Query: rat visual cortex neurotransmitter

title: Nerve growth factor and brain derived neurotrophic factor increase neurotransmitter release in the rat visual cortex
abstract: A number of experiments have shown that neurotrophins are involved in the development and plasticity of the visual cortex (Bonhoeffer, T. Curr. Op. Neurobiol. 6, 119 1996) A possible mechanism underlying these effects is the neurotrophin modulation of synaptic transmission. We investigated whether nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) can modulate the release of neurotransmitter in the rat visual cortex at the peak of the critical period for plasticity (P23) The release of glutamate, acetylcholine and gamma aminobutyric acid (GABA) from visual cortical synaptosomes was analysed in continuous perfusion conditions. We found that NGF enhances the depolarization evoked release of glutamate 90% and acetylcholine 35% but not that of GABA. By contrast, BDNF enhances the depolarization evoked release of all three neurotransmitters investigated 30% BDNF and NGF were ineffective on basal release of neurotransmitters. The effect of NGF was not blocked by cholinergic antagonists atropine and mecamylamine. NGF and BDNF potentiation of transmitter release was strongly but not completely blocked by K252a, a tyrosine kinase inhibitor. The role of TrkA and p75NTR receptors was investigated in NGF induced potentiation of glutamate release. Block of NGF binding to p75NTR using specific blocking antibodies (REX IgG) slightly but significantly reduced the effect of NGF. Activation of TrkA in isolation by RTA IgG, an antibody that specifically activates TrkA, was less effective than activation of both receptors by NGF. These results show that neurotrophin action on neurotransmitter release was mostly mediated by Trk receptors with p75NTR having a little but significant positive role. Antigen blot analysis showed the presence of TrkA, TrkB and p75NTR receptors in the visual cortex.

title: Topographic Organization of Cholinergic Innervation From the Basal Forebrain to the Visual Cortex in the Rat
abstract: Acetylcholine is an important neurotransmitter for the regulation of visual attention, plasticity, and perceptual learning. It is released in the visual cortex predominantly by cholinergic projections from the basal forebrain, where stimulation may produce potentiation of visual processes. However, little is known about the fine organization of these corticopetal projections, such as whether basal forebrain neurons projecting to the primary and secondary visual cortical areas (V1 and V2, respectively) are organized retinotopically. The aim of this study was to map these basal forebrain V1/V2 projections. Microinjections of the fluorescent retrograde tracer cholera toxin b fragment in different sites within V1 and V2 in Long Evans rats were performed. Retrogradely labeled cell bodies in the horizontal and vertical limbs of the diagonal band of Broca (HDB and VDB, respectively) nucleus basalis magnocellularis, and substantia innominata (SI) were mapped ex vivo with a computer assisted microscope stage controlled by stereological software. Choline acetyltranferase immunohistochemistry was used to identify cholinergic cells. Our results showed a predominance of cholinergic projections coming from the HDB. These projections were not retinotopically organized but projections to V1 arised from neurons located in the anterior HDB/SI whereas projections to V2 arised from neurons located throughout the whole extent of HDB/SI. The absence of a clear topography of these projections suggests that BF activation can stimulate visual cortices broadly.

title: Three distinct families of GABAergic neurons in rat visual cortex.
abstract: In the cortex inhibition is mediated predominantly by GABAergic interneurons. Although all of these neurons use the same neurotransmitter, studies in the rat frontal cortex have shown that they are molecularly and physiologically diverse. It is not known whether similar subgroups of GABAergic neurons exist in primary visual cortex and how these different inhibitory neurons are inserted into specific cortical circuits. We have used immunostaining with antibodies against gamma aminobutyric acid (GABA) parvalbumin (PV) calretinin (CR) somatostatin (SOM) calbindin (CB) and nitric oxide synthase (NOS) to probe for colocalization of known markers of GABAergic interneurons. The results show that the majority of PV (100% SOM (89.8% and CR (93.9% staining neurons are GABA positive. PV immunoreactive neurons constitute a distinct group that show no overlap with CR, SOM and NOS expressing cells and only a minor overlap (5.3% with CB. PV immunoreactive cells account for 50.8% of GABAergic neurons. A second group of SOM expressing neurons accounts for 16.9% of GABAergic cells. None of these cells colocalize PV or CR, but 1.7% of SOM neurons stain for NOS and 86.3% show CB immunoreactivity. The third distinct group of CR expressing cells accounts for 17.0% of GABAergic neurons. All of these are PV, CB, SOM and NOS negative. CB expressing neurons represent a heterogeneous group that includes GABAergic and non GABAergic cells. Our findings indicate that GABAergic neurons in rat area 17 are organized in at least three separate families that can be identified by the expression of PV, CR and SOM. These cells account for 84.9% of GABAergic neurons. These results extend previous observations in rat frontal agranular cortex and suggest that in visual cortex the inhibitory network is composed of similar cell types.

