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Rouba Kozak

Publications and source records attributed to Rouba Kozak.

7 recordsLinked to original sources

More attention must be paid: the neurobiology of attentional effort.

Increases in attentional effort are defined as the motivated activation of attentional systems in response to detrimental challenges on attentional performance, such as the presentation of distractors, prolonged time-on-task, changing target stimulus characteristics and stimulus presentation parameters, circadian phase shifts, stress or sickness. Increases in attentional effort are motivated by the expected performance outcome; in the absence of such motivation, attentional performance continues to decline or may cease altogether. The beneficial effects of increased attentional effort are due in part to the activation of top-down mechanisms that act to optimize input detection and processing, thereby stabilizing or recovering attentional performance in response to challenges. Following a description of the psychological construct "attentional effort", evidence is reviewed indicating that increases in the activity of cortical cholinergic inputs represent a major component of the neuronal circuitry mediating increases in attentional effort. A neuronal model describes how error detection and reward loss, indicating declining performance, are integrated with motivational mechanisms on the basis of neuronal circuits between prefrontal/anterior cingulate and mesolimbic regions. The cortical cholinergic input system is activated by projections of mesolimbic structures to the basal forebrain cholinergic system. In prefrontal regions, increases in cholinergic activity are hypothesized to contribute to the activation of the anterior attention system and associated executive functions, particularly the top-down optimization of input processing in sensory regions. Moreover, and influenced in part by prefrontal projections to the basal forebrain, increases in cholinergic activity in sensory and other posterior cortical regions contribute directly to the modification of receptive field properties or the suppression of contextual information and, therefore, to the mediation of top-down effects. The definition of attentional effort as a cognitive incentive, and the description of a neuronal circuitry model that integrates brain systems involved in performance monitoring, the processing of incentives, activation of attention systems and modulation of input functions, suggest that 'attentional effort' represents a viable construct for cognitive neuroscience research.

Animals↗

Hypothalamic orexigenic peptides are overexpressed in young Long-Evans rats after early life exposure to fat-rich diets.

Nutritional factors have a critical influence during prenatal life on the development and regulation of networks involved in body weight and feeding regulation. To establish the influence of the macronutrient type on feeding regulatory mechanisms and more particularly on stimulatory pathways (galanin and orexins), we fed female rats on either a high-carbohydrate (HC), a high-fat (HF), or a well-balanced control diet during gestation and lactation, and measured peptide expression in the hypothalamus and important hormones (leptin, insulin) in their pups at weaning. HF weanlings were 30% lighter than control and HC pups (P<0.001). They were characterized by reduced plasma glucose and insulin levels (P<0.01 or less). Their galanin and orexin systems were upregulated as shown by the significant augmentation of mRNA expression in the paraventricular nucleus and lateral hypothalamus, respectively. Inhibitory peptides like corticotropin-releasing hormone and neurotensin were not affected by this dietary treatment during early life. There was, therefore, a more intense drive to eat in HF pups, perhaps to compensate for the lower body weight at weaning. HF diets during early life had meanwhile some positive consequences: the lower metabolic profile might be beneficial in precluding the development of obesity and metabolic syndrome later in life. This is however valid only if the orexigenic drive is normalized after weaning.

Aging↗

Increased capacity and density of choline transporters situated in synaptic membranes of the right medial prefrontal cortex of attentional task-performing rats.

Cholinergic neurons innervating the cortex have been conceptualized as a major component of the attention system of the brain. Because of recent evidence indicating plastic mechanisms regulating choline transporter (CHT)-mediated high-affinity choline uptake, which is the rate-limiting step of acetylcholine synthesis, the present experiment determined the capacity of cholinergic terminals to transport choline, and the proportion of choline transporters localized in the membrane of synaptic terminals, in several brain regions of rats performing a cognitive vigilance task (CVT) and a simple reaction time task (SRTT) and nonperforming (NP) rats. Compared with evidence from NP rats, increased choline transporter capacity [as indicated by maximum transporter velocity (Vmax)] and an increased density of CHTs situated in synaptic plasma membrane, relative to intracellular locations, were observed in the medial prefrontal cortex of the right but not left hemisphere of CVT-performing animals. Furthermore, right medial prefrontal Vmax values of CVT-performing rats correlated positively and left medial Vmax values correlated negatively with the animals' performance in signal trials. Measures of CHT function in the brains of SRTT-performing animals did not differ significantly from those in NP rats. The present data support the hypothesis that an increased capacity of choline transporters in the right medial prefrontal cortex, primarily attributable to increased trafficking of transporters from intracellular compartments to the terminal membrane, represents a cellular mechanism contributing to the mediation of attentional performance.

