Systemic and local administration of estradiol into the prefrontal cortex or hippocampus differentially alters working memory

The influence of estradiol on learning and memory is dependent on a number of factors. The effects of physiological levels of estradiol on the acquisition of a spatial working memory task mediated by the prefrontal cortex (PFC) and the hippocampus were examined in Experiment 1. Ovariectomized Long-Evans rats received daily injections of estradiol or vehicle were tested on the win-shift version of the radial arm maze. A high dose of estradiol benzoate (5 microg) enhanced acquisition of the task, whereas a low dose of estradiol (0.3 microg) increased the number of errors committed over 17 days of testing. Experiment 2 was conducted to examine site-specific influences of estradiol on spatial working memory in well-trained rats. Saline and estradiol cyclodextrin (0.1 and 0.9 microg) were infused into the prelimbic region of the PFC or dorsal hippocampus 40 min prior to testing on the win-shift task. Infusions of estradiol into both brain areas attenuated saline-infusion disruptions in working memory. Specifically, the higher dose of estradiol facilitated working memory when infused into the PFC, whereas the lower dose of estradiol facilitated performance when infused into the dorsal hippocampus. Moreover, working memory was significantly impaired 24 h after infusions of estradiol into the dorsal hippocampus but not the PFC. These data provide further evidence for the notion that estradiol can dose-dependently alter memory processes and suggest that facilitation or disruptions of working memory by estradiol are site- and time-specific.     

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Learning involves not only the establishment of memory per se, but also the specific details of its contents. In classical conditioning, the former concerns whether an association was learned while the latter discloses what was learned. The neural bases of associativity have been studied extensively while neural mechanisms of memory specificity have been neglected. Stimulation of the cholinergic nucleus basalis (NBs) paired with a preceding tone induces CS-specific associative memory. As different levels of acetylcholine may be released naturally during different learning situations, we asked whether the level of activation of the cholinergic neuromodulatory system can control the degree of detail that is encoded and retrieved. Adult male rats were tested pre- and post-training for behavioral responses (interruption of ongoing respiration) to tones of various frequencies (1-15 kHz, 70 dB, 2 s). Training consisted of 200 trials/day of tone (8.0 kHz, 70 dB, 2 s) either paired or unpaired with NBs (CS-NBs = 1.8 s) at moderate (65.7+/-9.0 microA, one day) or weak (46.7+/-12.1 microA, three training days) levels of stimulation, under conditions of controlled behavioral state (pre-trial stable respiration rate). Post-training (24 h) responses to tones revealed that moderate activation induced both associative and CS-specific behavioral memory, whereas weak activation produced associative memory lacking frequency specificity. The degree of memory specificity 24 h after training was positively correlated with the magnitude of CS-elicited increase in gamma activity within the EEG during training, but only in the moderate NBs group. Thus, a low level of acetylcholine released by the nucleus basalis during learning is sufficient to induce associativity whereas a higher level of release enables the storage of greater experiential detail. gamma waves, which are thought to reflect the coordinated activity of cortical cells, appear to index the encoding of CS detail. The findings demonstrate that the amount of detail in memory can be directly controlled by neural intervention.     

Medial prefrontal cortex lesions abolish contextual control of competing responses

There is much debate as to the extent and nature of functional specialization within the different subregions of the prefrontal cortex. The current study was undertaken to investigate the effect of damage to medial prefrontal cortex subregions in the rat. Rats were trained on two biconditional discrimination tasks, one auditory and one visual, in two different contexts. At test, they received presentations of audiovisual compounds of these training stimuli in extinction. These compounds had dictated either the same (congruent trials) or different (incongruent trials) responses during training. In sham-operated controls, contextual cues came to control responding to conflicting information provided by incongruent stimulus compounds. Experiment 1 demonstrated that this contextual control of responding was not evident in individual rats with large amounts of damage that included the prelimbic and cingulate subregions of the prefrontal cortex. Experiment 2 further dissociated the result of Experiment 1, demonstrating that lesions specific to the anterior cingulate cortex were sufficient to produce a deficit early on during presentation of an incongruent stimulus compound but that performance was unimpaired as presentation progressed. This early deficit suggests a role for the anterior cingulate cortex in the detection of response conflict, and for the medial prefrontal cortex in the contextual control of competing responses, providing evidence for functional specialization within the rat prefrontal cortex.     

Activation of adenosine receptors in the posterior cingulate cortex impairs memory retrieval in the rat

Adenosine A1 and A2A receptor agonists and antagonists have been reported to alter learning and memory. The aim of our study was to investigate the involvement of adenosinergic system in memory retrieval into posterior cingulate cortex (PCC) of Wistar rats. To clarify this question, we tested specifics agonist and antagonists of adenosine A1 and A2A receptors in rats submitted to a one-trial inhibitory avoidance task. The stimulation of adenosine A1 and A2A receptors by CPA and CGS21680, respectively, impaired memory retrieval for inhibitory avoidance task, into PCC. These findings provide behavioral evidence for the role of adenosinergic system in the memory retrieval into PCC.     

