The immunocytochemical localization of somatostatin-containing neurons in the rat central nervous system

Finley, James C. W.; Maderdrut, Jerome L.; Roger, L. J.; Petrusz, Peter

doi:10.1016/0306-4522(81)90006-3

Cited by 483 publications

(108 citation statements)

References 54 publications

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“…Both somatostatin (Finley, Maderdrut, Roger & Petrusz, 1981) and cholecystokinin (Greenwood, Godar, Reaves & Hayward, 1981;Handelmann, Meyer, Beinfeld & Oertel, 1981) have been identified with immunohistochemical techniques in interneurones in the CAI region of the hippocampus. Recent studies (Pittman & Siggins, 1981) suggest that somatostatin does indeed hyperpolarize hippocampal neurones by increasing potassium conductance, although other studies suggest an excitatory action for both somatostatin and cholecystokinin (Dodd & Kelly, 1978.…”

Section: Discussionmentioning

confidence: 99%

A bicuculline‐resistant inhibitory post‐synaptic potential in rat hippocampal pyramidal cells in vitro.

Newberry¹

1984

The Journal of Physiology

319

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SUMMARY1. Experiments were performed on rat hippocampal CAI pyramidal cells in vitro in order to elucidate the origin of the late hyperpolarizing potential, which follows the y-aminobutyric acid (GABA)-mediated inhibitory post-synaptic potential (GABA-i.p.s.p.).2. The late hyperpolarizing potential could be evoked by orthodromic stimulation via stratum radiatum or stratum oriens but not by selective antidromic stimulation.3. The membrane soluble analogue of cyclic AMP, 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br cyclic AMP), which blocks calcium-activated potassium hyperpolarizations (GK(Ca)), did not reduce the late hyperpolarizing potential.4. The enkephalin analogue, (D-ala2-met5)-enkephalinamide (DALA) reversibly reduced both the GABA-i.p.s.p. and the late hyperpolarizing potential.5. The late hyperpolarizing potential and GABA-i.p.s.p. were more sensitive to low doses of the calcium antagonist, cadmium, than the excitatory post-synaptic potential (e.p.s.p.).6. The local application of cadmium to the pyramidal cell layer blocked the antidromic i.p.s.p. but the orthodromically evoked late hyperpolarizing potential was less affected.7. In contrast to the GABA-i.p.s.p., the late hyperpolarizing potential was not reversed by chloride injection and was enhanced, rather than depressed, by bicuculline.8. We conclude that the late hyperpolarizing potential is a bicuculline-resistant i.p.s.p. The unidentified transmitter for this i.p.s.p. is released from feed-forward interneurones primarily onto the dendrites of the pyramidal cell and may act by increasing the potassium permeability of the membrane.9. The epileptiform burst after-hyperpolarization evoked in the presence of GABA antagonists is composed ofat least two components, a long-duration hyperpolarization mediated by GK(Ca) and an earlier and shorter late hyperpolarizing potential.10. Blockade of the GK(ca) by 8-Br cyclic AMP did not alter the duration of epileptiform bursts but did markedly increase the frequency of their occurrence. This suggests that GK(ca) is involved in controlling the interval between bursts.

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Section: Discussionmentioning

confidence: 99%

A bicuculline‐resistant inhibitory post‐synaptic potential in rat hippocampal pyramidal cells in vitro.

Newberry¹

1984

The Journal of Physiology

319

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“…The presence of SOM in the pineal gland was shown for the first time by Pelletier et al (1975) in the rat (and later on by Pévet et al, 1980b;Finley et al, 1981;Webb et al, 1984;Møller et al, 1995) then in the hamster, gerbil, mouse (Webb et al, 1984), sheep, pig (Lew and Lawson-Willey, 1987), cow (Peinado et al, 1989;Møller et al, 1992), and human (Bouras et al, 1987). The rat pineal gland contains approximately 0.3 to 3 ng SOM/mg protein (Webb et al, 1985).…”

mentioning

confidence: 99%

Generation of the Melatonin Endocrine Message in Mammals: A Review of the Complex Regulation of Melatonin Synthesis by Norepinephrine, Peptides, and Other Pineal Transmitters

