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PubMed2007

Osmotic regulation of neuronal nitric oxide synthase expression in the rat amygdala: functional role for nitric oxide in adaptive responses?

Water-deprivation-induced osmotic stress leads to activation of a number of adaptive responses. Nitric oxide (NO) has been implicated in the modulation of these responses, as the amygdala has been implicated in ingestive behavior and modulation of autonomic homeostatic functions. Here we investigated the effects of water deprivation on neuronal nitric oxide synthase (nNOS) expression within the rat amygdala; a brain area involved in modulating ingestive behavior and autonomic function. Water deprivation resulted in significant increases in nNOS immunoreactivity (-ir) within different regions of the amygdala compared with euhydrated rats. Maximal increases were observed in the anteroventral (118 +/- 9 vs. 47 +/- 3 neurons), anteriodorsal (133 +/- 9 vs. 77 +/- 3), and posterioventral (175 +/- 5 vs. 71 +/- 5) parts of the medial amygdala. The basomedial nucleus (65 +/- 4 vs. 39 +/- 3) and posterior basolateral nucleus (19 +/- 2 vs. 5 +/- 1) of the amygdala and the capsular (21 +/- 2 vs. 6 +/- 1) and medial (44 +/- 6 vs. 22 +/- 3) parts of the central nucleus of the amygdala also showed increased nNOS-ir in dehydrated rats. Water deprivation had no effect on nNOS-ir in areas such as the cortical, anterior basolateral, and intercalated nuclei of the amygdala. Microinjection of an NO donor, DEA-NONOate, into the central amygdala resulted in a pressor and tachycardic response that was attenuated by a soluble guanylate cyclase inhibitor. These observations suggest that activation of the nitrergic system is prevalent throughout the amygdala following water deprivation and suggest that the up-reguation of nNOS could play a significant role in the integrative response to osmotic stress.

Adaptation, Physiological↗
PubMed1996

Attack priming in female Syrian golden hamsters is associated with a c-fos-coupled process within the corticomedial amygdala.

Allowing a resident hamster a single "priming" attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a second intruder presented within the next 30 min. We present two lines of evidence identifying the corticomedial amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the corticomedial amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce corticomedial amygdala c-fos expression of the same pattern or magnitude. The corticomedial amygdala contribution to the priming effect involves more than a non-specific arousal, since corticomedial amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the corticomedial amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by corticomedial amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the corticomedial amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the corticomedial amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.

Aggression↗
PubMed1987

Structurally stable burst and synchronized firing in human amygdala neurons: auto- and cross-correlation analyses in temporal lobe epilepsy.

Burst structure and synchronized firing of bursts were studied, in the interictal period, using auto- and cross-correlation analyses in human amygdala neurons in temporal lobe epilepsy patients diagnosed as having a unilateral limbic seizure focus in anterior hippocampus and/or amygdala. Satisfactory single unit recordings were obtained from chronically implanted microelectrodes in 51 amygdala neurons, and auto-correlation analysis identified 27 of 51 neurons where burst firings recurred with regular interspike interval structures (structurally stable burst: S-burst). This structural stability was characteristic only for a short burst, or at the beginning of a series of repetitive firings, involving 2-5 action potentials. In 'non-epileptic' amygdala neurons located contralateral to the seizure focus, the average duration of S-burst was 15 msec and the number of action potentials (spikes) in the S-burst was inversely related to the interspike intervals in the S-burst, suggesting that endogenous membrane characteristics of non-epileptic amygdala neurons determine the patterns of S-burst. In contrast, in the seizure focus amygdala ('epileptic'), the duration of the S-burst was prolonged among epileptic neurons, not because of the occurrence of more action potentials within the S-burst, but because of a prolonged interspike interval within the S-burst. Furthermore, there was no relationship between the interspike interval and the number of action potentials in the S-burst, suggesting that synaptic inputs and/or extracellular environmental factors may affect an intrinsic mechanism for generating stable S-burst in epileptic neurons. Cross-correlation analysis identified synchronized firings in epileptic neurons: when two epileptic neurons both exhibited S-bursts, when either epileptic neuron exhibited S-burst, but never when neither exhibited S-bursts. Conversely, non-epileptic neurons rarely fired synchronously; even though they showed S-bursts. The difference in the pattern of S-bursts between epileptic and non-epileptic amygdala neurons seems to be the degree of firing synchrony. Our results provide, for the first time, direct evidence that human epileptogenic amygdala neurons recorded in vivo have unique burst firing patterns and significant synchronous excitatory interactions, different from a burst pattern found in non-epileptogenic amygdala neurons during the interictal period.

Action Potentials↗
PubMed2005

Temporary inactivation of the medial and basolateral amygdala differentially affects TMT-induced fear behavior in rats.

Trimethylthiazoline (TMT) is a component of fox feces and is thought to be a stimulus with innate fear-eliciting properties for rodents. Naive laboratory rats that are exposed to TMT display freezing behavior, a known behavioral sign of fear and anxiety. Early studies examining the neural basis of TMT-induced fear showed that the bed nucleus of the stria terminalis is important for this behavior. In contrast, the central and lateral nuclei of the amygdala does not seem to participate in the neural processing of TMT-induced fear. However, a study investigating c-fos expression in response to TMT-exposure revealed a strong activation of the medial as well as a weak activation of the basolateral amygdala. Therefore, the present study examined the effects of temporary inactivation of the medial and basolateral amygdala on TMT-induced freezing. Temporary inactivation was accomplished by local injections of the GABA(A) receptor agonist muscimol into the areas of interest. TMT-induced freezing was completely blocked by temporary inactivation of the medial amygdala. Temporary inactivation of the basolateral amygdala resulted in a delay of the onset of the freezing response to TMT. These results clearly demonstrate that the medial amygdala is crucial for TMT-induced freezing, whereas the basolateral amygdala seems to play a modulatory role in this type of fear behavior. Since the medial amygdala is also involved in the processing of cat odor-induced fear, the finding of the present study points towards a general role of the medial amygdala in the processing of predator odor-induced fear.

Amygdala↗
PubMed2005

Lateral and medial amygdala of anuran amphibians and their relation to olfactory and vomeronasal information.

The amygdala of anurans is currently considered as a complex of nuclei that share many features with their counterparts in amniotes. In the present study, the subdivisions of the amygdala that are directly related to olfactory and vomeronasal information, were investigated in the anurans Rana perezi and Xenopus laevis. In particular, the connectivity of the main and accessory olfactory bulbs and their related amygdaloid nuclei was studied by means of in vivo and in vitro tract-tracing with dextran amines. The projections observed from the main olfactory bulb clearly innervate the newly redefined lateral amygdala within the ventral pallium and, to a lesser extent, the rostral portion of the medial amygdala. Injections into the accessory olfactory bulb exclusively revealed projections to the medial amygdala. Tracer applications into the lateral and medial nuclei revealed abundant intra-amygdaloid connections. The dual flow of olfactory and vomeronasal projections throughout the telencephalon was not strictly segregated since the lateral pallium and the lateral amygdala, both receiving olfactory information, were found to project to the medial amygdala (the only target of vomeronasal information), which in turn projects to the lateral amygdala. Additionally, both the lateral and the medial amygdala strongly project to the hypothalamus through the anuran equivalent of the stria terminalis. The main hodological features found in the present study suggest that forerunners of the olfactory and vomeronasal amygdaloid nuclei can be distinguished in anurans. This supports the notion that all tetrapods share a common pattern of organization of the amygdaloid complex, which links environmental (olfactory/vomeronasal) information and the behavioural response of the animal.

Amygdala↗
PubMed2005

Novel fearful faces activate the amygdala in healthy young and elderly adults.

Activation of the amygdala to emotionally valenced stimuli, and particularly to fearful faces, has been widely demonstrated in healthy young adults. However, recent studies assessing amygdala responses to fearful emotional faces in the normal elderly have not shown similar results. The reason for this is uncertain, but it may relate to life-span developmental changes in processing emotional stimuli or structural alterations in the amygdala with aging. In order to examine whether the amygdala could be activated in the elderly, we developed a paradigm designed to engage the amygdala on several levels. Based on recent imaging work indicating that novelty and stimulus change activates the amygdala, we assessed amygdala responses in young and elderly adults to novel fearful faces (versus familiar neutral ones). We demonstrate a robust activation in both groups, indicating that the amygdala remains responsive in aging. This activation did not differ between the two groups when we examined regions of interest in the amygdala based on functional or structural criteria. However, there were significantly greater activations in the inferior temporal cortex in the young versus elderly subjects.

