In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 11 ( 1998-06-01), p. 4001-4007
Abstract:
Weaver ( wv ) mice carry a point mutation in the pore region of a G-protein-gated inwardly rectifying K + channel subunit (Kir3.2). wv Kir3.2 conducts inward currents that may cause the loss of neurons in the cerebellum and substantia nigra. Although Kir3.2 is widely expressed in the CNS, significant morphological or physiological changes have not been reported for other brain areas. We studied the role of wv Kir3.2 in hippocampal slices of young [postnatal day (P) 4–18] and adult wv/wv (≥P24) mice, because protein levels of Kir 3.1 and Kir3.2 appear to be normal in the first 3 postnatal weeks and only decrease thereafter. In disinhibited slices, the GABA B receptor agonist R -baclofen reduced burst activity in wv/wv mice but was much more potent in wild-type mice. Mean resting membrane potential, slope input resistance, and membrane time constant of CA3 neurons of adult wv/wv and wild-type mice were indistinguishable. However, R -baclofen or chloroadenosine did not induce K + currents or any other conductance change in wv/wv mice. Moreover, electrical or chemical stimulation of inhibitory neurons did not evoke slow IPSPs in adult wv/wv mice. Only in a few cells of young wv/wv mice did GABA B receptor activation by R -baclofen or presynaptic stimulation induce small inward currents, which were likely caused by a Na + ion influx through wv Kir3.2 channels. The data show that the pore mutation in wv Kir3.2 channels results in a hippocampal phenotype resembling Kir3.2-deficient mutants, although it is not associated with the occurrence of seizures.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.18-11-04001.1998
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
1998
detail.hit.zdb_id:
1475274-8
SSG:
12
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