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PubMed2005

Changes in the biogenic amine content of the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens of rats submitted to single and repeated sessions of the elevated plus-maze test.

It has been demonstrated that exposure to a variety of stressful experiences enhances fearful reactions when behavior is tested in current animal models of anxiety. Until now, no study has examined the neurochemical changes during the test and retest sessions of rats submitted to the elevated plus maze (EPM). The present study uses a new approach (HPLC) by looking at the changes in dopamine and serotonin levels in the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens in animals upon single or double exposure to the EPM (one-trial tolerance). The study involved two experiments: i) saline or midazolam (0.5 mg/kg) before the first trial, and ii) saline or midazolam before the second trial. For the biochemical analysis a control group injected with saline and not tested in the EPM was included. Stressful stimuli in the EPM were able to elicit one-trial tolerance to midazolam on re-exposure (61.01%). Significant decreases in serotonin contents occurred in the prefrontal cortex (38.74%), amygdala (78.96%), dorsal hippocampus (70.33%), and nucleus accumbens (73.58%) of the animals tested in the EPM (P < 0.05 in all cases in relation to controls not exposed to the EPM). A significant decrease in dopamine content was also observed in the amygdala (54.74%, P < 0.05). These changes were maintained across trials. There was no change in the turnover rates of these monoamines. We suggest that exposure to the EPM causes reduced monoaminergic neurotransmission activity in limbic structures, which appears to underlie the "one-trial tolerance" phenomenon.

Amygdala↗

PubMed2005

Influence of cocaine self-administration on learning related to prefrontal cortex or hippocampus functioning in rats.

RATIONALE: Individuals who abuse cocaine have cognitive deficits, particularly in functions associated with the orbitofrontal cortex. It is not clear to what extent the impact of cocaine on cognitive functioning is related to its role as a behavioral reinforcer. A preclinical means to investigate this issue is to use a yoked-triad procedure in which sets of three animals either contingently self-administer cocaine or receive passive administration of cocaine or saline in a noncontingent manner. OBJECTIVE: Using this procedure, we assessed cocaine's effect on learning that requires a functionally intact prefrontal cortex (prelimbic or insular/orbital subregions) or hippocampus. METHODS: Rats self-administering 1-mg/kg unit doses of cocaine responded under a fixed-ratio 5, time-out 20-s schedule of drug delivery. Testing took place in a radial-arm maze within the first 30 min after 2-hr drug sessions ended, beginning after 2.5 months of cocaine or saline exposure. RESULTS: Rats self-administering cocaine earned 14-18 infusions on average throughout different phases of the study. In groupwise comparisons, learning in the visually guided delayed win-shift (prelimbic prefrontal cortex-related) and win-shift (hippocampus-related) tasks was not influenced by contingent or noncontingent cocaine exposure. Session latency, though, was shorter in both cocaine-exposed groups during the win-shift task. During the odor-guided delayed win-shift task (insular/orbital prefrontal cortex-related), learning was disrupted in rats self-administering cocaine, with no influence of noncontingent cocaine exposure. CONCLUSIONS: Based on these and previous findings, learning related to functioning of the insular/orbital prefrontal cortex and amygdala is the most consistently disrupted in cocaine-intoxicated rats after long-term drug exposure.

Amygdala↗

PubMed1995

Intrinsic circuit organization of the major layers and sublayers of the dorsolateral prefrontal cortex in the rhesus monkey.

Intrinsic connections are likely to play important roles in cognitive information processing in the prefrontal association cortex. To gain insight into the organization of these circuits, intracortical connections of major laminar and sublaminar divisions were retrogradely labeled in Walker's area 9 and 46 in rhesus monkeys by using cholera toxin (B-subunit) conjugated to colloidal gold. Microinjections placed within particular cortical laminae produced unique patterns of retrograde labeling. Injections in layers II/III yielded labeling which was laterally widespread (2-7 mm) in supragranular layers, and more narrowly focused, i.e., conforming to a column, in layers IV-VI. In contrast, local circuits associated with layers IV and Vb displayed a regular, cylindrical organization, whereas intrinsic connections of layer Va were laterally extensive (3-5 mm) in layers III and Va. Finally, injections in layer VI gave rise to a narrow column of cell labeling traversing all layers, augmented by laterally extensive labeling (approximately 7 mm) in layer VI. The intrinsic connections of the prefrontal cortex were arrayed within mediolaterally elongated stripes which were often distributed asymmetrically in either the medial or lateral direction. In addition, labeled cells within these mediolaterally oriented fields were frequently grouped within discrete clusters or narrow bands. The intrinsic connections identified in this study differ from the local circuits of corresponding layers reported for primary visual cortex; the unique intrinsic wiring diagram of the prefrontal cortex may be related to its specialized cognitive and mnemonic functions.

