On the relation between conceptual priming, neural priming, and novelty assessment

A consistently reported finding in functional neuroimaging studies which compare processing of new information to processing of old information is a reduction in blood flow, and hence neural activity, associated with the old condition. This deactivation has been labeled neural priming. Some investigators have hypothesized that neural priming is the physiological mechanism underlying conceptual priming—a facilitation in the semantic processing of repeated information. Others, however, have hypothesized that neural priming reflects novelty assessment—a mechanism which minimizes the probability that redundant information will be stored in long‐term memory. In this paper, the conceptual priming and novelty assessment hypotheses are compared and contrasted in order to ask, and tentatively answer, the question: Are conceptual priming and novelty assessment cognitively and neurophysiologically distinct? Based on a review of the literature, it is suggested that whereas novelty assessment and conceptual priming are distinct cognitive entities, they cannot be presently separated neurophysiologically. That is, some novelty assessment deactivations may in fact reflect priming, and some priming deactivations may in fact reflect novelty assessment.     

The awareness of thirst: proposed neural correlates

The neural and endocrine bases of the generation of thirst are reviewed. Based on this review, a hierarchical system of neural structures that regulate water conservation and acquisition is proposed. The system includes primary sensory-receptive areas; secondary sensory structures (circumventricular organs), which detect levels of hormones, including angiotensin II and vasopressin, which are involved in generating thirst; preoptic and hypothalamic structures; and an area within the ventrolateral quadrant of the periaqueductal gray matter. Hodological and other data are used to determine the hierarchical organization of the system. Based on studies of the effects of lesions to various structures within the hierarchy of the system, it is proposed that the awareness of thirst in rodents is either entirely or predominantly due to neuronal activities in a subsection of the ventrolateral periaqueductal gray matter. It is also hypothesized that the awareness of thirst in primates is due to neuronal activities in both the ventrolateral periaqueductal gray and in a region within the medial prefrontal and anterior cingulate cortex.     

Beyond family‐level adversities: Exploring the developmental timing of neighborhood disadvantage effects on the brain

A growing literature suggests that adversity is associated with later altered brain function, particularly within the corticolimbic system that supports emotion processing and salience detection (e.g., amygdala, prefrontal cortex [PFC]). Although neighborhood socioeconomic disadvantage has been shown to predict maladaptive behavioral outcomes, particularly for boys, most of the research linking adversity to corticolimbic function has focused on family‐level adversities. Moreover, although animal models and studies of normative brain development suggest that there may be sensitive periods during which adversity exerts stronger effects on corticolimbic development, little prospective evidence exists in humans. Using two low‐income samples of boys (n = 167; n = 77), Census‐derived neighborhood disadvantage during early childhood, but not adolescence, was uniquely associated with greater amygdala, but not PFC, reactivity to ambiguous neutral faces in adolescence and young adulthood. These associations remained after accounting for several family‐level adversities (e.g., low family income, harsh parenting), highlighting the independent and developmentally specific neural effects of the neighborhood context. Furthermore, in both samples, indicators measuring income and poverty status of neighbors were predictive of amygdala function, suggesting that neighborhood economic resources may be critical to brain development.     

Somatic Markers and Response Reversal: Is There Orbitofrontal Cortex Dysfunction in Boys with Psychopathic Tendencies?

This study investigated the performance of boys with psychopathic tendencies and comparison boys, aged 9 to 17 years, on two tasks believed to be sensitive to amygdala and orbitofrontal cortex functioning. Fifty-one boys were divided into two groups according to the Psychopathy Screening Device (PSD, P. J. Frick & R. D. Hare, in press) and presented with two tasks. The tasks were the gambling task (A. Bechara, A. R. Damasio, H. Damasio, & S. W. Anderson, 1994) and the Intradimensional/Extradimensional (ID/ED) shift task (R. Dias, T. W. Robbins, & A. C. Roberts, 1996). The boys with psychopathic tendencies showed impaired performance on the gambling task. However, there were no group differences on the ID/ED task either for response reversal or extradimensional set shifting. The implications of these results for models of psychopathy are discussed.     

