hz (indicating atropine-sensitive type 2 theta) occurring in amygdalo-hippocampal pathways during conditioned fear responses. This type of rhythmic network activity is associated with the retrieval of long-term fear memory following cued and contextual fear conditioning, but is not related to the expression of fear behavior per se or to short-term fear memory. Synchronization at theta frequencies is suggested to represent activity in amygdalo-hippocampal pathways associated with system consolidation of fear memory, which is supported by the cholinergic system.

Action Potentials↗
PubMed2006

Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat.

In the present study, we investigated in the rat whether vertex- or primary somatosensory cortex-recorded somatosensory-evoked potentials (Vx-SEP/SI-SEP, respectively) signal unpleasantness of noxious stimuli. Therefore, initially we characterised fentanyl effects (0, 20, 40 or 50 microg/kg/h) on somatosensory and auditory processing by recording Vx-/SI-SEPs and vertex- and primary auditory cortex-recorded auditory-evoked potentials (Vx-/AI-AEPs, respectively). Subsequently, in a separate experiment, the animals were subjected to a Pavlovian fear-conditioning paradigm. The noxious stimuli applied to evoke Vx-/SI-SEPs (unconditioned stimulus (US)) were paired to a tone (conditioned stimulus (CS)) under 'steady state' conditions of 0, 20, 40 or 50 microg/kg/h fentanyl. Vx-/SI-SEPs were recorded simultaneously during these trials. After CS-US presentation, CS-induced fear-conditioned behaviour was analysed in relation to the SEPs recorded during CS-US presentation and the AEPs recorded in the first experiment. While the SI-SEP and AI-AEP were minimally but significantly affected, fentanyl dose-dependently decreased the Vx-SEP and Vx-AEP. The decrease of the Vx-SEP and Vx-AEP was parallelled by the dose-dependent decrease of the amount of CS-induced fear-conditioned behaviour. These results suggest that the dose-dependent decrease of the Vx-SEP amplitude, rather than of the SI-SEP, indicates that the US was experienced as less unpleasant. Next to an altered US processing, altered CS processing contributed to the decrease of the amount of CS-induced fear-conditioned behaviour as indicated by the dose-dependent decrease of the Vx-AEP.

Analgesics, Opioid↗
PubMed2000

The predator odor, TMT, displays a unique, stress-like pattern of dopaminergic and endocrinological activation in the rat.

Predator odors may provide a species relevant aversive stimuli to study the central effects of stress in rats and may have several benefits over currently applied models. Here, we examined one such odor, TMT, isolated from the fox, a predator of the rat, on fear-induced behaviors, serum corticosterone, and central dopamine metabolism. Habituated rats were exposed to TMT, or a control odor, butyric acid, in an open field. For comparison, other rats were subjected to a model of conditioned fear - a traditional fear model. Several similarities between the two stresses were observed including increased serum corticosterone and increased dopamine metabolism in the medial prefrontal cortex. Differences were also observed. TMT, but not conditioned fear, activated dopamine metabolism in the amygdala, but not the nucleus accumbens core and shell. Rats exposed to conditioned fear, but not TMT odor, demonstrated altered behaviors associated with fear, including locomotion, grooming and immobility. Finally, rats reexposed to TMT after a 24-h delay did not demonstrate any of the changes observed with acute exposure to TMT. These data indicate acute exposure to a predator odor, TMT, can result in a unique pattern of biochemical activation that is similar, but not identical, to conditioned fear. The differences may indicate unique features of a central 'fear arousal' pathway that responds to innate, unlearned stressful stimuli, such as predator odors.

Animals↗
PubMed2002

The group I metabotropic glutamate receptor mGluR5 is required for fear memory formation and long-term potentiation in the lateral amygdala.

The group I metabotropic glutamate receptor subtype mGluR5 has been shown to play a key role in the modulation of synaptic plasticity. The present experiments examined the function of mGluR5 in the circuitry underlying Pavlovian fear conditioning using neuroanatomical, electrophysiological, and behavioral techniques. First, we show using immunocytochemical and tract-tracing methods that mGluR5 is localized to dendritic shafts and spines in the lateral nucleus of the amygdala (LA) and is postsynaptic to auditory thalamic inputs. In electrophysiological experiments, we show that long-term potentiation at thalamic input synapses to the LA is impaired by bath application of a specific mGluR5 antagonist, 2-methyl-6-(phenyle-thynyl)-pyridine (MPEP), in vitro. Finally, we show that intra-amygdala administration of MPEP dose-dependently impairs the acquisition, but not expression or consolidation, of auditory and contextual fear conditioning. Collectively, the results of this study indicate that mGluR5 in the LA plays a crucial role in fear conditioning and in plasticity at synapses involved in fear conditioning.