Animals↗

PubMed2005

Anterior prefrontal cortex and the recollection of contextual information.

Recollective memory can involve the retrieval of many different kinds of contextual information, including where and when an event took place, as well as our thoughts and feelings at the time. The brain regions associated with this ability were examined in an event-related fMRI experiment, where participants made decisions about words or famous faces which were presented either on the left or right of a monitor screen. Subsequently, the studied words and faces were again presented and participants underwent fMRI brain scanning while recollecting either which of the decisions they had made on each item ("task memory"), or whether it had been presented on the left or right of the screen ("position memory"). A functional dissociation was observed within anterior prefrontal cortex (principally Brodmann's area 10), with activation in lateral regions associated with remembering either type of information (relative to baseline), and a medial anterior PFC region showing significantly greater activation during the "task memory" conditions. These results suggest different roles for lateral and medial anterior prefrontal cortex in recollection.

Adult↗

PubMed2006

Differential activation of ventrolateral prefrontal cortex during working memory retrieval.

Brain imaging studies have suggested a predominant involvement of prefrontal areas during retrieval of information from working memory (WM). This study used event-related functional magnetic resonance imaging to assess the gradual recruitment of brain areas during verbal WM-retrieval with a parametrically varied modified version of the Sternberg Item Recognition Paradigm. In particular, we were interested in activation differences during retrieval of negative and positive probes. Fifteen subjects performed a WM-task which required the retrieval of a probe letter from a set of a maximum of three letters. The analysis of the retrieval period regardless of probe type revealed bilateral VLPFC activation during retrieval from a single remembered item. These initially activated regions showed a gradual activation increase of left VLPFC (BA 47) and anterior PFC (BA 10) as well as and bilateral DLPFC (BA 9) with increasing retrieval demand, i.e. during retrieval of two and three previously remembered letters. The comparison of negative and positive probes (non-targets versus targets) revealed greater activity in VLPFC (BA 47) in response to negative than to positive probes. These findings demonstrate that ventral areas of prefrontal cortex seem to be differentially engaged during the discrimination of a non-target from a previously manipulated set.

Adult↗

PubMed2003

Lesions of the medial prefrontal cortex or nucleus accumbens core do not impair inhibitory control in rats performing a stop-signal reaction time task.

The 'stop-signal' task measures the ability to inhibit a response that has already been initiated, i.e. the ability to stop. Human subjects who have been classified as 'impulsive', for example, those with attention-deficit/hyperactivity disorder (ADHD), are slower to react to the stop signal, and are often less sensitive to changes in the timing of signals to stop. Imaging studies have implicated fronto-striatal circuitry in the mediation of this form of response control. We report inhibition functions on the stop-signal reaction time (SSRT) task for normal rats, and following damage to the medial prefrontal cortex or to the nucleus accumbens core. Neither group of excitotoxic lesions produced significant deficits on task performance. Subsequent treatment with D-amphetamine (0.3 and 1.0mg/kg) resulted in quicker go-trial reaction times (mRT) overall, but had no significant effect on SSRT. Neither medial prefrontal cortex nor nucleus accumbens lesions had any differential effects on performance following D-amphetamine. These results are discussed with respect to the fronto-striatal circuitry involved in the mediation of behavioural inhibition.

Animals↗

PubMed1976

Attenuation of self-stimulation from substantia nigra but not dorsal tegmental noradrenergic bundle by lesions of sulcal prefrontal cortex.

