摘要:

AbstractThese experiments were designed to compare phencyclidine (PCP) and s̀ (sigma) receptor binding sites in the rat spinal cord by using receptor binding and autoradiographic techniques. Binding sites for3H‐TCP (3H‐1‐[1‐(2‐thienyl)cyclohexy]piperidine), a PCP receptor agonist, and (+)3H‐3‐PPP (3H‐(+)‐3‐(3‐hydroxyphenyl)‐N‐(1‐propyl)piperidine), a s̀ receptor agonist, in the rat spinal cord were shown to represent two populations of recognition sites. Inhibition studies revealed that ligands with high affinity for the PCP receptor (MK‐801 and PCP) were potent competitors at3H‐TCP binding sites whereas the putative s̀ receptor ligands (±)pentazocine and haloperidol were potent competitors at (+)3H‐3‐PPP binding sites. The autoradiographic distribution of3H‐TCP and (+)3H‐3‐PPP binding sites in adjacent sections of rat spinal cord demonstrated the occurrence of two distinct populations of binding sites.3H‐TCP binding sites were localized primarily in laminae I and II in cervical and thoracic spinal segments. Binding sites in lamina I decreased in density along a rostral to caudal gradient in the spinal cord. The highest density of (+)3H‐3‐PPP binding sites was found in the ventral horn (lamina VIII and IX) and over perikarya in dorsal root ganglia. Significantly elevated densities of (+)3H‐3‐PPP binding sites were also found in lamina X within thoracic and lumbar segments and in the intermediolateral cell column. The results of the present study show that PCP and s̀ receptor binding sites are differentially localized in the rat spinal cord and suggest t

ISSN:0887-4476    

DOI:10.1002/syn.890040102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractThe effect of prolonged glutamate (GLU) application was examined on 60 CA1 pyramidal neurons in the in vitro rat hippocampal slice preparation. Continuous application of L‐GLU, either by bath perfusion (0.5–2mM) of the slices or iontophoresis (200 mM) into the dendritic region of the neurons, elicited a transient depolarization which faded to a mean of 53% of the initial peak amplitude despite continued exposure to the agonist. Membrane depolarization to aspartate (ASP) and the d‐isomer of GLU also faded with time. In contrast, the depolarizing response to the excitatory amino acid agonists N‐methyl‐D, L‐aspartate (NMA), quisqualate (QUIS), and kainate (KA) did not fade significantly during continuous application. The fade of the GLU depolarization was not affected by the NMDA antagonist D‐2‐amino‐5‐phosphonovalerate (APV) or by blocking synaptic transmission with tetrodotoxin. At the time of maximum fade of the GLU depolarization, there was no change in input resistance or GLU reversal potential. In addition, fade of the response was not a consequence of changes in extracellular potassium concentration, GLU uptake mechanisms, or the electrogenic pump. The most likely explanation for fade is postsynaptic recep

ISSN:0887-4476    

DOI:10.1002/syn.890040103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractOn the basis of animal studies, grafts of fetal human dopaminergic cells have been suggested as a therapy for Parkinson's disease. The purpose of this study was to characterize the ultrastructure and immunocytochemistry of human ventral mesencephalic xenografts placed into the catecholamine‐depleted striata of athymic “nude” rats.Human fetal tissue was obtained from tissue fragments derived from elective abortions during the first trimester of pregnancy. Small pieces of the basal mesencephalon were grafted into the catecholamine‐depleted striata of four athymic nude rats. The rats were allowed to survive from 3 to 6 months after grafting; following fixation, the striatal tissue containing the grafts was labeled with antibodies against tyrosine hydroxylase and serotonin.Immunocytochemistry revealed tyrosine‐hydroxylase‐like‐immunoreactive (THLI) and serotoninlike‐immunoreactive (5HTLI) cell bodies within the human grafts. Both 5HTLI and THLI fibers crossed the graft‐host interface and innervated the previously lesioned striatum. Both types of fibers also entered the host cortex from the adjacent human graft.At the ultrastructural level, THLI and 5HTLI fibers and synaptic terminals were observed in the host neuropil. THLI and 5HTLI dendrites and axon terminals were also observed in the neuropil of the grafts themselves. THLI axon terminals are not normally present in the substantia nigra. The results of our study indicate that human xenografts can survive in the neuropil of the host striatum and form morphologically appropriate synapses with

