Relativistic Electrons Produced by Foreshock Disturbances Observed Upstream of Earth's Bow Shock.

Charged particles can be reflected and accelerated by strong (i.e., high Mach number) astrophysical collisionless shock waves, streaming away to form a foreshock region in communication with the shock. Foreshocks are primarily populated by suprathermal ions that can generate foreshock disturbances-large-scale (i.e., tens to thousands of thermal ion Larmor radii), transient (∼5-10 per day) structures. They have recently been found to accelerate ions to energies of several keV. Although electrons in Saturn's high Mach number (M>40) bow shock can be accelerated to relativistic energies (nearly 1000 keV), it has hitherto been thought impossible to accelerate electrons beyond a few tens of keV at Earth's low Mach number (1≤M<20) bow shock. Here we report observations of electrons energized by foreshock disturbances to energies up to at least ∼300 keV. Although such energetic electrons have been previously observed, their presence has been attributed to escaping magnetospheric particles or solar events. These relativistic electrons are not associated with any solar or magnetospheric activity. Further, due to their relatively small Larmor radii (compared to magnetic gradient scale lengths) and large thermal speeds (compared to shock speeds), no known shock acceleration mechanism can energize thermal electrons up to relativistic energies. The discovery of relativistic electrons associated with foreshock structures commonly generated in astrophysical shocks could provide a new paradigm for electron injections and acceleration in collisionless plasmas.

From impulses to maladaptive actions: the insula is a neurobiological gate for the development of compulsive behavior.

Impulsivity is an endophenotype of vulnerability for compulsive behaviors. However, the neural mechanisms whereby impulsivity facilitates the development of compulsive disorders, such as addiction or obsessive compulsive disorder, remain unknown. We first investigated, in rats, anatomical and functional correlates of impulsivity in the anterior insular (AI) cortex by measuring both the thickness of, and cellular plasticity markers in, the AI with magnetic resonance imaging and in situ hybridization of the immediate early gene zif268, respectively. We then investigated the influence of bilateral AI cortex lesions on the high impulsivity trait, as measured in the five-choice serial reaction time task (5-CSRTT), and the associated propensity to develop compulsivity as measured by high drinking levels in a schedule-induced polydipsia procedure (SIP). We demonstrate that the AI cortex causally contributes to individual vulnerability to impulsive-compulsive behavior in rats. Motor impulsivity, as measured by premature responses in the 5-CSRTT, was shown to correlate with the thinness of the anterior region of the insular cortex, in which highly impulsive (HI) rats expressed lower zif268 mRNA levels. Lesions of AI reduced impulsive behavior in HI rats, which were also highly susceptible to develop compulsive behavior as measured in a SIP procedure. AI lesions also attenuated both the development and the expression of SIP. This study thus identifies the AI as a novel neural substrate of maladaptive impulse control mechanisms that may facilitate the development of compulsive disorders.

Divergent effects of D2/3 receptor activation in the nucleus accumbens core and shell on impulsivity and locomotor activity in high and low impulsive rats.

RATIONALE: Previously we demonstrated reduced D2/3 receptor availability in the ventral striatum of hyper-impulsive rats on the five-choice serial reaction time task (5-CSRTT). However, the anatomical locus of D2/3 receptor dysfunction in high impulsive (HI) rats is unknown. OBJECTIVE: In the present study, we investigated whether D2/3 receptor dysfunction in HI rats is localised to the core or shell sub-regions of the nucleus accumbens (NAcb). METHODS: Rats were selected for low (low impulsive, LI) and high impulsivity on the 5-CSRTT and implanted with guide cannulae targeting the NAcb core and shell. The D2/3 receptor agonist quinpirole was locally injected in the NAcb (0.1, 0.3 and 1 µg per infusion) and its effects investigated on the performance of LI and HI rats on the 5-CSRTT as well as spontaneous locomotor activity in an open field. RESULTS: Intra-NAcb core quinpirole increased premature responding in HI rats but not in LI rats. In contrast, intra-NAcb shell quinpirole strongly increased locomotor activity in HI rats, unlike LI rats. This effect was blocked by intra-NAcb shell infusions of the D2/3 receptor antagonist nafadotride (0.03 µg). However, nafadotride was ineffective in blocking the effects of intra-NAcb core quinpirole on premature responding in HI rats. CONCLUSIONS: These findings indicate that impulsivity and hyperactivity are separately regulated by core and shell sub-regions of the NAcb and that HI rats show an enhanced response to D2/3 receptor activation in these regions. These results suggest that the symptom clusters of hyperactivity and impulsivity in attention-deficit hyperactivity disorder may be neurally dissociable at the level of the NAcb.