Rats that self-stimulated from electrodes implanted in either the substantia nigra pars compacta (SNC) or the dorsal tegmental noradrenergic bundle (DTB) received bilateral electrolytic lesions of the prefrontal cortex dorsal to the rhinal sulcus. Immediately after the lesions, animals with SNC electrodes (n = 9) showed significant and permanent reductions in self-stimulation rates. The average reduction in the SNC group was 67% of prelesion bar-pressing scores. In contrast, rats with DTB electrodes (n = 11) were not significantly affected by similar sulcal lesions. Subsequent examination of the brains for prograde degeneration using procedure I of Fink and Heimer 11 revealed a descending system of sulcal efferents that was very dense in the region of the SNC but only scattered in the area of the DTB. The close relation between the effects of sulcal lesions on self-stimulation and the resultant density of degeneration as a function of stimulation site is discussed in terms of the contribution of prefrontal cortex to self-stimulation in general, and of the implications for the catecholamine hypothesis of self-stimulation in particular.

Animals↗

PubMed2005

Information processing flow and neural activations in the dorsolateral prefrontal cortex in the Stroop task in schizophrenic patients. A spatially filtered MEG analysis with high temporal and spatial resolution.

Using a spatially filtered magnetoencephalography analysis (synthetic aperture magnetometry), we estimated neural activations in the Stroop task in nearly real time for schizophrenic patients with/without auditory hallucinations and for normal control subjects. In addition, auditory hallucinations were examined through the information processing flow of the brain neural network, including the frontal regions. One hundred unaveraged magnetoencephalography signals during the incongruent stimulus responses were analyzed with a time window of 200 ms in steps of 50 ms. In the 25-60-Hz band, cortical regions that showed significant current source density changes were examined for each time window. The three groups showed significantly decreased current source density, corresponding to neural activation, with temporal overlap along the fundamental cognitive information processing flow: sensory input system, executive control system, motor output system. Transient neural activations in the dorsolateral prefrontal cortex were bilateral with left-side dominancy for normal controls, left-lateralized for nonhallucinators and right-lateralized for hallucinators. Our results suggest that the dysfunction in the left dorsolateral prefrontal cortex was related to auditory hallucinations, while the information processing flow was unaffected in the schizophrenic subjects in the Stroop task.

Adolescent↗

PubMed1998

Response of the ventral pallidal/mediodorsal thalamic system to antipsychotic drug administration: involvement of the prefrontal cortex.

Intracellular recordings were obtained from rat ventral pallidal (VP) and mediodorsal thalamic (MD) cells in vivo and the effects of antipsychotic drugs on their basal and evoked electrophysiological characteristics were assessed. Administration of either haloperidol or clozapine caused a significant decrease in the average firing rate, accompanied by a hyperpolarization of the membrane potential in the VP cells recorded. However, neither drug induced a substantial change in the other basic membrane properties of the MD cells or VP cells tested. In addition, in 50% of the MD cells tested, both antipsychotic drugs caused a change in spike discharge from an oscillatory pattern to a tonic discharge mode. In rats that had received ibotenic acid lesions of the prefrontal cortex (PFCtx) 4-8 weeks prior to recording, cells in the VP exhibited similar changes in firing frequency in response to haloperidol administration as those in the intact rats. However, in contrast to the intact rats, MD cells recorded from rats with PFCtx lesions exhibited a significant increase in firing rate after haloperidol administration. The results from this study suggest that the prefrontal cortex plays a role in modulating the response of the thalamus to antipsychotic drugs.

Animals↗

PubMed2005

Presynaptic D1 dopamine receptors in primate prefrontal cortex: target-specific expression in the glutamatergic synapse.

Dopaminergic modulation of glutamate neurotransmission in prefrontal cortex (PFC) microcircuits is commonly perceived as a basis for cognitive operations. Yet it appears that although the control of recurrent excitation between deep-layer prefrontal pyramids may involve presynaptic and postsynaptic D1 receptor (D1R) mechanisms, pyramid-to-interneuron communication will engage a postsynaptic D1R component. The substrate underlying such target-specific neuromodulatory patterns was investigated in the infragranular PFC with immunoelectron microscopy for D1R and parvalbumin, a marker for fast-spiking interneurons. In addition to their proverbial postsynaptic expression, gold-labeled D1Rs were distinctly distributed on perisynaptic/extrasynaptic membranes and the axoplasm of 13% of excitatory-like, presumably glutamatergic varicosities. Most importantly, presynaptic D1Rs were highly specific with regard to the cellular compartment and neurochemical identity of the postsynaptic neuron, being present in spine-targeting varicosities but distinctly absent from those synapsing with parvalbumin profiles often coexpressing D1Rs. We define therein an axonal D1 heteroreceptor component, apparently mediating volume neurotransmission, yet strategically positioned to convey target cell-specific modulation of the glutamatergic drive. We also indicate that presynaptic D1R mechanisms may indeed be associated with recurrent excitation in prefrontal microcircuits, consistent with physiological evidence for a role of these receptors in modulating the persistent activity-profile of neurons essential for working memory.

