Socially-mediated activation in the snake social-decision-making network.

Brain areas important for social perception, social reward, and social behavior - collectively referred to as the social-decision-making network (SDN) - appear to be highly conserved across taxa. These brain areas facilitate a variety of social behaviors such as conspecific approach/avoidance, aggression, mating, parental care, and recognition. Although the SDN has been investigated across taxa, little is known about its functioning in reptiles.

Toluene decreases Purkinje cell output by enhancing inhibitory synaptic transmission in the cerebellar cortex.

Toluene belongs to a class of psychoactive drugs known as inhalants. Found in common household products such as adhesives, paint products, and aerosols, toluene is inhaled for its intoxicating and euphoric properties. Additionally, exposure to toluene disrupts motor behaviors in a manner consistent with impairments to cerebellar function.

Age-dependent time courses of recovery for motor functions following acute toluene intoxication in rats.

Toluene is a psychoactive chemical found in many household products including adhesives and thinners. Inhalation of these vapors can cause euphoria and impairments in motor control and neurological functioning. Misuse and abuse of toluene is most common in children, which may in part be due to an age-dependent neurobehavioral sensitivity to toluene.

Binge inhalation of toluene vapor produces dissociable motor and cognitive dysfunction in water maze tasks.

Binge inhalation of toluene, a psychoactive chemical found in many household and industrial products, leads acutely to intoxication with comorbid impairments in motor function and cognitive abilities that appear to recover quickly. Recent evidence, however, indicates that the administration of toluene results in marked changes in neurons of the medial prefrontal cortex that persist for relatively longer periods compared with other brain regions. To elucidate the potential toluene-induced (∼5000 ppm) cognitive dysfunctions that continue following the recovery of locomotor abilities, rats were entered into a series of water maze tasks.

Toluene inhalation modulates dentate gyrus granule cell output in vivo.

Toluene, a psychoactive volatile solvent found in adhesives and other products, is inhaled for its euphoric and intoxicating effects. Toluene inhalation additionally results in cognitive disturbances including impairments in select types of spatial and non-spatial memory, which converging evidence suggests may involve neurons of the dentate gyrus. In the present study we examined the effects of acute binge-like (~5000 ppm) toluene inhalation on dentate gyrus granule cell output and perforant path synaptic transmission, using extracellular field potential recordings in anesthetized adult rats in vivo.

Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells.

Encoding sensory input requires the expression of postsynaptic ion channels to transform key features of afferent input to an appropriate pattern of spike output. Although Ca(2+)-activated K(+) channels are known to control spike frequency in central neurons, Ca(2+)-activated K(+) channels of intermediate conductance (KCa3.1) are believed to be restricted to peripheral neurons.

Distribution of c-Fos immunoreactivity in the rat brain following abuse-like toluene vapor inhalation.

Inhalation of vapors from toluene-containing products results in euphoria accompanied by a variety of cognitive impairments and motor dysfunctions. The profound behavioral changes observed during and following toluene inhalation suggest changes in the activity of cells in potentially many brain regions; however, a comprehensive assessment of the neuroanatomical structures activated by toluene vapor has not been completed. Thus in the present study we systematically mapped in over 140 brain structures the distribution of c-Fos immunoreactivity (c-Fos IR), a proxy for neural activation, following exposure to an abuse-like concentration (~5000 ppm) of toluene vapor for 0, 5, 10 or 30 min.

Endogenous biotin in rat brain: implications for false-positive results with avidin-biotin and streptavidin-biotin techniques.

The interaction between avidin and biotin or streptavidin and biotin forms the basis of several widely used immunohistochemical techniques. An assumption inherent to these techniques is that endogenous biotin is not present in the tissue in detectable quantities, as neither avidin nor streptavidin can discriminate between endogenous biotin and biotinylated antibodies. However, biotin is a known cofactor for numerous carboxylases required in oxidative metabolism, raising the possibility for potential false-positive results in many tissues.

Regulation of synaptic transmission and plasticity by neuronal nicotinic acetylcholine receptors.

Nicotinic acetylcholine receptors (nAChRs) are widely expressed throughout the central nervous system and participate in a variety of physiological functions. Recent advances have revealed roles of nAChRs in the regulation of synaptic transmission and synaptic plasticity, particularly in the hippocampus and midbrain dopamine centers. In general, activation of nAChRs causes membrane depolarization and directly and indirectly increases the intracellular calcium concentration.

Climbing fiber discharge regulates cerebellar functions by controlling the intrinsic characteristics of purkinje cell output.

The contribution of Purkinje cells to cerebellar motor coordination and learning is determined in part by the chronic and acute effects of climbing fiber (CF) afferents. Whereas the chronic effects of CF discharge, such as the depression of conjunctive parallel fiber (PF) inputs, are well established, the acute cellular functions of CF discharge remain incompletely understood. In rat cerebellar slices, we show that CF discharge presented at physiological frequencies substantially modifies the frequency and pattern of Purkinje cell spike output in vitro.

Ca(V)3 T-type calcium channel isoforms differentially distribute to somatic and dendritic compartments in rat central neurons.

Spike output in many neuronal cell types is affected by low-voltage-activated T-type calcium currents arising from the Ca(v)3.1, Ca(v)3.2 and Ca(v)3.

Specific T-type calcium channel isoforms are associated with distinct burst phenotypes in deep cerebellar nuclear neurons.

T-type calcium channels are thought to transform neuronal output to a burst mode by generating low voltage-activated (LVA) calcium currents and rebound burst discharge. In this study we assess the expression pattern of the three different T-type channel isoforms (Ca(v)3.1, Ca(v)3.

Physiological and morphological development of the rat cerebellar Purkinje cell.

Cerebellar Purkinje cells integrate multimodal afferent inputs and, as the only projection neurones of the cerebellar cortex, are key to the coordination of a variety of motor- and learning-related behaviours. In the neonatal rat the cerebellum is undeveloped, but over the first few postnatal weeks both the structure of the cerebellum and cerebellar-dependent behaviours mature rapidly. Maturation of Purkinje cell physiology is expected to contribute significantly to the development of cerebellar output.

Kv1 K+ channels control Purkinje cell output to facilitate postsynaptic rebound discharge in deep cerebellar neurons.

Purkinje cells (PCs) generate the sole output of the cerebellar cortex and govern the timing of action potential discharge from neurons of the deep cerebellar nuclei (DCN). Here, we examine how voltage-gated Kv1 K+ channels shape intrinsically generated and synaptically controlled behaviors of PCs and address how the timing of DCN neuron output is modulated by manipulating PC Kv1 channels. Kv1 channels were studied in cerebellar slices at physiological temperatures with Kv1-specific toxins.

Biotin is endogenously expressed in select regions of the rat central nervous system.

The vitamin biotin is an endogenous molecule that acts as an important cofactor for several carboxylases in the citric acid cycle. Disorders of biotin metabolism produce neurological symptoms that range from ataxia to sensory loss, suggesting the presence of biotin in specific functional systems of the CNS. Although biotin has been described in some cells of nonmammalian nervous systems, the distribution of biotin in mammalian CNS is virtually unknown.