Adult↗
PubMed2005

Noradrenaline mediates amygdala activation in men and women during encoding of emotional material.

The amygdala is a pivotal structure in humans for encoding of emotional information, as shown by recent imaging studies. It is unknown which neurotransmitters are specifically involved in the human amygdala, although in animal studies noradrenaline was shown to be essential. In our study, participants received the betablocker propranolol (which blocks the noradrenergic response) or placebo when watching neutral to highly negative arousing pictures. Amygdala activation, monitored with functional magnetic resonance imaging (fMRI), increased with emotional intensity of the pictures under placebo condition. Betablockade selectively decreased amygdala activation for emotional pictures of the second highest category, but not for the highest or lower (neutral) category pictures. Two findings add to the existing knowledge in this area. First, the activation pattern in the amygdala under placebo condition shows a nonlinearity related to the emotional categories of the pictures. Second, propranolol disturbs this activation pattern in the amygdala. Explorations with respect to gender show a similar effect of betablockade on amygdala activation in both men and women, but a difference in its effect on long-term memory for emotional pictures. This study supports the hypothesis that the neurotransmitter noradrenaline also mediates amygdala activity in humans when processing emotional stimuli and that betablockers can disrupt the normal activation pattern in the amygdala.

Adolescent↗
PubMed2005

Trauma modulates amygdala and medial prefrontal responses to consciously attended fear.

Effective fear processing relies on the amygdala and medial prefrontal cortex (MPFC). Post-trauma reactions provide a compelling model for examining how the heightened experience of fear impacts these systems. Post-traumatic stress disorder (PTSD) has been associated with excessive amygdala and a lack of MPFC activity in response to nonconscious facial signals of fear, but responses to consciously processed facial fear stimuli have not been examined. We used functional MRI to elucidate the effect of trauma reactions on amygdala-MPFC function during an overt fear perception task. Subjects with PTSD (n = 13) and matched non-traumatized healthy subjects (n = 13) viewed 15 blocks of eight fearful face stimuli alternating pseudorandomly with 15 blocks of neutral faces (stimulus duration 500 ms; ISI 767 ms). We used random effects analyses in SPM2 to examine within- and between-group differences in the MPFC and amygdala search regions of interest. Time series data were used to examine amygdala-MPFC associations and changes across the first (Early) versus second (Late) phases of the experiment. Relative to non-traumatized subjects, PTSD subjects showed a marked bilateral reduction in MPFC activity (in particular, right anterior cingulate cortex, ACC), which showed a different Early-Late pattern to non-traumatized subjects and was more pronounced with greater trauma impact and symptomatology. PTSD subjects also showed a small but significant enhancement in left amygdala activity, most apparent during the Late phase, but reduction in Early right amygdala response. Over the time course, trauma was related to a distinct pattern of ACC and amygdala connections. The findings suggest that major life trauma may disrupt the normal pattern of medial prefrontal and amygdala regulation.

Adult↗
PubMed2004

Stress induces CRF release in the paraventricular nucleus, and both CRF and GABA release in the amygdala.

In the hypothalamus, corticotropin-releasing factor (CRF) initiates the hypothalamic-pituitary-adrenal (HPA) axis response to stress, resulting in the release of glucocorticoids, including cortisol. Extrahypothalamic CRF, particularly in the limbic system, also appears to play a role in the stress response. To further define brain CRF response to stress, immunosensor-based microdialysis probes were used to measure the extracellular levels of CRF in the paraventricular nucleus of the hypothalamus (PVN) and in the amygdala of sheep during a predator (dog) exposure stress. In addition, gamma amino butyric acid (GABA) was measured in the amygdala and cortisol was measured in venous blood. Exposure to the predator stress increased CRF in the PVN and both CRF and GABA in the amygdala. These were followed in time by a rise in venous cortisol. Application of a CRF antagonist to the amygdala, immediately prior to stress, had a small effect on the subsequent observed stress responses. This treatment, however, significantly reduced the responses to a repeat stress administered 2 days later, compared to nontreated animals. Application of a GABA antagonist to the amygdala prior to stress had no effect on the subsequent observed stress response but increased the response to the stress repeated 2 days later. Perfusion with 4-aminopyridine, a neuronal depolarising agent, into the PVN induced a release of CRF accompanied shortly thereafter by a small increase in CRF in the amygdala, and 5-10 min later by an increase in venous cortisol. Perfusion into the amygdala increased the levels of both CRF and GABA but had no effect on either PVN CRF or venous cortisol. These data support roles for both the PVN and amygdala in stress responsiveness. It suggests further that actions at the amygdala can strongly influence subsequent responsiveness to a further stress, mediated in part by both CRF and GABA actions.