Animals↗

PubMed1994

Indirect nucleus accumbens input to the prefrontal cortex via the substantia nigra pars reticulata: a combined anatomical and electrophysiological study in the rat.

The nucleus accumbens is a major component of the ventral striatum through which most of the limbic affiliated cortical areas gain access to the basal ganglia circuitry. In this study, the organization of the pathways linking the nucleus accumbens to the thalamus, via the substantia nigra pars reticulata, was examined in the rat using anatomical and electrophysiological methods. Use of anterograde and retrograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase has established that the core of the nucleus accumbens innervates a dorsal region of the substantia nigra pars reticulata which projects to subfields of the mediodorsal and ventral medial thalamic nuclei. These subfields consist of the rostral pole of the mediodorsal nucleus with the exception of its central segment and a region of the ventral medial nucleus, medial to the mammillothalamic tract. Confirming the existence of a nucleus accumbens nigrothalamic link, we have observed that electrical or chemical stimulation of the nucleus accumbens induces an inhibition of the spontaneous discharges of the nigral cells which project to the mediodorsal and ventral medial thalamic nuclei. Finally, the cortical projections of the thalamic subfields involved in the nucleus accumbens nigrothalamic circuit were determined using the anterograde and retrograde axonal transport of wheatgerm agglutinin conjugated with horseradish peroxidase. These subfields innervate mainly the prelimbic and to a lesser degree the orbital areas of the prefrontal cortex. The present data show that the substantia nigra pars reticulata is a major link between the core of the nucleus accumbens and the prefrontal cortex and provide further evidence for the concept of a parallel architecture in the basal ganglia thalamocortical circuits of the ventral striatum.

Action Potentials↗

PubMed2006

Dissociating task-set selection from task-set inhibition in the prefrontal cortex.

Patients with focal lesions in the left (n=7) and right (n=4) prefrontal cortex were compared with controls (n=16) in a task-switching experiment using four different, simple spatial tasks. Each of these tasks involved a left-right decision, either regarding an arrow, the word "left" or "right," a circle position, or the direction of a moving line. We compared performance on trials that required rule switches versus rule repetitions (local switch costs) and we compared performance between blocks with bivalent stimuli (two dimensions present) and blocks with univalent stimuli (only one dimension present) to assess global switch costs. Patients with left prefrontal lesions, but not patients with right prefrontal lesions, exhibited increased costs on trials in which the relevant dimension switched (local switch costs), but also on no-switch trials with bivalent stimuli (global costs). We also assessed task-set inhibition in the form of the backward-inhibition effect [increased response times to recently abandoned tasks; Mayr, U., & Keele, S. Changing internal constraints on action: The role of backward inhibition. Journal of Experimental Psychology: General, 129, 4-26, 2000]. Although left frontal patients showed normal inhibition, right frontal patients showed no evidence for inhibition. These results suggest a neurocognitive dissociation between task-set selection and inhibition.

Acoustic Stimulation↗

PubMed2001

Validating cortical surface analysis of medial prefrontal cortex.

This paper describes cortical analysis of 19 high resolution MRI subvolumes of medial prefrontal cortex (MPFC), a region that has been implicated in major depressive disorder. An automated Bayesian segmentation is used to delineate the MRI subvolumes into cerebrospinal fluid (CSF), gray matter (GM), white matter (WM), and partial volumes of either CSF/GM or GM/WM. The intensity value at which there is equal probability of GM and GM/WM partial volume is used to reconstruct MPFC cortical surfaces based on a 3-D isocontouring algorithm. The segmented data and the generated surfaces are validated by comparison with hand segmented data and semiautomated contours, respectively. The L(1) distances between Bayesian and hand segmented data are 0.05-0.10 (n = 5). Fifty percent of the voxels of the reconstructed surface lie within 0.12-0.28 mm (n = 14) from the semiautomated contours. Cortical thickness metrics are generated in the form of frequency of occurrence histograms for GM and WM labelled voxels as a function of their position from the cortical surface. An algorithm to compute the surface area of the GM/WM interface of the MPFC subvolume is described. These methods represent a novel approach to morphometric chacterization of regional cortex features which may be important in the study of psychiatric disorders such as major depression.