Amygdala↗
PubMed1994

Modulation of hypoalgesia by morphine and number of shock trials: covariation of a measure of context fear and hypoalgesia.

In a recent series of studies, we observed that exposure to prolonged foot shock increased hypoalgesia induced by morphine. This increase was observed only when testing was conducted in the presence of shock-associated cues, suggesting that it resulted from context-conditioned fear. However, we do not know whether the extended stressor parameters employed in that study are necessary for an observance of the effect. Therefore, in the present study, we assessed the effect of the number of shock trials (either 0, 20, 100, or 200) on the hypoalgesia observed following morphine administration. In addition, we measured activity as an independent index of context-conditioned fear, because in prior studies there had been no independent behavioral assessment of the conditioning of fear to the context. Although others have shown a covariation of conditioned fear and context-induced hypoalgesia using shock parameters and test paradigms different from our own, we sought to assess whether the same covariation would hold for conditioned fear and the hypoalgesia observed following the administration of morphine. The results showed increased hypoalgesia in all groups exposed to foot shock, demonstrating that prolonged exposure to foot shock is not necessary for an observance of this effect. In addition, the results revealed a linear relationship between number of trials of shock and hypoalgesia, but a U-shaped relationship between trials and activity. The pattern of results is considered in light of Fanselow's Perceptual-Defensive-Recuperative model.

Animals↗
PubMedDate not supplied

Environmental enrichment modifies the PKA-dependence of hippocampal LTP and improves hippocampus-dependent memory.

cAMP-dependent protein kinase (PKA) is critical for the expression of some forms of long-term potentiation (LTP) in area CA1 of the mouse hippocampus and for hippocampus-dependent memory. Exposure to spatially enriched environments can modify LTP and improve behavioral memory in rodents, but the molecular bases for the enhanced memory performance seen in enriched animals are undefined. We tested the hypothesis that exposure to a spatially enriched environment may alter the PKA dependence of hippocampal LTP. Hippocampal slices from enriched mice showed enhanced LTP following a single burst of 100-Hz stimulation in the Schaffer collateral pathway of area CA1. In slices from nonenriched mice, this single-burst form of LTP was less robust and was unaffected by Rp-cAMPS, an inhibitor of PKA. In contrast, the enhanced LTP in enriched mice was attenuated by Rp-cAMPS. Enriched slices expressed greater forskolin-induced, cAMP-dependent synaptic facilitation than did slices from nonenriched mice. Enriched mice showed improved memory for contextual fear conditioning, whereas memory for cued fear conditioning was unaffected following enrichment. Our data indicate that exposure of mice to spatial enrichment alters the PKA dependence of LTP and enhances one type of hippocampus-dependent memory. Environmental enrichment can transform the pharmacological profile of hippocampal LTP, possibly by altering the threshold for activity-dependent recruitment of the cAMP-PKA signaling pathway following electrical and chemical stimulation. We suggest that experience-dependent plasticity of the PKA dependence of hippocampal LTP may be important for regulating the efficacy of hippocampus-based memory.

Action Potentials↗
PubMed2003

Posttraining lesion of the superior colliculus interferes with feature-negative discrimination of fear-potentiated startle.

Though much is known about the neural circuits involved in the elicitation of fear, little is known about the neural circuits responsible for the reduction of fear. The present experiments investigated the contribution of the superior colliculus (SC) and the dorsal periacquaductal gray (dPAG) in the reduction of conditioned fear produced by an auditory feature trained in a feature-negative discrimination procedure. In this procedure, light plus foot shock training trials are interspersed with trials in which the light is preceded by a noise and this noise and light compound is not followed by foot shock. At the end of this feature-negative discrimination training, rats were given excitotoxic lesions of the SC or dPAG. Feature-negative discrimination of fear was assessed with the fear-potentiated startle effect in which conditioned fear is operationally defined as potentiated startle amplitude in the presence versus the absence of the light. Feature-negative discrimination of fear is evidenced by a reduction in fear-potentiated startle to the light when the noise feature accompanies the light. Lesions of the SC, but not the dPAG, interfered with feature-negative discrimination of fear-potentiated startle suggesting that the SC plays a role in feature-negative discrimination of fear. Both SC and dPAG lesions facilitated startle amplitude in the absence of the light suggesting that these structures may exert a tonic inhibition on the acoustic startle reflex. The SC receives polymodal sensory information and is known to project forebrain areas involved in the production of conditioned fear. Thus, the SC may be an important component of the feature-negative discrimination circuit.

