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ABSTRACT: The insular cortex (IC) processes multimodal sensory information including gustatory, visceral, nociceptive, and thermal sensation, and is considered to play a role in the regulation of homeostasis. The IC receives dense histaminergic projection from the tuberomamillary nucleus in the hypothalamus, and recent studies have demonstrated that the blockage of histaminergic receptors impairs physiological functions in the IC. However, little is known about the effects of histamine on the electrophysiological properties of the IC. To explore the effects of histamine on the subthreshold responses and action potential properties in the IC, intracellular recording with a sharp glass electrode was obtained from IC pyramidal cells in cortical slice preparations. Application of histamine (30 μM) increased the frequency of repetitive spike firing in response to a long depolarizing current pulse injection; accompanied by an increase in input resistance. The frequency of repetitive spike firing was estimated by the slope of the frequency-current (f/I) curve. Histamine caused an increase from 23.3±2.3 Hz/nA to 40.3±4.3 Hz/nA. The histamine-induced facilitation of repetitive spike firing was blocked by pre-application of 50 μM cimetidine, an H(2) receptor antagonist, but not 30 μM pyrilamine, an H(1) receptor antagonist. R-α-methylhistamine (10 μM), an H(3) autoreceptor agonist, had little effect on the slope of the f/I curve. These results suggest that the histamine-induced facilitation of firing frequency is mediated via H(2) and not H(1) receptors. In addition, H(3) receptors have a minor role in the intrinsic membrane and firing properties of IC pyramidal cells.
Neuroscience Letters 05/2012; 518(1):55-9. · 2.11 Impact Factor
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ABSTRACT: Release of GABA is controlled by presynaptic GABA receptor type B (GABA(B)) autoreceptors at GABAergic terminals. However, there is no direct evidence that GABA(B) autoreceptors are activated by GABA release from their own terminals, and precise profiles of GABA(B) autoreceptor-mediated suppression of GABA release remain unknown. To explore these issues, we performed multiple whole-cell, patch-clamp recordings from layer V rat insular cortex. Both unitary inhibitory and excitatory postsynaptic currents (uIPSCs and uEPSCs, respectively) were recorded by applying a five-train depolarizing pulse injection at 20 Hz. In connections from both fast-spiking (FS) and non-FS interneurons to pyramidal cells, the GABA(B) receptor antagonist CGP 52432 had little effect on the initial uIPSC amplitude. However, uIPSCs, responding to later pulses, were effectively facilitated. This CGP 52432-induced facilitation was prominent in the fourth uIPSCs, which were evoked 150 ms after the first uIPSC. The facilitation of uIPSCs was accompanied by an increase in the paired-pulse ratio. In addition, analysis of the coefficient of variation suggests the involvement of presynaptic mechanisms in CGP 52432-induced uIPSC facilitation. Paired-pulse stimulation (interstimulus interval = 150 ms) of presynaptic FS cells revealed that the second uIPSC was also facilitated by CGP 52432, which had little effect on the amplitude and interevent interval of miniature IPSCs. In contrast, uEPSCs, responding to all five stimulations of a presynaptic pyramidal cell, were less affected by CGP 52432. These results suggest that a single presynaptic action potential is sufficient to activate GABA(B) autoreceptors and to suppress GABA release in the cerebral cortex.
Journal of Neurophysiology 12/2011; 107(5):1431-42. · 3.32 Impact Factor
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ABSTRACT: Neural plasticity in the gustatory area of the insular cortex (IC) plays a critical role in detecting novel taste and taste memory formation, which require extracellular signal-regulated kinase 1-2 (ERK1-2) phosphorylation. However, the distribution patterns of phosphorylated ERK1-2 (pERK) responses to gustatory stimulation remain unknown. This study examined distribution patterns of gustatory stimulation-driven pERK expression in the IC of anesthetized and alert rats. In both pentobarbital-anesthetized and alert rats, gustatory stimulation (10% sucrose) induced pERK-like immunoreactivity in pyramidal cells of all IC subdivisions: agranular (AI), dysgranular (DI), and granular IC (GI). Alert naïve rats exhibited approximately 10-fold larger number of pERK-like immunopositive (pERK-LI) cells than anesthetized naïve rats in response to sucrose application. Most pERK-LI cells were located in layers II/III but not deeper layers and almost no parvalbumin/somatostatin-immunopositive cells expressed pERK. In the AI, rostral regions exhibited more pERK-LI cells than caudal regions, whereas most pERK-LI cells existed in the DI/GI around the intersection of the rhinal fissure and middle cerebral artery (MCA), where in vivo optical imaging revealed activation during sucrose application in addition to the ventral primary and secondary somatosensory cortices. Gustatory experience affected the number of pERK-LI cells in the IC: sucrose stimulation induced more pERK-LI cells in the DI/GI of alert naïve rats than sucrose-exposed rats, which had received sucrose solution for 1 week. These results suggest that pyramidal cells in the upper layers of the gustatory region are highly susceptible to ERK1-2 phosphorylation by gustatory stimulation, which may induce neuroplastic changes in the IC.
Synapse 12/2009; 64(4):323-34. · 2.94 Impact Factor