4-Aminopyridine↗
PubMed1998

Opioid supraspinal analgesic synergy between the amygdala and periaqueductal gray in rats.

Analgesia can be elicited following microinjections of morphine, mu-selective agonists and beta-endorphin into the amygdala. These analgesic responses are mediated by opioid synapses in the periaqueductal gray (PAG) since general (naltrexone), mu (beta-funaltrexamine) and delta2 (naltrindole isothiocyanate) opioid antagonists administered into the PAG significantly reduce both morphine and beta-endorphin analgesia elicited from the amygdala. Supraspinal multiplicative opiate analgesic interactions have been observed between the PAG and rostroventromedial medulla (RVM), the PAG and locus coeruleus (LC), and the RVM and LC. The present study further examined the relationship between the amygdala and PAG in analgesic responsiveness by determining whether multiplicative analgesic interactions occur following paired administration of subthreshold doses of morphine into both structures, beta-endorphin into both structures, morphine into one structure and beta-endorphin into the other structure, or morphine and beta-endorphin into one structure. Co-administration of subthreshold doses of morphine into both the amygdala and PAG results in a profound synergistic interaction on the jump test, but not the tail-flick test. Co-administration of subthreshold doses of beta-endorphin into both structures also results in a profound test-specific synergistic interaction. In both cases, the magnitude of the interaction was similar regardless of the site receiving the fixed dose of the opioid, and the site receiving the variable dose of the opioid. Co-administration of beta-endorphin (1 microg) into the amygdala and morphine (1 microg) into the PAG produced a potent interaction, but co-administration of morphine (1 microg) into the amygdala and beta-endorphin (1 microg) into the PAG failed to produce interactive effects. Finally, co-administration of morphine (1 microg) and beta-endorphin (1 microg) into either the amygdala alone or the PAG alone failed to produce an interaction, indicating the importance of regional opioid activation. These data are discussed in terms of the test-specificity of nociceptive processing in the amygdala, in terms of the multiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, and in terms of whether the interactions are either mediated by anatomical connections between the amygdala and PAG or by mechanisms initiated by these two sites converging at another site or sites.

Amygdala↗
PubMed2001

Differential amygdala activation during emotional decision and recognition memory tasks using unpleasant words: an fMRI study.

This study used fMRI to examine the response of the amygdala in the evaluation and short-term recognition memory of unpleasant vs. neutral words in nine right-handed healthy adult women. To establish specificity of the amygdala response, we examined the fMRI BOLD signal in one control region (visual cortex). Alternating blocks of unpleasant and neutral trials were presented. During the emotional decision task, subjects viewed sets of three unpleasant or three neutral words while selecting the most unpleasant or neutral word, respectively. During the memory task, subjects identified words that were presented during the emotional decision task (0.50 probability). Images were detrended, filtered, and coregistered to standard brain coordinates. The Talairach coordinates for the center of the amygdala were chosen before analysis. The BOLD signal at this location in the right hemisphere revealed a greater amplitude signal for the unpleasant relative to the neutral words during the emotional decision but not the memory task, confirmed by Time Course x Word Condition ANOVAs. These results are consistent with the memory modulatory view of amygdala function, which suggests that the amygdala facilitates long-term, but not short-term, memory consolidation of emotionally significant material. The control area showed only an effect for Time Course for both the emotional decision and memory tasks, indicating the specificity of the amygdala response to the evaluation of unpleasant words. Moreover, the right-sided amygdala activation during the unpleasant word condition was strongly correlated with the BOLD response in the occipital cortex. These findings corroborate those by other researchers that the amygdala can modulate early processing of visual information in the occipital cortex. Finally, an increase in subject's state anxiety (evaluated by questionnaire) while in the scanner correlated with amygdala activation under some conditions.

Adult↗
PubMed1997

Neonatal androgen manipulation differentially affects the development of monoamine systems in rat cerebral cortex, amygdala and hypothalamus.

