Coloboma Hyperactive Mutant Mice Exhibit Regional and Transmitter‐Specific Deficits in Neurotransmission

@article{Raber1997ColobomaHM,
  title={Coloboma Hyperactive Mutant Mice Exhibit Regional and Transmitter‐Specific Deficits in Neurotransmission},
  author={Jacob Raber and P P Mehta and Max Kreifeldt and Loren H. Parsons and F Weiss and Floyd E. Bloom and M. Curtis Wilson},
  journal={Journal of Neurochemistry},
  year={1997},
  volume={68}
}
Abstract: 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 crucial role for SNAP‐25 in the release of both classical neurotransmitters and neuropeptides. In the present study, we compared the release of specific neurotransmitters in vitro from… Expand
Coloboma mouse mutant as an animal model of hyperkinesis and attention deficit hyperactivity disorder
  • M. C. Wilson
  • Medicine, Psychology
  • Neuroscience & Biobehavioral Reviews
  • 2000
TLDR
Despite the ubiquitous role of SNAP-25 in synaptic transmission, and uniformly decreased expression in the mutants, coloboma mice show marked deficits in Ca2+-dependent dopamine release selectively in dorsal but not ventral striatum, which suggests that haploinsufficiency of Snapchat reveals a specific vulnerability of the nigrostriatal pathway which regulates motor activity. Expand
Transgenic rescue of SNAP-25 restores dopamine-modulated synaptic transmission in the coloboma mutant
TLDR
The hypothesis that alteration of monoaminergic neurotransmission, which can be reversed by the indirect agonist, amphetamine, is particularly sensitive to alterations in the expression of SNAP-25 is supported. Expand
Norepinephrine regulates locomotor hyperactivity in the mouse mutant coloboma
TLDR
It is suggested that NE regulation in the CNS plays an important role in the expression of hyperactivity in this mouse model, consistent with results of human studies and current models of ADHD. Expand
Abnormal presynaptic catecholamine regulation in a hyperactive SNAP-25-deficient mouse mutant
TLDR
Norepinephrine (NE) concentration was significantly increased in the striatum and nucleus accumbens of the hyperactive mutant mice, suggesting the increase in NE may regulate the hyperactivity in these mice, as suggested by current hypotheses of the mechanisms underlying attention-deficit hyperactivity disorder (ADHD) and Tourette's syndrome. Expand
THE MOLECULAR AND BEHAVIORAL CONSEQUENCES OF ABNORMAL NORADRENERGIC NEUROTRANSMISSION IN THE HYPERACTIVE SNAP-25 DEFICIENT MOUSE MUTANT COLOBOMA
TLDR
The mouse mutant coloboma is identified as an animal model for examining the neurological basis of hyperactivity with a well-defined genetic abnormality and the role of norepinephrine in the regulation of locomotor hyperactivity is examined. Expand
Neuromuscular transmission and muscle contractility in SNAP-25-deficient coloboma mice.
TLDR
It is concluded that spinal motor neurons up-regulate SNAP-25 to preserve vital neuromuscular function in muscle function and prevent weakness and paralysis of skeletal muscle due tooxication by BoNT/A, /C1 or /E. Expand
Neurobiology of animal models of attention-deficit hyperactivity disorder
  • V. Russell
  • Medicine, Psychology
  • Journal of Neuroscience Methods
  • 2007
TLDR
Results obtained with animal studies suggest that dopamine neurons are functionally impaired, however, evidence obtained from some animal models suggests that the noradrenergic and serotonergic neurotransmitter systems may be the target of drugs that ameliorate ADHD symptoms. Expand
Reprint of “Neurobiology of animal models of attention-deficit hyperactivity disorder”
  • V. Russell
  • Psychology, Medicine
  • Journal of Neuroscience Methods
  • 2007
TLDR
Results obtained with animal studies suggest that dopamine neurons are functionally impaired, however, evidence obtained from some animal models suggests that the noradrenergic and serotonergic neurotransmitter systems may be the target of drugs that ameliorate ADHD symptoms. Expand
Synaptosomal-associated protein 25 (SNAP-25) and attention deficit hyperactivity disorder (ADHD): evidence of linkage and association in the Irish population
TLDR
Using HHRR and TDT, a large number of ADHD nuclear families from Ireland were analysed and found increased preferential transmission of SNAP-25/DdeI allelel to ADHD cases, but it is not clear what the role ofSNAP-25 in ADHD is. Expand
Astrocyte-Specific Disruption of SynCAM1 Signaling Results in ADHD-Like Behavioral Manifestations
TLDR
Results indicate that disruption of SynCAM1-dependent astroglial function results in behavioral abnormalities similar to those described in animals model of attention-deficit hyperactive disorder (ADHD), and suggest a hitherto unappreciated contribution of glial cells to the pathophysiology of this disorder. Expand
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TLDR
It has been previously demonstrated that dopamine neurotransmission is essential for induction of one type of hippocampal theta rhythm and also may modulate hippocampal LTP, suggesting that alterations in DA synaptic transmission may underlie the behavioral abnormalities, in particular the hyperactivity, associated with Cm/+ mutant mice. Expand
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