Acoustic Stimulation↗
PubMed2002

Social stress does not interact with paradoxical sleep deprivation-induced memory impairment.

Extensive evidence has linked both paradoxical sleep (PS) and stress to memory processing. The purpose of the present study was to examine the effect of social instability stress on memory and to verify whether this stress interferes with the amnesic effect of PS deprivation using the modified multiple platform method. In addition to the PS-deprived group (put onto narrow platforms inside the deprivation tanks) two control groups were used: one of them remained in its home-cages and the other was placed inside the deprivation tanks, onto a grid that contained large platforms on it. All groups were subdivided in socially stable and unstable conditions. Immediately after 96 h of sleep deprivation, the animals were trained in three different memory tasks: inhibitory avoidance, classical fear conditioning to a discrete stimulus and contextual fear conditioning. Twenty-four hours after training, the animals were tested in order to assess task acquisition. The results showed that social instability did not impair the performance of animals nor interacted with PS deprivation in any of the tasks. Grid control animals presented a selective impairment in the inhibitory avoidance task and contextual, but not in the classical, fear conditioning task, compared to cage control rats. This finding could be due to the stress to which grid control animals were exposed (humidity and luminosity) during the manipulation period. PS-deprived animals exhibited poorer performance than the other groups in all tasks. As they also showed an increased threshold to shock-induced vocalisation, but not to flinch response, it is not possible to completely rule out a decreased response to noxious stimulation as a contributing factor for the present results with PS deprivation.

Animals↗
PubMed2001

Contextual control over the expression of fear in rats conditioned under a benzodiazepine.

RATIONALE: Benzodiazepines disrupt fear conditioning, but this disruption is context-specific; if rats have been conditioned under a benzodiazepine, their fear is recovered if they are tested in a different context. The present experiments investigated how the conditioning context controls fear in rats conditioned under a benzodiazepine. OBJECTIVES: The experiments had three aims: (1) to replicate the finding that fear is recovered when rats are tested in a different context, (2) to test whether the conditioning context reduces fear generally or only for the specific stimulus conditioned in that context and (3) to test whether latent inhibition of the conditioning context reduces its control over fear. METHODS: Rats were injected with the benzodiazepine midazolam (1.25 mg/kg) or saline and exposed to a conditioned stimulus (CS) and shock in a distinctive chamber. Latent inhibition of the chamber was induced by extensively preexposing the rats to the chamber. The day after conditioning, fear was assessed by presenting the CS while rats were in either the conditioning chamber or a different chamber. RESULTS: The midazolam-induced reduction of fear was reversed (i.e. fear was partially recovered) if rats were tested in the different context, and was completely prevented if the conditioning context had been latently inhibited. These two effects were not additive since, when the conditioning context had been latently inhibited, rats showed less fear in the different context than in the conditioning context. CONCLUSIONS: We argue that midazolam does not disrupt conditioning, but imbues the conditioning context with control over retrieval of the CS-shock association. In this regard, the effects of midazolam closely parallel those of extinction.

Animals↗
PubMed2001

In vivo neurotransmitter release in the locus coeruleus--effects of hyperforin, inescapable shock and fear.

Hyperforin, the main antidepressant constituent of Hypericum perforatum, influences the extracellular concentrations of transmitters in vitro and in vivo. In vivo experiments have shown that hyperforin enhances the extracellular concentrations of dopamine, norepinephrine, serotonin and glutamate in the locus coeruleus. Hyperforin-free Hypericum extract also elevates the extracellular concentrations of dopamine and norepinephrine in the locus coeruleus, but, in contrast to hyperforin, the extracellular concentration of serotonin is diminished. The differing profiles of hyperforin and hyperforin-free Hypericum extract on the extracellular transmitter concentrations point to the presence of an additional biologically active compound in Hypericum perforatum. Inescapable shock increases the release of monoamines and several amino acids, as well as motility, blood pressure and heart rate. Conditioned fear, similar to hyperforin-free Hypericum extract, decreases the release of serotonin in the locus coeruleus. Conditioned fear also leads to tachycardia. The latter finding shows that telemetric heart rate recording is a good index for conditioned fear. In vivo findings confirm the idea that the anti-depressive properties of Hypericum extract and hyperforin result from increases in extracellular neurotransmitter concentrations. Since hyperforin-free extract, like conditioned fear, reduces the extracellular concentration of serotonin, hyperforin may be more beneficial than Hypericum extract in the treatment of depressive disorders.

Animals↗