Neural tissue during perinatal life is sufficiently plastic to respond to the presence of testicular androgens. Here we studied the effect of neonatal androgen manipulation (castration of male and androgenization of female rats) on monoamine neurotransmitter systems in the cerebral cortex and sexually dimorphic regions of brain (hypothalamus and amygdala). Norepinephrine (NE) and dopamine (DA) concentrations in cortex, amygdala and hypothalamus of rats were assayed by HPLC at days 25, 60, 120, 180, 240 and 300. Results show that NE levels in all groups of rats at day 25 were higher in the hypothalamus (5-9 ng/mg protein) compared to the amygdala (0.5-3 ng/mg protein) and the cortex (0.5-1 ng/mg protein). Levels of DA at day 25 in the hypothalamus and the amygdala were comparable (up to 3.5 ng/mg) but higher than in the cortex (1.25-1.75 ng/mg protein). NE and DA concentrations in sham-castrated male and androgen-treated females were higher at day 25 compared to castrated male and control females in both amygdala and hypothalamus; however, levels of NE and DA remained unchanged in the cortex. Pattern of NE concentrations started reversing with increase in age, i.e., NE levels in control females and castrated males increased almost 4-fold in amygdala and 2-fold in hypothalamus by day 300, but there was no significant change in the cortex. Compared to that, NE levels decreased in sham-castrated male (2-fold) and androgen-treated females (3-fold) in amygdala as well as in the hypothalamus (2-fold) in both these groups. A similar pattern of reversal of DA levels was found in both amygdala and hypothalamus, however, at day 300 DA levels were comparable in all the four groups. These studies suggest that androgen manipulation (castration or androgen administration) induces age-dependent short- and long-term effects on the development of noradrenergic and dopaminergic systems in the sexually dimorphic regions of brain, amygdala and hypothalamus, without a significant change in the cerebral cortex.

Amygdala↗
PubMed1997

Opposite effects on two different measures of retention following unilateral inactivation of the amygdala.

We previously reported finding differential effects of unilateral infusion of lidocaine into the right and left amygdalae prior to a retention test 24 h after one-trial inhibitory avoidance training. The present study was undertaken to determine whether the degree of training in an escape task influences the effects of unilateral inactivation of the amygdala with lidocaine prior to the retention test. Male Sprague-Dawley rats, implanted with bilateral cannulae aimed at the amygdaloid complex received 0 (no shock), 2, or 10 training trials in a footshock-motivated escape task (0.4 mA). Forty-eight h later, the rats received bilateral microinfusions into the amygdalae of either buffer, or lidocaine into one amygdala and buffer in the other, 5 min before they were tested for retention of the escape training using a continuous multiple trial inhibitory avoidance (CMIA) procedure (0.4 mA). Forty-eight h after CMIA training the animals were retested, this time without influence of drugs. As indicated by initial response latencies on the first retention test, unilateral inactivation of either the right or the left amygdala severely impaired retention performance for the escape training regardless of the number of prior escape training trials received. However, unilateral inactivation of either amygdala had no effect on acquisition of CMIA. Furthermore, unilateral inactivation of either amygdala during CMIA training did not affect retention tested 48 h later. These results suggest that the differential involvement of the right and left amygdalae may be limited to certain training conditions. Furthermore, these findings demonstrate opposite effects on 2 different measures of retention indicating that the method of testing retention affects the interpretation of the memory impairment induced by infusion of lidocaine into the amygdala.

Amygdala↗
PubMed2004

Amygdala volume reductions in pediatric patients with obsessive-compulsive disorder treated with paroxetine: preliminary findings.