ISSN:0887-4476    

DOI:10.1002/syn.890040104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractPreviously we reported that acetylcholine (ACh) and acetyl‐beta‐methacholine (MCh) modify responses of neurons in auditory cortex to individual frequencies. The purpose of this study was to determine whether muscarinic agonists produce frequency‐specific alterations or general changes in cellular responses. Frequency‐specific modifications would be evident in alterations of frequency receptive fields (FRF) that differed across frequencies while general effects would be seen as changes that were more or less the same over frequencies. Responses of single neurons to designated sets of tones were recorded in the auditory cortex of chronically prepared awake cats before, during, and following ejection of ACh or MCh by iontophoresis or micropressure using multibarrel micropipettes. Frequency receptive fields were determined by presenting isointensity tones across a range of frequencies including the cell's best frequency (BF) to tone onset. FRF for “off” and “sustained (through)” responses were also determined quantitatively. The effects of ACh and MCh were predominantly frequency‐specific (77%, 39/51 cells); general changes (19%, 10/51) and no effects (4%, 2/51) were less likely. Frequency‐specific effects involved both facilitation and reduction of the same response component to different frequencies within the same neuron. For responses to tone onset (but not “through” and “off” responses), agonists were more likely to produce a decrease at the BF while simultaneously increasing responses to other frequencies. Agonists could increase or decrease frequency selectivity. Effects of agonists could be blocked by atropine, suggesting involvem

ISSN:0887-4476    

DOI:10.1002/syn.890040105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractExogenously applied muscarinic agonists—for example, acetylcholine (ACh) and acetyl‐beta‐methacholine (MCh)—modify frequency receptive fields in auditory cortex of unanesthetized animals in a frequency‐specific rather than global manner. The present study sought to relate these findings to endogenous actions of ACh by using the anticholinesterase agents eserine sulphate and soman (0‐1,2,2‐trimethylpropylmethylphosphonofluoridate) to facilitate the effects of endogenous ACh. Frequency receptive fields (FRF) were determined by presenting sequences of different isointensity tones before, during, and after application of ACh, MCh, eserine, or soman; also the cholinesterase blockers were applied between applications of ACh or MCh. The major effects produced by the inhibitors were similar to those of the agonists. Predominant effects were frequency‐specific changes in FRF. Further, eserine and soman, similar to ACh and MCh, produced shifts in the best frequency (BF) of FRF due mainly to coordinated depression of responses to the BF and increased responses to adjacent, non‐BF. The results indicate that exogenous and endogenous ACh, acting via muscarinic receptors, can significantly influence the physiological functioning of cortical neurons and consequently their processing of se

ISSN:0887-4476    

DOI:10.1002/syn.890040106

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractIt is proposed that taurine is an inhibitory neurotransmitter/neuromodulator in the CNS. The present study localized taurine‐containing neurons within the rat hippocampus with the use of a monoclonal antibody against conjugated taurine (Tau2) in conjuction with an antiserum against cysteine sulfinic acid decarboxylase (CSADC), a synthesizing enzyme for taurine. Taurine‐like immunoreactivity (Tau‐LI) and CSADC‐LI were colocalized in neurons of the dentate gyrus, CA1(/CA2), CA3, and CA4. Of all the cells examined, pyramidal basket cells within the granule cell layer of the dentate gyrus were most intensely stained with both Tau2 and CSADC. Granule cells were also double‐labeled with Tau‐LI and CSADC‐LI Cell nuclei and dendrites in the CA1 region stained more intensely with Tau2 than somata. CSADC‐LI was colocalized with Tau‐LI within these neurons. Light staining with both Tau2 and the CSADC antiserum was inconsistently present in CA3 and CA4 neurons and was found to be highly dependent on the type of fixation and delay to fixation. Tau‐LI was more consistently present in increased numbers of neurons in CA3 when glutaraldehyde was added to the paraformaldehyde fixative solution. Hippocampi which were immersion‐fixed in paraformaldehyde following a 0‐, 6‐, or 24‐hour postmortem delay exhibited a lack of Tau2 staining in the CA3 region in the majority of animals studied, similar to some paraformaldehyde perfusion‐fixed rats. These studies suggest that taurine was present in the majority of neurons within the major cell layers of the rat hippocampus, but Tau‐LI was more easily lost from neurons in the CA3 region following delay to fixation. The localization of Tau‐LI in excitatory neurons such as granule cells and pyramidal cells is not consistent with its proposed inhibitory transmitter role. However, the prominent Tau2 staining in dendrites of the CA1 region provides anatomical support for the hypothesis that taurine may be released from dendrites in the CA1 region and may function as a neuromodulator of calciu