Adult↗

PubMed2005

Effects of repeated cocaine on the release and clearance of dopamine within the rat medial prefrontal cortex.

Previous data suggest that cocaine-induced dopamine (DA) transmission within the medial prefrontal cortex (mPFC) undergoes time-dependent changes during withdrawal from repeated cocaine administration. The current studies assessed two potential mechanisms that may underlie this neuroadaptation. One set of experiments examined alterations in DA clearance in the mPFC of rats that had been pretreated with four administrations of cocaine (15 mg/kg, i.p.; once per day for 4 days) and were withdrawn 1, 7, or 30 days. No significant changes in mPFC DA uptake into crude mPFC synaptosomes or in mPFC DA transporter levels were observed at any of the time points examined. Uptake assay and Western blotting sensitivity was confirmed with prefrontal 6-hydroxydopamine lesions, which significantly reduced [3H]DA uptake and DA transporter immunoreactivity in mPFC synaptosomes. To evaluate temporal changes in DA release resulting from repeated cocaine, additional experiments utilized in vivo microdialysis to locally infuse KCl (10, 30, or 100 mM) into the mPFC over the same withdrawal time course used in the uptake studies. After 1-7 days of withdrawal, KCl-stimulated DA release was significantly reduced in the mPFC of cocaine-pretreated animals. However, after 30 days of withdrawal the evoked release of DA in the mPFC of saline- and cocaine-pretreated animals was similar. These data suggest that previously reported modulation of cocaine-induced mPFC DA transmission occurring upon withdrawal from repeated cocaine might arise from transient changes in DA releasability rather than clearance. The relevance of these findings is discussed in relation to mPFC involvement in psychostimulant sensitization.

Adrenergic Agents↗

PubMed2001

Effects of imidazoline antihypertensive drugs on sympathetic tone and noradrenaline release in the prefrontal cortex.

1. The aim of the present study was to compare the effects of the centrally acting antihypertensive drugs rilmenidine, moxonidine, clonidine and guanabenz on sympathetic tone with their effects on noradrenaline release in the cerebral cortex. In particular, the hypothesis was tested that rilmenidine and moxonidine, due to their high affinity for sympatho-inhibitory imidazoline I(1) receptors and low affinity for alpha(2)-adrenoceptors, lower sympathetic tone without causing an alpha(2)-adrenoceptor-mediated inhibition of cerebrocortical noradrenaline release. 2. In rats anaesthetized with urethane, blood pressure and heart rate were measured and the concentration of noradrenaline in arterial blood plasma was determined. The release of noradrenaline in the medial prefrontal cortex was estimated by microdialysis. Intravenous administration of rilmenidine (30, 100, 300 and 1000 microg kg(-1)), moxonidine (10, 30, 100 and 300 microg kg(-1)), clonidine (1, 3, 10 and 30 microg kg(-1)) and guanabenz (1, 3, 10 and 30 microg kg(-1)) led to dose-dependent hypotension and bradycardia; the plasma noradrenaline concentration also decreased. After the two highest doses, all four drugs lowered noradrenaline release in the prefrontal cortex. At doses eliciting equal hypotensive and sympatho-inhibitory responses, rilmenidine and moxonidine inhibited cerebral cortical noradrenaline release at least as much as clonidine and guanabenz. 3. The results show that rilmenidine and moxonidine lower cerebrocortical noradrenaline release at doses similar to those which cause sympatho-inhibition. This effect was probably due to an alpha(2)-adrenoceptor-mediated inhibition of the firing of locus coeruleus neurons and, in addition, to presynaptic inhibition of noradrenaline release at the level of the axon terminals in the cortex. The results argue against the hypothesis that rilmenidine and moxonidine, due to their selectivity for sympatho-inhibitory I(1) imidazoline receptors, do not suppress noradrenergic neurons in the central nervous system.

Animals↗

PubMed1996

Local infusion of the serotonin antagonists ritanserin or ICS 205,930 increases in vivo dopamine release in the rat medial prefrontal cortex.