The amygdala is believed to be highly relevant to the pathophysiology of obsessive-compulsive disorder (OCD) given its prominent role in fear conditioning and because it is an important target of the serotonin reuptake inhibitors (SRIs), the pharmacotherapy of choice for OCD. In the present study, we measured in vivo volumetric changes in the amygdala in pediatric patients with OCD following 16 weeks of monotherapy with the selective SRI, paroxetine hydrochloride. Amygdala volumes were computed from contiguous 1.5 mm magnetic resonance (MR) images in 11 psychotropic drug-naive patients with OCD prior to and then following treatment. Eleven healthy pediatric comparison subjects also had baseline and follow-up scans, but none of these subjects received medication. Patients demonstrated significant asymmetry of the amygdala (L>R) prior to pharmacologic intervention in contrast to healthy comparison subjects who showed no asymmetry at the time of their baseline scan. Mixed model analyses using age and total brain volume as time varying covariates indicated that left amygdala volume decreased significantly in patients following treatment. The reduction in left amygdala volume in patients correlated significantly with higher paroxetine dosage at the time of the follow-up scan and total cumulative paroxetine exposure between the scans. No significant changes in either right or left amygdala volume were evident among healthy comparison subjects from the baseline to the follow-up scan. These preliminary findings suggest that abnormal asymmetry of the amygdala may play a role in the pathogenesis of OCD and that paroxetine treatment may be associated with a reduction in amygdala volume.

Adolescent↗
PubMed1998

Basolateral amygdala stimulation evokes glutamate receptor-dependent dopamine efflux in the nucleus accumbens of the anaesthetized rat.

Afferents from the basolateral amygdala and dopamine projections from the ventral tegmental area to the nucleus accumbens have both been implicated in reward-related processes. The present study used in vivo chronoamperometry with stearate-graphite paste electrodes in urethane-anaesthetized rats to determine how basolateral amygdala efferents to the nucleus accumbens synaptically regulate dopamine efflux. Repetitive-pulse (20 Hz for 10 s) electrical stimulation of the basolateral amygdala evoked a complex pattern of changes in monitored dopamine oxidation currents in the nucleus accumbens related to dopamine efflux. These changes were characterized by an initial increase that was time-locked to stimulation, a secondary decrease below baseline, followed by a prolonged increase in the dopamine signal above baseline. The effects of burst-patterned stimulation (100 Hz, 5 pulses/burst, 1-s interburst interval, 40 s) of the basolateral amygdala on the basal accumbens dopamine signal were similar to those evoked by 20 Hz stimulation, with the lack of a secondary suppressive component. Infusions of the ionotropic glutamate receptor antagonists (+/-)-2-amino-5-phosphonopentanoic acid (APV) or 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the nucleus accumbens dose-dependently blocked or attenuated the initial and prolonged increases in the dopamine signal following 20 Hz or burst-patterned basolateral amygdala stimulation. Infusions of the metabotropic glutamate receptor antagonist (+)-alpha-methyl-4-carboxyphenylglycine selectively blocked the intermediate suppressive effect of 20 Hz basolateral amygdala stimulation on dopamine oxidation currents. Blockade of glutamate receptors or inhibition of dopamine neuronal activity via infusions of either APV + DNQX, lidocaine or gamma-hydroxybutyric acid, respectively, into the ventral tegmental area did not effect the pattern of changes in the accumbens dopamine signal evoked by basolateral amygdala stimulation. These data suggest that the glutamatergic basolateral amygdala inputs to nucleus accumbens dopamine terminals synaptically facilitate or depress dopamine efflux, and these effects are independent of dopamine neuronal firing activity. Moreover, these results imply that changes in nucleus accumbens dopamine levels following presentation of reward-related stimuli may be mediated, in part, by the basolateral amygdala.

Amygdala↗
PubMed2004

The impact of early and late damage to the human amygdala on 'theory of mind' reasoning.

There is a burgeoning interest in the neural basis of the ability to attribute mental states to others; a capacity referred to as 'theory of mind' (ToM). We examined the effects of lesions of the amygdala which arise at different stages of development on this key aspect of social cognition. Tests of ToM, executive and general neuropsychological function were given to subjects with lesions of the amygdala arising congenitally or in early childhood ('early damage', n = 15), subjects who acquired damage to the amygdala in adulthood ('late damage' n = 11) and matched clinical (n = 14) and healthy comparison groups (n = 38). Subjects with early damage to the amygdala, particularly if the lesion was associated with childhood onset of seizures, were impaired relative to all other groups on more advanced tests of ToM reasoning, such as detecting tactless or ironic comments or interpreting non-literal utterances. These deficits held for subjects with either left or right early amygdala damage and encompassed the understanding of both the beliefs and emotional states of others. In contrast, subjects who acquired damage to the amygdala in adulthood (usually as part of an anterior temporal lobectomy) were not impaired in ToM reasoning relative to both clinical and healthy controls, supporting the position that the amygdala is not part of the neural circuitry mediating the 'on-line' performance of ToM reasoning. In line with theories which claim that ToM is an independent faculty of cognition, we found that the pattern of results held after co-varying for measures of executive function, memory and general intellectual functioning. We discuss the results in the light of recent theories which link early developmental insults to the amygdala with the ToM impairments which are thought to be a core neurocognitive deficit found in disorders such as autism. We conclude that the amygdala may play an important role in the neural systems supporting the normal development of ToM reasoning.

