Peptide Receptors

Burt, David R.; Sharif, Najam A.

doi:10.1007/978-1-4684-4568-8_13

Cited by 9 publications

(4 citation statements)

References 221 publications

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“…For example, TRH-containing fibers that emanate from the TRH-synthesizing neurons in ROb and RPa (Johansson et al,198 1;Lynn et al,199 1) are located near motoneurons (Hokfelt et al, 1975a,b;Johansson et al, 1981;Merchenthaler et al, 1988). In addition, TRH binding sites are found in motor nuclei (Manaker and Rizio, 1989;Sharif, 1989;Burt and Sharif, 1990) and motoneurons express mRNA encoding TRH receptor (Calza et al, 1992). Furthermore, TRH is known to have direct excitatory effects on adult motoneurons (Rekling, 1990;Bayliss et al, 1992a) and may mediate a slow excitatory postsynaptic potential in spinal motoneurons (Takahashi, 1985).…”

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confidence: 99%

Early postnatal development of thyrotropin-releasing hormone (TRH) expression, TRH receptor binding, and TRH responses in neurons of rat brainstem

et al. 1994

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We investigated the postnatal development of the thyrotropin-releasing hormone (TRH)-containing raphe system in the brainstem of neonatal rats. Postnatal changes in TRH expression in nucleus (n.) raphe obscurus (ROb) and n. raphe pallidus (RPa) were evaluated by in situ hybridization using an 35S-labeled oligonucleotide probe complementary to TRH precursor mRNA. TRH mRNA expression was low at birth [postnatal day 0 (P0)], but was clearly evident by P7 and increased from that time to reach sustained high levels from P14 to P28. Consistent with this postnatal increase in TRH expression, we found increases in the density of TRH-immunoreactive (IR) fibers, which are derived from ROb and RPa, in the hypoglossal nucleus (nXII). TRH-IR fibers in nXII were very sparse at P0, but increased markedly over the first 2 postnatal weeks. The change in TRH innervation of nXII was closely matched by concomitant increases in 3H-methyl-TRH binding in nXII; specific TRH binding increased from very low levels at birth to high levels of P14. Finally, we recorded intracellularly the electrophysiological responses to TRH of hypoglossal motoneurons (HMs; n = 42) of neonatal rats (P0-P21) in a brainstem slice preparation. The response of neonatal HMs to TRH, in contrast to adult HMs, was highly variable. In some neonatal HMs, even at P0, TRH caused a depolarization with a decrease in input conductance (GN) that was characteristic of the response of all adult HMs. However, in other neonatal HMs, TRH was either without effect or caused a slight depolarization with no apparent change in GN, responses that were unlike those of adult HMs. A response was considered typical (i.e., "adult-like") if GN decreased to < 85% of control. The percentage of cells responding in a typical manner increased progressively from 25% at P0-P2 to 100% after P11. In addition, we found that the density of TRH-sensitive current (normalized to cell capacitance) increased with postnatal age in HMs that responded in a typical manner, suggesting that expression of the TRH-sensitive conductance is also developmentally regulated. Together, these data indicate that the TRH raphe neuronal system of the rat brainstem is not fully mature at the time of birth but develops over the first few postnatal weeks. This was true of levels of TRH mRNA in caudal raphe nuclei, density of TRH-IR fibers and 3H-methyl-TRH binding in nXII, and also the manner and magnitude of electrophysiological responses of HMs to exogenously applied TRH.

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confidence: 99%

Early postnatal development of thyrotropin-releasing hormone (TRH) expression, TRH receptor binding, and TRH responses in neurons of rat brainstem

et al. 1994

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“…A number of neuropeptide hormones, including thyrotropin-releasing hormone (Prasad and Edwards, 1984), opioids (Roth et al, 1981), and somatostatin (Epelbaum et al, 1982), resemble neuro-transmitters in that their receptors are concentrated on nerve-ending preparations, i.e., synaptosomes. Furthermore, these neuropeptides resemble neurotransmitters in having marked variation in regional binding (Burt and Sharif, 1984).…”

