From unspecific to adjusted, how the BOLD response in the rat hippocampus develops during consecutive stimulations.

To determine the possibility to deconvolve measured BOLD responses to neuronal signals, the rat perforant pathway was electrically stimulated with 10 related stimulation protocols. All stimulation protocols were composed of low-frequency pulse sequences with superimposed high-frequency pulse bursts. Because high-frequency pulse bursts trigger only one synchronized spiking of granular cells, variations of the stimulation protocol were used: (a) to keep the spiking activity similar during the presentation of different numbers of pulses, (b) to apply identical numbers of pulses to induce different amounts of spiking activity, and (c) to concurrently vary the number of applied electrical pulses and resultant spiking activity. When complex pulse sequences enter the hippocampus, an unspecific default-like BOLD response is first generated, which relates neither to the number of incoming pulses nor to the induced spiking activity. Only during subsequent stimulations does the initial unspecific response adjust to a more adequate response, which in turn either strongly related to spiking activity when low-frequency pulses were applied or depended on the incoming activity when high-frequency pulse bursts were presented. Thus, only the development of BOLD responses during repetitive stimulations can predict the underlying neuronal activity and deconvolution analysis should not be performed during an initial stimulation period.

From Shortage to Surge: A Developmental Switch in Hippocampal-Prefrontal Coupling in a Gene-Environment Model of Neuropsychiatric Disorders.

Cognitive deficits represent a major burden of neuropsychiatric disorders and result in part from abnormal communication within hippocampal-prefrontal circuits. While it has been hypothesized that this network dysfunction arises during development, long before the first clinical symptoms, experimental evidence is still missing. Here, we show that pre-juvenile mice mimicking genetic and environmental risk factors of disease (dual-hit GE mice) have poorer recognition memory that correlates with augmented coupling by synchrony and stronger directed interactions between prefrontal cortex and hippocampus. The network dysfunction emerges already during neonatal development, yet it initially consists in a diminished hippocampal theta drive and consequently, a weaker and disorganized entrainment of local prefrontal circuits in discontinuous oscillatory activity in dual-hit GE mice when compared with controls. Thus, impaired maturation of functional communication within hippocampal-prefrontal networks switching from hypo- to hyper-coupling may represent a mechanism underlying the pathophysiology of cognitive deficits in neuropsychiatric disorders.

Frontal alpha-asymmetry in adults with attention deficit hyperactivity disorder: replication and specification.

Recent findings suggest that adults suffering from attention deficit hyperactivity disorder (ADHD) display an atypical pattern of hemispheric asymmetry, assessed through the alpha band in resting-state electroencephalogram. In the context of the approach-withdrawal model of hemispheric asymmetry, this pattern has been identified as a correlate of approach-related behavior, particularly in anterior brain regions. The current study sought to replicate previous findings on alpha asymmetry in ADHD, and to specify them based on the assumption that ADHD represents a disorder of excessive approach tendencies. A group of ADHD patients (n=19) was compared to a group of healthy controls (n=19) on measures of alpha asymmetry and aggression, an approach-related trait. Observed region-specific group differences in alpha asymmetry approximated assumptions of the approach-withdrawal model. In addition ADHD subjects displayed elevated levels of a subcomponent of aggression. These results provide support for a conceptualization of ADHD as a disorder of excessive approach tendencies.