The Limbic System and the Soul: Evolution and the Neuroanatomy of Religious Experience

The evolutionary neurological foundations of religious experience are detailed. Human beings have been burying and preparing their dead for the Hereafter for more than 100,000 years. These behaviors and beliefs are related to activation of the amygdala, hippocampus, and temporal lobe, which are responsible for religious, spiritual, and mystical trancelike states, dreaming, astral projection, near-death and out-of-body experiences, and the hallucination of ghosts, demons, angels, and gods. Abraham, Moses, Muhammad, and Jesus Christ, and others who have communed with angels or gods display limbic system hyperactivity, whereas patients report religious hallucinations or out-of-body experiences when limbic structures are stimulated or excessively activated. It is postulated that limbic and temporal lobe structures account for the sexual and violent aspects of religious behavior and also serve as a "transmitter to God," and that the evolution of these structures made spiritual experience possible.     

Is There Savings for Pavlovian Fear Conditioning after Neurotoxic Basolateral Amygdala Lesions in Rats?

Considerable evidence indicates an important role for amygdaloid nuclei in both the acquisition and expression of Pavlovian fear conditioning. Recent reports from my laboratory have focused on the impact of neurotoxic lesions of the basolateral complex of the amygdala (BLA) on conditional freezing behavior in rats. In these studies, I have observed severe effects of posttraining BLA lesions on the expression of conditional freezing even after extensive presurgical overtraining (25-75 trials). Moreover, I have found no evidence for sparing of fear memory (i.e., savings) in these rats when I assess their rate of reacquisition relative to BLA rats receiving minimal training (1 trial). In these experiments, freezing behavior was assessed using a conventional time-sampling procedure and expressed as a response probability. Although this measure is well established in the literature, it is conceivable that it is not sensitive to spared memory in rats with BLA lesions. To address this issue, I present a more detailed analysis of freezing behavior that quantifies latency to freeze, the number of freezing bouts, the duration of freezing bouts, and the probability distribution of bout lengths. I also include control data from untrained (no-shock) rats. Consistent with my earlier reports, I find no evidence of savings of fear memory in rats with neurotoxic BLA lesions using several measures of freezing behavior. These results reiterate the conclusion that fear memory, as it is expressed in freezing behavior, requires neurons in the BLA.     

杏仁体与情绪及感觉功能的关系

近来研究表明杏仁体与感觉、情绪和记忆关系密切。对恐惧条件反射的研究发现杏仁体是情绪活动的关键性结构;导致恐惧条件反射的细胞及分子机制研究征实杏仁体具有情绪学习与记忆机能;杏仁体在向中感觉信息的筛选和凋制中具有显著作用和重要意义。本文将综述这方面的进展。     

Does medial prefrontal cortex activity during self‐knowledge reference reflect the uniqueness of self‐knowledge?1

Abstract: For this study, functional magnetic resonance imaging was used to examine whether medial prefrontal cortex (MPFC) activity during self‐knowledge reference reflects the uniqueness of self‐knowledge. Experiment 1 investigated neural activity during self‐knowledge reference (“Does the word describe you?”) and self‐monitoring (“Does the word make you feel pleasant?”). The results showed that self‐knowledge reference and self‐monitoring activate common neural substrates within the MPFC. Experiment 2 compared neural activity produced by self‐knowledge reference, other‐knowledge (acquaintance‐knowledge) reference (“Does this word describe the person?”), and evaluation (“Is this word socially desirable?”). Results showed no increase in MPFC activity during self‐knowledge reference relative to other‐knowledge reference. Furthermore, self‐knowledge reference and other‐knowledge reference share common neural substrates within the MPFC. The results described indicate that it is unlikely that MPFC activity during self‐knowledge reference reflects the uniqueness of self‐knowledge. The feature, as reflected in MPFC activity, is discussed.     