ISSN:0887-4476    

DOI:10.1002/syn.890040107

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractA monoclonal antibody against taurine conjugated to KLH was used to identify and describe taurine‐like immunoreactive processes in the rat hippocampus. Tissue from perfused rats was processed for immunohistochemical visualization of taurine and embedded for electron microscopy. Representative tissue samples from three regions, the dentate gyrus, CA3, and CA1, were sectioned, examined, and photographed. In the dentate gyrus, both granule cells and pyramidal basket cells were taurine‐like immunoreactive. Some axon terminals in the dentate gyrus molecular layer as well as some mossy fiber boutons in the hilus were also taurine‐like immunoreactive. In the CA3 region both pyramidal neurons and glial cells were taurine‐like immunoreactive. A few small‐diameter axon terminals in stratum radiatum and some mossy fiber boutons in stratum lucidum were taurine‐like immunoreactive. In CA1, pyramidal neurons and some glia were intensely taurine‐like immunoreactive. A few immunoreactive axon terminals were seen in stratum radiatum and stratum oriens. In all regions, dendritic staining predominated. Our results support the hypothesis that while taurine may act as a neurotransmitter in a small portion of hippocampal terminals, its main function is probably as a neuromodulator or io

ISSN:0887-4476    

DOI:10.1002/syn.890040108

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractWe have examined the effects of intracerebroventricular administration of corticotropin‐releasing factor (CRF) (5.25 nmol in 10 μl of saline) on glucose utilization, an index of cerebral function, in 65 anatomically discrete regions of rat brain by using the14C‐2‐deoxyglucose quantitative autoradiographic technique. CRF administration increased plasma glucose concentrations with a temporal onset and magnitude of response similar to those previously reported. CRF differentially affected glucose utilization (GU) in discrete regions of rat brain. Consonant with the hypophysiotropic role for CRF, pronounced increases in GU were seen in median eminence and lateral nucleus of the hypothalamus. CRF also increased GU in brain regions implicated in mediating responses to stress including locus coeruleus and median raphe nucleus. In contrast, reductions in GU were observed in prefrontal cortex and nucleus accumbens. Punctate increases in GU were noted in the cerebellar cortex. Furthermore, large increases in GU occurred in vermis, inferior olive, and red nucleus substantiating a neurotransmitter role for CRF in the olivocerebellar pathway. Additional brain areas showing significant alterations in GU in response to CRF included anteroventral, anterior pretectal, and posterolateral nuclei of the thalamus, fornix, dorsal tegmental nucleus, spinal trigeminal nucleus, and cuneate nucleus. These data demonstrating regional changes in GU in response to CRF administration further elucidate the neuroanatomical substrates underlying the actions of CRF in brain and support the role of this neuropeptide in coordinating responses to

ISSN:0887-4476    

DOI:10.1002/syn.890040109

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractSeveral excitatory amino acid receptors encoded by rat brain mRNA were expressed inXenopusoocytes. Experimental protocols using an open channel blocker (MK‐801) were designed to test the common receptor‐channel hypothesis in which N‐methyl‐D‐aspartate (NMDA) and kainate activate the same ion channel but induce different open channel conformations with different ionic permeabilities. The present data demonstrate that NMDA exposes previously trapped MK‐801 molecules to the transmembrane field and accelerates their dissociation from the channel at positive potentials, while kainate lacks this effect, Therefore, kainate does not activate the same ion channel as NMDA does. Furthermore, differential inhibition of the NMDA response or the kainate response by the competitive antagonists D‐2‐amino‐5‐phosphonopentanoic acid (D‐AP5) and 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) indicates that NMDA and kainate do not share the same binding site. Thus, these several lines of evidence demonstrate that two distinct receptor‐channels are activated

ISSN:0887-4476    

DOI:10.1002/syn.890040110

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

ISSN:0887-4476    

DOI:10.1002/syn.890040112

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY