Dopamine D1/5 receptor-mediated long-term potentiation of intrinsic excitability in rat prefrontal cortical neurons:: Ca2+-dependent intracellular signaling

被引:55
作者
Chen, Long
Bohanick, Joseph D.
Nishihara, Makoto
Seamans, Jeremy K.
Yang, Charles R. [1 ]
机构
[1] Eli Lilly & Co, Lilly Corp Ctr, Neurosci Discovery, Indianapolis, IN 46285 USA
[2] Nanjing Univ Tradit Chinese Med, Natl Stand Lab Pharmacol Chinese Mat Med, Res Ctr Acupuncture & Pharmacol, Nanjing, Peoples R China
[3] Univ Arizona, Arizona Res Labs, Div Neural Syst Memory & Aging, Tucson, AZ USA
[4] Univ British Columbia, Dept Psychiat, Vancouver, BC V5Z 1M9, Canada
[5] Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 1M9, Canada
关键词
D O I
10.1152/jn.00317.2006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Prefrontal cortex (PFC) dopamine D1/5 receptors modulate long- and short-term neuronal plasticity that may contribute to cognitive functions. Synergistic to synaptic strength modulation, direct postsynaptic D1/5 receptor activation also modulates voltage-dependent ionic currents that regulate spike firing, thus altering the neuronal input-output relationships in a process called long- term potentiation of intrinsic excitability (LTP-IE). Here, the intracellular signals that mediate this D1/5 receptor-dependent LTP-IE were determined using whole cell current-clamp recordings in layer V/VI rat pyramidal neurons from PFC slices. After blockade of all major amino acid receptors (V-hold = -65 mV) brief tetanic stimulation ( 20 Hz) of local afferents or application of the D1 agonist SKF81297 (0.2-50 mu M) induced LTP-IE, as shown by a prolonged (> 40 min) increase in depolarizing pulse-evoked spike firing. Pretreatment with the D1/5 antagonist SCH23390 ( 1 mu M) blocked both the tetani- and D1/5 agonist-induced LTP-IE, suggesting a D1/5 receptor-mediated mechanism. The SKF81297-induced LTP-IE was significantly attenuated by Cd2+, [Ca2+](i) chelation, by inhibition of phospholipase C, protein kinase-C, and Ca2+/calmodulin kinase-II, but not by inhibition of adenylate cyclase, protein kinase-A, MAP kinase, or L-type Ca2+ channels. Thus this form of D1/5 receptor-mediated LTP-IE relied on Ca2+ influx via non-L-type Ca2+ channels, activation of PLC, intracellular Ca2+ elevation, activation of Ca2+-dependent CaMKII, and PKC to mediate modulation of voltage-dependent ion channel(s). This D1/5 receptor-mediated modulation by PKC coexists with the previously described PKA-dependent modulation of K+ and Ca2+ currents to dynamically regulate overall excitability of PFC neurons.
引用
收藏
页码:2448 / 2464
页数:17
相关论文
共 170 条
[1]   Relationships between intracellular calcium and afterhyperpolarizations in neocortical pyramidal neurons [J].
Abel, HJ ;
Lee, JCF ;
Callaway, JC ;
Foehring, RC .
JOURNAL OF NEUROPHYSIOLOGY, 2004, 91 (01) :324-335
[2]   Prefrontal DA transmission at D1 receptors and the pathology of schizophrenia [J].
Abi-Dargham, A ;
Moore, H .
NEUROSCIENTIST, 2003, 9 (05) :404-416
[3]   LOCALIZED CALCIUM SPIKES AND PROPAGATING CALCIUM WAVES [J].
ALLBRITTON, NL ;
MEYER, T .
CELL CALCIUM, 1993, 14 (10) :691-697
[4]  
ALZHEIMER C, 1993, J NEUROSCI, V13, P660
[5]   Methylphenidate increases cortical excitability via activation of alpha-2 noradrenergic receptors [J].
Andrews, GD ;
Lavin, A .
NEUROPSYCHOPHARMACOLOGY, 2006, 31 (03) :594-601
[6]  
[Anonymous], RAT BRAIN STEREOTAXI
[7]   5-HYDROXYTRYPTAMINE2 AND 5-HYDROXYTRYPTAMINE1A RECEPTORS MEDIATE OPPOSING RESPONSES ON MEMBRANE EXCITABILITY IN RAT-ASSOCIATION CORTEX [J].
ARANEDA, R ;
ANDRADE, R .
NEUROSCIENCE, 1991, 40 (02) :399-412
[8]   Activation of protein kinase C increases neuronal excitability by regulating persistent Na+ current in mouse neocortical slices [J].
Astman, N ;
Gutnick, MJ ;
Fleidervish, IA .
JOURNAL OF NEUROPHYSIOLOGY, 1998, 80 (03) :1547-1551
[9]  
Augustine G J, 1992, Curr Opin Neurobiol, V2, P302, DOI 10.1016/0959-4388(92)90119-6
[10]   Abnormalities in the dopamine system in schizophrenia may lie in altered levels of dopamine receptor-interacting proteins [J].
Bai, J ;
He, F ;
Novikova, SI ;
Undie, AS ;
Dracheva, S ;
Haroutunian, V ;
Lidow, MS .
BIOLOGICAL PSYCHIATRY, 2004, 56 (06) :427-440