Neurochemical mechanisms underlying amygdaloid modulation of aggressive behavior in the cat

Studies designed to determine the respective roles of substance P, excitatory amino acids, and enkephalins in amygdaloid modulation of defensive rage behavior in the cat are presented. The basic design of these studies involved three stages. In stage I, cannula electrodes for stimulation and drug infusion were implanted into medial hypothalamic or midbrain periaqueductal gray (PAG) sites from which defensive rage behavior could be elicited. Then, a stimulating electrode was implanted into a site within the medial, basal, or central nuclear complex from which modulation of the defensive rage response could be obtained. Amygdaloid modulation of defensive rage was determined in the following manner: it employed the paradigm of dual stimulation in which comparisons were made of response latencies between alternate trials of dual (i. e., amygdala = medial hypothalamus [or PAG]) and single stimulation of the hypothalamus or PAG alone. Thus, stage I established the baseline level ofmodulation (i. e., facilitation or suppression of defensive rage) in the predrug stimulation period. In stage II, a selective or nonselective receptor antagonist for a given transmitter system was administered either peripherally or intracerebrally at the defensive rage site, after which time the same dual stimulation paradigm was then repeated over the ensuing 180 min postinjection period in order to determine the effects of drug delivery upon amygdaloid modulation of defensive rage. Stage III of the study took place at the completion of the pharmacological testing phase. The retrograde axonal tracer, Fluoro-Gold, was microinjected into the defensive rage site within the medial hypothalamus or PAG, and following a 6-14 day survival period, animals were sacrificed and brains were processed for histological and immunocytochemical analyses for the neurotransmitters noted above. This procedure thus permitted identification of cells within the amygdala which were labeled retrogradely and which were also immunostained positively for substance P, excitatory amino acids, or enkephalin. For studies involving substance P, defensive rage was elicited from the medial hypothalamus and for studies examining the roles of excitatory amino acids and enkephalin, defensive rage was elicited from the PAG. In the first study, facilitation of hypothalamically elicited defensive rage was obtained with dual stimulation of the medial nucleus of the amygdala. In separate experiments, the selective NK₁ non-peptide antagonist, CP 96,345, was administered both peripherally as well as intracerebrally into the hypothalamic defensive rage sites in doses of 0.5-4.0 mg/kg (i. p.) and 0.5-2.5 nmol (i. c.). Following drug delivery, the facilitatory effects of medial amygdaloid stimulation were blocked in a dose- and time-dependent manner in which the effects were noted as early as 5 min postinjection. The maximum drug dose (4.0 mg/kg) employed for peripheral administration resulted in a 42% reduction in the facilitatory effects of the medical amygdala (P < 0.002). This drug, when microinjected directly into medial hypothalamic defensive rage sites at the maximum dose level of 2.5 nmol, resulted in an 84% reduction of the suppressive effects of amygdaloid stimulation (P < 0.5) at 5 min postinjection. In the next study, an N-methyl-D-aspartate (NMDA) antagonist, DL-α-amino-7-phosphonoheptanoic acid (AP-7), was administered either peripherally (0.1-1.0 mg/kg) or intracerebrally (0.2 and 2.0 nmol) into PAG defensive rage sites. Facilitation of defensive rage behavior, which was observed following dual stimulation of the basal amygdala and PAG, was significantly reduced by either route of drug administration in a dose- and time-dependent manner. At the maximum dose level of peripheral administration, AP-7 reduced amygdaloid facilitation of defensive rage by 63% (P < 0.001) for 60 min, postinjection. A smaller (i. e., 19%) but still significant (P < 0.05) reduction in facilitation was obtained following intracerebral administration of the drug. In a third study, the non-selective opioid receptor antagonist, naloxone (27.5 nmol), infused directly into PAG defensive rage sites, totally blocked the suppressive effects of central amygdaloid stimulation for a period of 30 min (P < 0.05) in a dose- and time-dependent manner. The anatomical phase of this study revealed the following relationships: 1) that large numbers of neurons projecting to the medial hypothalamus from the medial amygdala immunoreact positively for substance P; 2) that neurons projecting to the PAG from the basal complex of amygdala immunoreact positively for glutamate and aspartate; and 3) that neurons located within the central nucleus of the amygdala which project to the PAG immunoreact positively for met-enkephalin. Collectively, these observations provide new evidence which characterizes the likely neurotransmitters linked with specific amygdaloid pathways subserving the modulation of defensive rage behavior in the cat.