Auditory repetition priming is impaired in pure alexic patients

Alexia without agraphia, or "pure" alexia, is an acquired impairment in reading that leaves writing skills intact. Repetition priming for visually presented words is diminished in pure alexia. However, it is not possible to verify whether this priming deficit is modality-specific or modality independent because reading abilities are compromised. Hence, auditory repetition priming was assessed with lexical decision and word stem completion tasks in pure alexic patients with lesions in left inferior temporal-occipital cortex and the splenium. Perceptually based, modality-specific priming models predict intact auditory priming, since auditory association cortex is spared in the patients. Alternatively, modality-independent models, which suggest that priming reflects the temporary modification of an amodal system, might predict impairments. Baseline performance was matched in the patients and controls, although lexical decision priming measures showed an interaction between group and repetition lag. The patients showed intact immediate priming but significantly less priming than controls at longer delays. Furthermore, word stem completion priming was abolished in the patients. One explanation for the deficit is that left inferior temporal-occipital cortex supports amodal aspects of priming, as suggested by recent neuroimaging results. Another possibility is that long-term auditory priming relies on covert orthographic representations which were unavailable in the patients. The results provide support for interactive models of word identification.     

What, if anything, is the medial temporal lobe, and how can the amygdala be part of it if there is no such thing?

Should the medial temporal lobe (MTL) of primates--which includes allocortical structures such as the hippocampus, neocortical structures such as the parahippocampal cortex, and nuclear structures such as the basolateral amygdala--be considered a single "thing"? According to the prevailing view, here termed the reification theory, the answer is yes. According to this theory, the MTL functions as an amalgamated entity that provides the neuronal mechanisms for declarative memory; the greater the damage to the MTL or any of its components, the greater the deleterious effects on declarative memory. A countervailing view, here called the balkanization theory, holds that the various components of the MTL process and store different kinds of information. According to this theory, damage to each part of the MTL causes a unique set of behavioral deficits-some involving memory, others involving perception, and yet others involving response selection. The empirical neuropsychological evidence favors the balkanization theory, as do some new concepts in theoretical neuroanatomy.     

左前额叶参与非相关词对的语义编码过程──来自光学成像的佐证

通过研究左前额叶在非相关同对的语义编码过程中的作用,探讨近红外光学成像技术用于脑高级认知活动检测的可行性。被试在两种实验条件下分别学习视觉呈现的20个汉字非相关词对,要求被试或将词对组成一个有意义的句子(深加工),或判断两个词是否具有相同的结构组合(浅加工)。光学成像器即时记录连续光透过额骨及前额皮层后760nm和850nm的漫射光强变化,以此推测相应脑组织的血容量变化。结果表明,与浅加工相比,左下前额叶在深加工时的血容量增多,尤其是背外侧部分。     

The role of inferior frontal cortex in phonological processing

Recent neuroimaging studies of language processing are examining the neural substrate of phonology because of its critical role in mapping sound information onto higher levels of language processing (e.g., words) as well as providing codes in which verbal information can be temporarily stored in working memory. However, the precise role of the inferior frontal cortex in spoken and written phonological tasks has remained elusive. Although lesion studies have indicated the presence of selective deficits in phonological processing, the location of lesions underlying these impairments has not revealed a consistent pattern. Despite efforts to refine methods and tasks, functional neuroimaging studies have also revealed variability in activation patterns. Reanalysis of evidence from these neuroimaging studies suggests that there are functional subregions within the inferior frontal gyrus that correspond to specific components of phonological processing (e.g., orthographic to phonological conversion in reading, and segmentation in speech).     

Lesions in the Central Nucleus of the Amygdala: Discriminative Avoidance Learning, Discriminative Approach Learning, and Cingulothalamic Training-Induced Neuronal Activity

The amygdala is critically involved in discriminative avoidance learning. Large lesions of the amygdala block discriminative avoidance learning and abolish cingulothalamic training-induced neuronal activity. These results indicated that amygdalar processing is critical for cingulothalamic plasticity. The larger lesions did not allow differentiation of the specific functioning of various amygdalar nuclei. Anatomical analysis showed that damage in the central (CE) nucleus of the amygdala was correlated with the severity of the behavioral deficit. The present study was carried out to determine whether smaller lesions, centered in the CE nucleus, would impair discriminative avoidance learning and block cingulothalamic plasticity. In addition, the possible role of the CE nucleus in appetitively motivated discriminative approach learning was examined for the first time. New Zealand White rabbits with CE nuclear lesions were first trained in the discriminative approach task. After attaining asymptotic performance, discriminative avoidance training sessions were alternated with continuing approach training sessions, one session each day. The rabbits with lesions were severely impaired in avoidance learning but showed no impairment of approach learning. Surprisingly, the attenuating effects of the lesions on cingulothalamic training-induced neuronal activity were more prevalent during approach learning than during avoidance learning. These results indicated that avoidance learning can be impaired by lesions centered in the CE nucleus that leave cingulothalamic plasticity largely intact and that the CE nucleus is involved in extra-cingulothalamic learning processes.