Quantitative Autoradiography on Ontogenic Development of alpha-Adrenoceptor in the Rat Cerebral Cortex / 대한해부학회지

Adrenoceptors mediate response to catecholamines throughout the body. To investigate postnatal ontogenic development of alpha1- and alpha2- adrenoceptors in the rat cerebral cortex, in vitro autoradiography was done on frontal, parietal and temporal cortex in P0, P5, P10, P15, P20, P30 and adult animals. Binding sites for the alpha1-adrenergic receptor ligand, [3H]-prazosin, and the alpha2-adrenergic receptor ligand, [3H]-rauwolscine, were visualized by in vitro autoradiography, and anatomically localized by comparing the autoradiogram to Nissl-stained sections. Nonspecific binding was detected with unlabeled phentolamine (alpha1) and yohimbine (alpha2). There is uniform increase in alpha1- and alpha2- adrenoceptors from birth through first three or four postnatal weeks, followed by a decrease to adult level. Two alpha-adrenoceptors have very different ontogenic patterns of distribution during postnatal development. alpha1- adrenoceptors were expressed differentially in different cortical (frontal, temporal, parietal) regions and in different cortical layers (layers V, II-IV, VI) at same age. alpha2- adrenoceptor was expressed homogenously in throughout regions and layers. These findings may provide evidence that alpha1- adrenoceptors are involved in regulating cortical development or function more specifically than alpha2- adrenoceptors during postnatal development.

Effect of a Rostral Basal Forebrain Lesion on Neuropeptide Containing Neurons in the Rat Cerebral Cortex / 대한해부학회지

The present study was designed to elucidate the effects of rostral basal forebrain lesions on neuropeptide containing neurons in the cerebral cortex. Nine male Sprague-Dawley rats[250-300gm] received bilateral injections of ibotenic acid into the basal forebrain[A : +0.7mm, L : 2.3mm, D : 8.6mm] and additional five served as sham operated animals. Brains were removed at 8-14 days after lesioning and frozen coronal sections of 40 micrometer thickness were made. Immunohistochemical staining was performed against the somatostatin[SOM], neuropeptide Y[NPY], and vasoactive intestinal polypeptide[VIP]. No differences were observed in the number of the SOM-immunoreactive[SOM-ir] or NPY-ir neurons between the lesioned and the control groups. Density of the NPY-ir fibers also did not show any significant difference between the two groups. In contrast, the number of VIP-ir neurons in the frontal cortex was significantly reduced following the basal forebrain lesioning. These results suggest the functional relationship between the basal forebrain and the cortical VIP-ir neurons.

Double Immunohistochemical Study on the Postnatal Development of Somatostatin - and Neuropeptide Y - Immunoreactive Neurons in Rat Cerebral Cortex / 대한해부학회지

The postnatal development of somatostatin [SOM]- and neuropeptide Y[NPY]- immunoreactive[ir] neurons were examined in rat cerebral cortex considering their coexistence in cortical neurons. Using double immunohistochemical staining for SOM and NPY with diaminobenzidine and benzidine dihydrochloride as chromogens, we subdivided immunoreactive cells into double-labeled SOM/NPY-, SOM only-, and NPY only-ir neurons. Interestingly, SOM/NPY- and SOM only-ir neurons were detectable even at the day of birth, in contrast to NPY only-ir cells which first appeared in most cortices from two weeks of age. The morphological features of double-labeled SOM/NPY neurons were not identical to those SOM only- and NPY only-ir neurons. No apparent changes in the shape and size of single-labeled neurone occurred with age ; throughout their postnatal life they were round and ovoid, had a thin rim of perinuclear cytoplasm, and short processes. In contrast, the features of SOM/NPY-ir neurons were not consistent during postnatal life. By day P7, these neurons showed immature features ; they began to show more advanced neuronal characteristics by week P2, when they had a larger and more intensely-stained cytoplasm. In addition, their processes were longer, thicker and more complex than at earlier ages. At this age, SOM/NPY-ir somata were close to their maximum size. From week P4, they became smaller and were lightly labeled. SOM/NPY-ir somata were larger than SOM only- and NPY only-ir somata at and after two weeks of age. The present results showing different postnatal maturation patterns such as time of appearance and morphological features suggest that double-labeled SOM/NPY and single-labeled neurons might be different populations regulated by different mechanisms in their development, and with different functional properties during development.

Mechanisms of release of 3H Hydroxytryptamine evoked by hypoxia and hypoglycemia in rat cerebral cortex slices

Pathophysiology of brain ischemia is characterixed by a complex cascade of hemodynamic, electrophysiological and biochemical processes. It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induce neurotramsmitter release from various brain tissues in ischemic milieu. In presen study, the mechanism for ischemia-induced [3HT]5-hydroxytryptamine(5-HT) from cerebral cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from Mg2+-free artificl cerebrospinal fluid, induced significiant release of [3H]5-HT(7.2+0.6% of total tissue content) from the tissues. This ischemia-induced release of [3H]5-HT from the slices was significiantly attenuated by TTX(1 yM), Mg2+(102mM). MK-801(10yM), ketamine(10yM), NMDA receptor antagonists, DNQX(30yM), a kainate/AMPA receptor antagonist, or carbetapentane(31yM), an inhibitor of glutamate release. Fluoxetine, a selective blocker for 5-HT transporter, inhibited the ischemia-induced release of [3H]5-HT. Omission of Ca2+ from incubation media potentiated ischemia-evoked [3H]5-HT release and the inhibitory effect of blockers for transporter. Dantrolene (30yM) and ryanodine(100 nM) and -conotoxinGVIA(100 nM), inhibitors of N-type Ca2+ channels, sifnificiantly attenuated the ischemia-induced release of [3H]5-HT, but verapamil(5 yM), an inhibitor of L-type Ca2+ channels, did not. Fluoxetine(100 nM), a relatively selective 5-HT transporter blocker, significiantly inhibited the ischemia-induced release of [3H]5-HT. Theses results suggest that glutamate is involned in ischemia-evoked [3H]5-HT release, and this release is achieved by Ca2+=dependent exocytosis and reverdsal of transporters, and can be modulated by various neuronal mechanisms.