Feature integration, attention, and fixations during visual search.

We argue that mechanistic premises of "item-based" theories are not invalidated by the fixation-based approach. We use item-based theories to propose an account that does not advocate strict serial item processing and integrates fixations. The main focus of this account is feature integration within fixations. We also suggest that perceptual load determines the size of the fixations.

Neurofeedback Therapy for Enhancing Visual Attention: State-of-the-Art and Challenges.

We have witnessed a rapid development of brain-computer interfaces (BCIs) linking the brain to external devices. BCIs can be utilized to treat neurological conditions and even to augment brain functions. BCIs offer a promising treatment for mental disorders, including disorders of attention. Here we review the current state of the art and challenges of attention-based BCIs, with a focus on visual attention. Attention-based BCIs utilize electroencephalograms (EEGs) or other recording techniques to generate neurofeedback, which patients use to improve their attention, a complex cognitive function. Although progress has been made in the studies of neural mechanisms of attention, extraction of attention-related neural signals needed for BCI operations is a difficult problem. To attain good BCI performance, it is important to select the features of neural activity that represent attentional signals. BCI decoding of attention-related activity may be hindered by the presence of different neural signals. Therefore, BCI accuracy can be improved by signal processing algorithms that dissociate signals of interest from irrelevant activities. Notwithstanding recent progress, optimal processing of attentional neural signals remains a fundamental challenge for the development of efficient therapies for disorders of attention.

SSVEP-modulation by covert and overt attention: Novel features for BCI in attention neuro-rehabilitation.

In this pilot study the effect of attention (covert and overt) on the signal detection and classification of steady-state visual-evoked potential (SSVEP) were investigated. Using the SSVEP-based paradigm, data were acquired from 4 subjects using 3 scalp electroencephalography (EEG) electrodes located on the visual area. Subjects were instructed to perform the attention task in which they attended covertly or overtly to either of the stimuli flickering with different frequencies (6, 7, 8 and 9Hz). We observed a decrease in signal power in covert compared to the overt attention. However, there was a consistent pattern in covert attention causing an increase in the power of the 2(nd) harmonic of the attended frequency. Encouraging results of this preliminary study indicates that it can be adapted and implemented in the brain-computer interface (BCI) system which could potentially be used as a neuro-rehabilitation tool for individuals with attention deficit.

Effects of apomorphine and ß-carbolines on firing rate of neurons in the ventral pallidum in the rats.

The ventral pallidum (VP) is a critical element of the mesocorticolimbic system that is inter-connected with motor and limbic structures and may be considered as an interface between motivational and effector neural signals. Dopamine is important in behavioral output of the VP, and dysfunctioning its dopamine quantity leads to various neuropsychiatric disorders. Understanding neural substrate underlying this phenomenon has become an important affair in recent years. In this study, neuronal activities were recorded from the VP in presence or absence of the mixed dopamine D1/D2 receptor agonist, apomorphine, and/or ß-carbolines, using an extracellular single-unit recording technique. We reported that subcutaneous administration of apomorphine (0.5mg/kg) decreased neural activity in the VP. In addition, neither harmine (7.8 mg/kg; i.p.) nor harmane (4 mg/kg; i.p.) and norharmane (2.5mg/kg; i.p.) had any effect on neural firing in the VP. Finally, pretreatment with ß-carbolines prevented the apomorphine-induced inhibition on VP firing rate. Thus, according to the results of aforementioned study and our results in the present study, we can conclude that presumably most responses in the VP are D2 dopamine dependent. Although the ß-carbolines were unable to alter neural activity in the VP, interestingly, pretreatment with ß-carbolines protect decreasing in firing rate of neurons in the VP followed by apomorphine administration. This protective effect could be explained by interaction between ß-carbolines and dopaminergic mechanisms.

Electrolytic lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats.

Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 microg/0.3 microl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 microg/0.3 microl saline per side) in rats after NRM electrolytic lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 (P<0.01) and 60 (P<0.05) but not 90-120 min after morphine microinjection into the CnF, compared with sham-lesion group. We concluded that morphine induces the analgesic effects through the opioid receptors in the CnF. It is also appeared that morphine-induced antinociception decreases following the NRM lesion but it seems that there are some other descending pain modulatory pathways that activate in the absence of NRM.