Previous research has indicated that atypical antipsychotic drugs like clozapine preferentially increase dopamine (DA) release from the mesocortical, relative to the nigrostriatal, system, While these drugs generally have weak affinity for the D2 receptor subtype, they are potent antagonists of the 5-hydroxytryptamine2 (5-HT2) receptor. Research into neurotransmitter interactions indicates that 5-HT modulates DA release, but the nature of this interaction may depend upon the specific 5-HT receptor subtype and the neuronal location of that subtype. The present research tested the hypothesis that 5-HT2 receptors localized near mesocortical DA nerve terminals regulate DA release. This was accomplished by infusing the specific 5-HT2 antagonist ritanserin directly into the medial prefrontal cortex through reverse dialysis in vivo in the rat. Cortical extracellular fluid was then extracted by microdialysis and DA was subsequently assayed by HPLC with electrochemical detection. These results were compared to the systemic administration of ritanserin (1.0-5.0 mg/kg i.p.) and the local application of ICS 205,930, an antagonist at the 5-HT3/4 receptor subtypes. Both 5-HT antagonists increased cortical DA levels when infused locally at concentrations of 100 microM (12 nmoles/60 min), and these results were concentration-dependent. Systemically administered ritanserin also dose-dependently increased cortical DA efflux. These results indicate that atypical antipsychotic drugs may increase mesocortical DA release by antagonizing 5-HT receptors located in the prefrontal cortex. Furthermore, 5-HT may normally inhibit cortical DA release by actions at the 5-HT2 receptor subtype.

Animals↗

PubMed1997

Persistent structural modifications in nucleus accumbens and prefrontal cortex neurons produced by previous experience with amphetamine.

Experience-dependent changes in behavior are thought to involve structural modifications in the nervous system, especially alterations in patterns of synaptic connectivity. Repeated experience with drugs of abuse can result in very long-lasting changes in behavior, including a persistent hypersensitivity (sensitization) to their psychomotor activating and rewarding effects. It was hypothesized, therefore, that repeated treatment with the psychomotor stimulant drug amphetamine, which produces robust sensitization, would produce structural adaptations in brain regions that mediate its psychomotor activating and rewarding effects. Consistent with this hypothesis, it was found that amphetamine treatment altered the morphology of neurons in the nucleus accumbens and prefrontal cortex. Exposure to amphetamine produced a long-lasting (>1 month) increase in the length of dendrites, in the density of dendritic spines, and in the number of branched spines on the major output cells of the nucleus accumbens, the medium spiny neurons, as indicated by analysis of Golgi-stained material. Amphetamine treatment produced similar effects on the apical (but not basilar) dendrites of layer III pyramidal neurons in the prefrontal cortex. The ability of amphetamine to alter patterns of synaptic connectivity in these structures may contribute to some of the long-term behavioral consequences of repeated amphetamine use, including amphetamine psychosis and addiction.

Amphetamine-Related Disorders↗

PubMed2000

Decreased benzodiazepine receptor binding in prefrontal cortex in combat-related posttraumatic stress disorder.

OBJECTIVE: Animals exposed to stress exhibit a decrease in benzodiazepine receptor binding in the frontal cortex. No studies have examined central benzodiazepine receptor binding in patients with posttraumatic stress disorder (PTSD). The purpose of this study was to examine measures of benzodiazepine receptor binding in PTSD. METHOD: From 13 patients with Vietnam combat-related PTSD and 13 case-matched healthy comparison subjects, a quantitative measure related to benzodiazepine receptor binding (distribution volume) was obtained with single photon emission computed tomography (SPECT) imaging of [(123)I]iomazenil binding and measurement of radioligand concentration in plasma. Distribution volume image data were analyzed by means of statistical parametric mapping. RESULTS: Lower distribution volumes were found in the prefrontal cortex (Brodmann's area 9) of PTSD patients than in comparison subjects. CONCLUSIONS: These findings of lower values for the benzodiazepine receptor binding measure of distribution volume are consistent with fewer benzodiazepine receptors and/or reduced affinity of receptor binding in the medial prefrontal cortex in patients with PTSD. Alterations in benzodiazepine receptor function in this area may underlie many of the symptoms of PTSD.

Adult↗