2003

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“…The main source of the somatostatinergic fiber system, reaching the mediobasal hypothalamus and the median eminence, is located in the anterior part of the periventricular nucleus of the hypothalamus in the rat (1). A limited number of somatostatin-containing perikarya have been localized outside the periventricular nucleus, such as in the arcuate nucleus, ventromedial nucleus and the lateral hypothalamus (10,13,52). Another explanation of the decreased sleep effect might be that a portion of the injected OCT may leak out from the cerebral ventricles into the systemic circulation (60) reaching the pituitary and inhibit GH secretion.…”

Section: Effect Of Somatostatin Analog Octreotidementioning

confidence: 99%

Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus

Péterfi

McGinty

Sarai

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Peterfi Z, McGinty D, Sarai E, Szymusiak R. Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus. Am J Physiol Regul Integr Comp Physiol 298: R147-R156, 2010. First published November 4, 2009 doi:10.1152/ajpregu.00494.2009.-We examined whether growth hormone-releasing hormone (GHRH) may promote non-rapid eye movement (NREM) sleep via activation of GABAergic neurons in the preoptic area. Male Sprague-Dawley rats were implanted with EEG, EMG electrodes and a unilateral intracerebroventricular cannula. Groups of rats received injections (3 l icv) with gonadotropinreleasing hormone (GHRH) (0.1 nmol/100 g body wt) or equal volume of physiological saline at the onset of the dark period and were permitted spontaneous sleep for 90 min. Separate groups of rats were sleep deprived by gentle handling for 90 min, beginning at the time of GHRH or saline injection, at the onset of the dark period. Other groups of rats received intracerebroventricular octreotide (somatostatin analog OCT) injections, intracerebroventricular injection of one of two doses of competitive GHRH antagonist, or intracerebroventricular saline injection at light onset and were then permitted 90 min spontaneous sleep-waking. Rats were killed immediately after the 90-min sleep/wake monitoring period. Brain tissue was processed for immunohistochemistry for c-Fos protein and glutamic acid decarboxylase (GAD). Single c-Fos and dual Fos-GAD cell counts were determined in the median preoptic nucleus (MnPN), and in the core and the extended parts of the ventrolateral preoptic nucleus (cVLPO and exVLPO). Intracerebroventricular GHRH elicited a significant increase in NREM sleep amount. Double-labeled FosϩGAD cell counts were significantly elevated after GHRH injection in the MnPN and VLPO in both undisturbed and sleep-deprived groups. OCT and GHRH antagonist significantly decreased NREM sleep amount compared with control rats. OCT injection increased single c-Fos-labeled cell counts in the MnPN, but not in the VLPO. Double-labeled cell counts were significantly reduced after OCT and the high dose of GHRH antagonist injection in all areas examined. These findings identify GABAergic neurons in the MnPN and VLPO as potential targets of the sleep-regulatory actions of GHRH. preoptic area; growth hormone-releasing hormone; somatostatin; octreotide; median preoptic nucleus; ventrolateral preoptic nucleus GROWTH HORMONE-RELEASING HORMONE (GHRH) is the main stimulatory neuropeptide that regulates growth hormone (GH) release by the pituitary. Exogenous GHRH stimulates sleep, especially, non-rapid eye movement (NREM) sleep (reviewed in Ref. 39). Intracerebroventricular (icv) administration of GHRH increases NREM sleep and enhances EEG slow-wave activity (SWA) in the neocortical EEG during NREM sleep in rats and rabbits (11,37,38). Intravenous administration of GHRH promotes sleep and EEG SWA in humans (25,33,54).In humans, the major daily pulse in GH release occurs early in the nocturnal sleep period, coinciding with the o...

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The immunocytochemical localization of somatostatin-containing neurons in the rat central nervous system

Cited by 483 publications

References 54 publications

A bicuculline‐resistant inhibitory post‐synaptic potential in rat hippocampal pyramidal cells in vitro.

A bicuculline‐resistant inhibitory post‐synaptic potential in rat hippocampal pyramidal cells in vitro.

Generation of the Melatonin Endocrine Message in Mammals: A Review of the Complex Regulation of Melatonin Synthesis by Norepinephrine, Peptides, and Other Pineal Transmitters

Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus

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