Analysis of Variance↗

Augmented prefrontal acetylcholine release during challenged attentional performance.

Previous research has demonstrated that attentional performance depends on the integrity of the cortical cholinergic input system and that such performance is associated with increases in cortical acetylcholine (ACh) release. The present experiment tested the hypothesis that the attentional impairments produced by bilateral basal forebrain infusions of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV) are associated with attenuation of performance-associated increases in ACh release. Rats were trained in a sustained attention task and equipped with three guide cannula for the bilateral infusion of the NMDA receptor antagonist APV (0, 3, 20 nmol) and for the insertion of a dialysis probe into the medial prefrontal cortex (mPFC). APV or vehicle was infused remotely following completion of the first of five blocks of trials. During the first block, attentional performance was associated with a 140% increase in ACh efflux. Infusions of APV decreased the animals' ability to detect signals and augmented the increases in ACh efflux observed prior to infusions. These data indicate a dissociation between levels of attentional performance and increases in mPFC ACh release. Augmentation of performance-associated increases in mPFC cholinergic transmission is hypothesized to mediate the increased demands on attentional 'effort' that are required to maintain performance under challenging conditions.

Acetylcholine↗

Excitotoxic lesions of the pedunculopontine tegmental nucleus in rats impair performance on a test of sustained attention.

Recent research has suggested that the pontomesencephalic tegmentum might be an important part of a network underlying sustained attention. The largest structure of the pontomesencephalic tegmentum is the pedunculopontine tegmental nucleus, which has ascending connections to thalamus and with corticostriatal systems. In this experiment we examined the performance of rats following bilateral excitotoxic lesions of the pedunculopontine tegmental nucleus on a test of sustained attention previously used to examine frontal cortical function. After an initial period of darkness, the rats had to attend continuously to a dim stimulus light that would, at unpredictable intervals, become transiently brighter. During this period of increased stimulus brightness the rats could press a lever to obtain a food reward. Rats were trained to a criterion level of performance before lesions were made. After surgery, sham lesioned rats (n=7) resumed accurate responding, with an average successful detection rate of approximately 70%. Pedunculopontine lesioned rats (n=7), however, only achieved a successful detection rate of approximately 40%. When the duration of the bright target stimulus was increased from 1.5 to 4 s, the performance of the pedunculopontine lesioned rats significantly improved. The observation that an increase in brightness duration caused a marked improvement in lesioned rats' performance suggests strongly that the impairment was in attention rather than motor ability or simple sensory processing. These data are taken to be consistent with the hypothesis that the pedunculopontine tegmental nucleus is an important part of a network maintaining attention.

Animals↗

Effects of changing reward on performance of the delayed spatial win-shift radial maze task in pedunculopontine tegmental nucleus lesioned rats.

Because it was designed to assess working memory, the delayed spatial win-shift (DSWS) radial maze task has been used to investigate the involvement of corticostriatal structures in executive processing. Excitotoxic lesions of the pedunculopontine tegmental nucleus (PPTg) produce profound deficits in performance of this task that are not accounted for by motor impairment. Thus, PPTg DSWS deficits are hypothesized to support a role for PPTg in complex cognitive processing. However, other studies indicate that the behaviour of PPTg lesioned rats varies depending on level of motivational excitement, assessed by the presence or absence of deprivation, or by manipulations of reward value. Since DSWS performance may also be affected by motivational dysfunction, the present experiment was conducted to examine the effects of post-surgical presentation of a more positive food reward (chocolate drops) on the DSWS retention performance of PPTg lesioned rats. Results confirmed a PPTg lesion deficit: lesioned rats made significantly more errors in both training and test phases, and made errors significantly earlier in their choice sequence in the test phase. Main effects of phase on number of errors indicated that the PPTg test phase deficit was not simply the result of a carry-over impairment from the training phase. PPTg rats receiving chocolate made significantly fewer errors than PPTg rats receiving food pellets. Results suggest that PPTg DSWS deficits are not the result of altered motivation or hedonic appreciation of reward value (or reward change) and therefore support the hypothesis of executive cognitive deficits in PPTg lesioned rats.

Animals↗