Adult↗
PubMed2003

The decreased phosphorylation of cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein in the central amygdala acts as a molecular substrate for anxiety related to ethanol withdrawal in rats.

BACKGROUND: Several lines of evidence indicate a high comorbidity between anxiety and alcohol abuse. This study investigated the molecular mechanisms in the amygdaloid neurocircuitry governing anxiety related to ethanol withdrawal and also the phenomenon of alcohol preference. METHODS: Male Sprague Dawley(R) rats were treated with ethanol or control diet for 15 days, and ethanol-fed rats were withdrawn for 0 and 24 hr. Ethanol-withdrawn or control diet-fed rats were bilaterally infused into central or basolateral amygdala with artificial cerebrospinal fluid or protein kinase A (PKA) activator or inhibitor. These rats were used to measure anxiety levels by the elevated plus-maze test. Protein levels of various signaling molecules related to cyclic adenosine monophosphate (cAMP)-response element binding (CREB) protein signaling in amygdaloid structures were determined by gold immunolabeling procedure. The messenger RNA levels of neuropeptide Y were determined by in situ polymerase chain reaction procedure. RESULTS: Ethanol withdrawal (24 hr) after chronic exposure (15 days) produced anxiety in rats as measured by elevated plus-maze test. Ethanol withdrawal but not treatment significantly decreased the phosphorylation of CREB protein and protein levels of Ca2+/calmodulin-dependent protein kinase IV without modulating the protein levels of total CREB and alpha-catalytic subunit of protein kinase A (PKA-Calpha) in the central and medial amygdala. However, these changes were not observed in the basolateral amygdala. We also investigated the effects of manipulation of the phosphorylation status of CREB in the central amygdala by infusion of the PKA activator (Sp-cAMPS) or inhibitor (Rp-cAMPS) on anxiety levels in rats during ethanol withdrawal. When Sp-cAMPS is specifically infused into the central amygdala, it dose-dependently normalizes the decrease in CREB phosphorylation and prevents the development of anxiety in rats during ethanol withdrawal. On the other hand, Rp-cAMPS infusions into the central or basolateral amygdala decrease CREB phosphorylation, but only infusion into the central amygdala provokes anxiety and increases alcohol preference in normal rats. We also found that alcohol preference provoked by decreased CREB phosphorylation is related to decreased expression of the neuropeptide Y gene in the central amygdala. CONCLUSIONS: These novel results suggest the possibility that decreased CREB phosphorylation in the central amygdala acts as a common molecular correlate for anxiety and alcohol-drinking behaviors and also is correlated with anxiety related to ethanol withdrawal.

Alcohol Drinking↗
PubMedDate not supplied

Impaired emotional declarative memory following unilateral amygdala damage.

Case studies of patients with bilateral amygdala damage and functional imaging studies of normal individuals have demonstrated that the amygdala plays a critical role in encoding emotionally arousing stimuli into long-term declarative memory. However, several issues remain poorly understood: the separate roles of left and right amygdala, the time course over which the amygdala participates in memory consolidation, and the type of knowledge structures it helps consolidate. We investigated these questions in eight subjects with unilateral amygdala damage, using several different measures. For comparison, our main task used stimuli identical to those used previously to investigate emotional declarative memory in patients with bilateral amygdala damage. Contrasts with both brain-damaged and normal control groups showed that subjects with left amygdala damage were impaired in their memory for emotional stimuli, despite entirely normal memory for neutral stimuli (because of a number of caveats, the findings from subjects with right amygdala damage were less clear). Follow-up experiments suggested that the normal facilitation of memory for emotional stimuli may develop over an extended time course (>30 min), consistent with prior findings, and that the specific impairment we report may depend in part on the lexical nature of the task used (written questionnaire). We stress the complex and temporally extended nature of memory consolidation and suggest that the amygdala may influence specific components of this process.

Adult↗