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confidence: 99%

Subcellular Localization of Rat Brain Insulin Binding Sites

Marks

Maddison

Eastman³

1988

Journal of Neurochemistry

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Fractions and subcellular structures were prepared from rat brain homogenate and their purity was assessed using enzyme markers, gamma-aminobutyric acid binding, DNA content, and electron microscopy. Insulin binding was highest on the plasma membrane preparations and approximately 50% less so on brain homogenate crude mitochondrial (P2), myelinated axon, and synaptosome preparations. Very low levels of binding were found on mitochondria and nuclei. Differences in binding between fractions were due to numbers of binding sites, and not variable binding affinity. There was a close relationship between insulin binding and the activity of Na/K ATPase (E.C. 3.6.1.4) in all fractions (r = 0.98). Insulin binding to the P2 was compared with plasma membrane fractions in seven brain regions, and the results demonstrated the same close relationship between insulin binding and plasma membrane content in all regions except hypothalamus. Plasma membrane insulin binding was well represented by the binding on P2 membranes in all regions except hypothalamus and brainstem. It was concluded that insulin binding is distributed evenly over the surface of brain cells and is not increased on nerve endings.

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“…Thus, in the present study, high-affinity [3H]-MeTRH binding sites in the rat OB have been identified as TRH receptors based on the close similarity of the biochemical and pharmacological features of these entities to those of the pituitary gland (Table l), where much functional evidence for the TRH receptors has been found (for reviews, see Burt and Sharif, 1984;Hinkle, 1984;Gershengorn, 1985;Sharif, 1985a). The possible functional relevance of the OB TRH receptors has been demonstrated indirectly via the in vivo down-regulation of these sites following The levels of endogenous TRH in different brain tissues were determined 2 weeks postlesion using a specific TRH antibody RIA as described in Materials and Methods.…”

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confidence: 84%

“…CNS administration of TRH has been shown to evoke many different behavioral and physiological changes, such as enhanced CNS arousal (analepsis), hyperthermia, increased respiratory and locomotor activity, increased vasoconstriction and cardiac stimulation, increased feeding, etc. (for reviews, see Jackson, 1982;Griffiths and Bennett, 1983;Burt and Sharif, 1984;Griffiths, 1985;Sharif, 19851;Horita et al, 1986). Recently, TRH and its analogs have proved beneficial in reducing spasticity and muscle weakness associated with motoneuron disease (Engel et al, 1983) and in reversing hypovolemic shock (Holaday et al, 198 1;Amir et al, 1984), and TRH has exhibited antinociceptive activity (Boschi et al, 1983;Webster et al, 1983).…”

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confidence: 99%

Chemical and Surgical Lesions of Rat Olfactory Bulb: Changes in Thyrotropin‐Releasing Hormone and Other Systems

Sharif

1988

Journal of Neurochemistry

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Stereotaxic injection of kainic acid (15 micrograms) into rat olfactory bulbs was accompanied by a 53% (n = 4; p less than 0.02) depletion of endogenous thyrotropin-releasing hormone (TRH) as compared to sham-operated controls 2 weeks postlesion. TRH levels remained unaltered in three other caudal regions. Bulbar kainate lesions produced a 58% (n = 5; p less than 0.001) decrease in TRH receptor binding capacity without affecting the receptor affinity. Kainate lesions also reduced bulbar muscarinic and benzodiazepine receptors by 60% and 48%, respectively. Again, no changes in TRH receptors were apparent in six other brain areas after bulbar kainate treatment. Injection of the dopaminergic neurotoxin, 6-hydroxydopamine (8 micrograms), into rat bulbs decreased TRH receptors by 35% (n = 4; p less than 0.05) 1 week postlesion. One month after surgical bulbectomy, TRH and TRH receptor levels in a number of brain areas were unaltered compared to those of control animals. These studies suggest that TRH in the olfactory bulb originates intrinsically and may be produced predominantly for local use. Secondly, TRH receptors in the bulb appear to be postsynaptically localized on intrinsic neurons, although a small proportion are also associated with presynaptic elements of dopaminergic noradrenergic neurons. Bulbar TRH receptors exhibited nanomolar affinity and a pharmacological selectivity akin to that of the pituitary gland and other brain regions.

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Peptide Receptors

Cited by 9 publications

References 221 publications

Early postnatal development of thyrotropin-releasing hormone (TRH) expression, TRH receptor binding, and TRH responses in neurons of rat brainstem

Early postnatal development of thyrotropin-releasing hormone (TRH) expression, TRH receptor binding, and TRH responses in neurons of rat brainstem

Subcellular Localization of Rat Brain Insulin Binding Sites

Chemical and Surgical Lesions of Rat Olfactory Bulb: Changes in Thyrotropin‐Releasing Hormone and Other Systems

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