coloboma/dopamine

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Transgenic rescue of SNAP-25 restores dopamine-modulated synaptic transmission in the coloboma mutant.

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Many of the molecular components constituting the exocytotic machinery responsible for neurotransmitter release have been identified, yet the precise role played by these proteins in synaptic transmission, and their impact on neural function, has not been resolved. The mouse mutation coloboma is a

Norepinephrine regulates locomotor hyperactivity in the mouse mutant coloboma.

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An imbalance between dopaminergic and noradrenergic systems is implicated in hyperactivity disorders such as attention deficit hyperactivity disorder (ADHD) and Tourette syndrome. We have identified the mouse mutant coloboma as an animal model for examining the neurological basis of hyperactivity.

Coloboma mouse mutant as an animal model of hyperkinesis and attention deficit hyperactivity disorder.

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Hyperkinesis and developmental behavioral deficiencies are cardinal signs of attention-deficit hyperactivity disorder. In mice, the mutation coloboma (Cm) corresponds to a contiguous gene defect that results in phenotypic abnormalities including spontaneous hyperactivity, head-bobbing, and ocular

Expression of catecholaminergic mRNAs in the hyperactive mouse mutant coloboma.

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The SNAP-25 deficient mouse mutant coloboma (Cm/+) is an animal model for investigating the biochemical basis of locomotor hyperactivity. The spontaneous hyperactivity exhibited by coloboma is three times greater than control mice and is a direct result of the SNAP-25 deletion. SNAP-25 is a

Coloboma contiguous gene deletion encompassing Snap alters hippocampal plasticity.

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Mice heterozygous for the semidominant mutation coloboma (Cm/+) display several distinct pathologies including head bobbing, ophthalmic deformation, and locomotor hyperactivity. The Cm/+ mutation comprises a contiguous gene defect which encompasses deletion of the gene Snap encoding the presynaptic

Coloboma hyperactive mutant mice exhibit regional and transmitter-specific deficits in neurotransmission.

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The mouse mutant coloboma (Cm/+), which exhibits profound spontaneous hyperactivity and bears a deletion mutation on chromosome 2, including the gene encoding synaptosomal protein SNAP-25, has been proposed to model aspects of attention-deficit hyperactivity disorder. Increasing evidence suggests a

D2-like dopamine receptors mediate the response to amphetamine in a mouse model of ADHD.

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The mechanisms underlying the effects of psychostimulants in attention deficit hyperactivity disorder (ADHD) are not well understood, but indirect evidence implicates D2 dopamine receptors. Here we dissect the components of dopaminergic neurotransmission in the hyperactive mouse mutant coloboma to

D2 dopamine receptor subtype-mediated hyperactivity and amphetamine responses in a model of ADHD.

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Low doses of psychostimulants produce beneficial behavioral effects in ADHD patients but the mechanisms underlying the response are not understood. Here we use the hyperactive mouse mutant coloboma to identify D2-like dopamine receptor subtypes that mediate the hyperactivity and response to

Gene-environment interactions affect long-term depression (LTD) through changes in dopamine receptor affinity in Snap25 deficient mice.

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Genes and environmental conditions interact in the development of cognitive capacities and each plays an important role in neuropsychiatric disorders such as attention deficit/hyperactivity disorder (ADHD) and schizophrenia. Multiple studies have indicated that the gene for the SNARE protein SNAP-25

Animal models of attention-deficit/hyperactivity disorder.

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Attention-deficit hyperactivity disorder (AD/HD) is a clinically heterogenous disorder including hyperactivity, impulsivity, and inattention. Both psychostimulant and non-psychostimulant drugs such as methylphenidate and atomoxetine, respectively, to modulate catecholeamine neurotransmission are

Abnormal presynaptic catecholamine regulation in a hyperactive SNAP-25-deficient mouse mutant.

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The consequences of a reduction in the presynaptic protein, SNAP-25, were investigated to determine the neurochemical basis of the marked hyperlocomotor activity in coloboma (Cm/+) mice. SNAP-25 is part of the minimal presynaptic machinery necessary for exocytotic neurotransmitter release. Reserpine

Overview of animal models of attention deficit hyperactivity disorder (ADHD).

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Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous, highly heritable, behavioral disorder that affects ∼5% to 10% of children worldwide. Although animal models cannot truly reflect human psychiatric disorders, they can provide insight into the disorder that cannot be obtained from

Rodent models of ADHD.

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The neonatal 6-OHDA-lesioned rat, coloboma mouse, DAT-KO mouse, and spontaneously hypertensive rat (SHR) models all bear a phenotypic resemblance to ADHD in that they express hyperactivity, inattention, and/or impulsivity. The models also illustrate the heterogeneity of ADHD: the initial cause

Animal models of attention-deficit hyperactivity disorder.

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Attention-deficit hyperactivity disorder (ADHD) involves clinically heterogeneous dysfunctions of sustained attention, with behavioral overactivity and impulsivity, of juvenile onset. Experimental models, in addition to mimicking syndromal features, should resemble the clinical condition in

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