title: Glycine modulates synaptic NR2A and NR2B containing NMDA receptor mediated responses in the rat visual cortex
abstract: In the central nervous system, activation of N methyl d aspartate receptor (NMDA R) glycine binding sites is a prerequisite for activation of synaptic NMDA Rs by the excitatory neurotransmitter glutamate. Here we used patch clamp recordings in transverse slice preparations to study whether the glycine binding site of the NMDA R saturates and to determine their subunit composition in layer II/III pyramidal neurons of the rat visual cortex. We found that the NMDA R mediated component of miniature excitatory postsynaptic currents (mEPSCs) could be potentiated by exogenously applied glycine. Similar results were obtained by exogenously applied d serine. A specific antagonist for NR2B NMDA Rs, Ro 25 6981, reduced NMDA R mediated mEPSCs, and glycine with Ro 25 6981 enhanced NMDA R mediated mEPSCs. Moreover, Zn2+ an NR2A NMDA R antagonist, also reduced NMDA mediated mEPSCs and glycine with Zn2+ enhanced the NMDA mediated mEPSCs. Our data indicate that the glycine binding site of synaptic NR2A containing and NR2B containing NMDA Rs does not saturate and that glycine may act as a modulator of NMDA R mediated transmission in layer II/III pyramidal neurons of the rat visual cortex.

title: Glycine binding sites of presynaptic NMDA receptors may tonically regulate glutamate release in the rat visual cortex.
abstract: In the CNS, activation of N methyl D aspartate receptor (NMDA R) glycine binding sites is a prerequisite for activation of postsynaptic NMDA Rs by the excitatory neurotransmitter glutamate. Here we provide electrophysiological evidence that the glycine binding sites of presynaptic NMDA Rs regulate glutamate release in layer II/III pyramidal neurons of the rat visual cortex. Specifically, our results reveal that the frequency of miniature excitatory postsynaptic currents is significantly reduced by 7 chloro kynurenic acid (7 Cl KYNA) a NMDA R glycine binding site antagonist, and glycine or D serine reverses this effect. Similar results are obtained when the open channel NMDA receptor blocker, MK 801, is included in the recording pipette. Our data indicate that the glycine binding site of postsynaptic NMDA Rs is not saturated. Moreover, they suggest that presynaptic NMDA Rs are located in layer II/III pyramidal neurons of the rat visual cortex and that the glycine binding site of presynaptic NMDA Rs tonically regulates glutamate release.

title: Effects of dopamine on gamma amino butyric acid activated currents in neutron of visual cortex of rat
abstract: As a main suppressing neurotransmitter in visual system,gamma aminobutyric acid (GABA) participates in the transmission and regulation of visual information.GABA and dopamine (DA) coexist in the visual cortex,and their mutual effects should be clarified. This study was to investigate the effect of DA on GABA activated current in vitro in cultured visual cortical neurons of rats. Neutrons from visual cortex of clean neonatal rats were isolated and cultured by explant culture method.The neutrons cultured for 11 to 14 days were collected for the record of whole cell currents of GABA A (IGABA) channels in vitro using patch clamp technique.The DA solution (100mmol/L),SKF38393 (10mmol/L) solution and quinpirole solution(10mmol/L) were prepared with double distilled water and then the extracellular fluid was added to different concentrations.The IGABA changing rate under the action of SKF38393+SCH23390,SKF38393+Quinpirole for different time was recorded respectively and compared with that of action of DA,SKF38393,SCH23390,Quinpirole.The IGABA activated by extracellular fluid along served as control. The IGABA was significantly attenuated after activated by =10mmol/L of DA or SKF38393 separately in comparison to that of extracellular fluid action (P<0.05).In various time of action,there were obviously differences in IGABA between DA or SKF38393 action and extracellular fluid (P<0.05,P<0.01).No evident change in IGABA changing rate was found after only SCH23390 action in comparison with extracellular cells (P<0.05).However,after combination of SCH23390 and SKF38393,IGABA changing rate reduced by 19.49%.No significant differences were found in the changing rates of IGABA among different concentrations of quinpirole action groups compared with extracellular fluid group (P>0.05);while when quinpirole was combined with SKF38393,the IGABA was elevated in comparison with only SKF38393 action group (P<0.05).Conclusion Dopamine participates in the transfer and regulation of visual information through suppressing GABA activated currents from neutrons of visual cortex at time dependent manner in vitro.  Dopamine; Gamma aminobutyric acid; Visual cortex; Patch clamp;

title: Multiple G protein coupled receptors mediate presynaptic inhibition at single excitatory synapses in the rat visual cortex
abstract: Modulation of excitatory synaptic transmission by agonists for several neurotransmitter receptors was investigated at intrinsic cortical synapses derived from single presynaptic neurons. Excitatory postsynaptic currents (EPSCs) were recorded from layer 5 pyramidal neurons in the rat visual cortex in response to minimal stimulation within the same layer. 5 hydroxytryptamine, adenosine, baclofen, carbachol and DCG IV all suppressed EPSCs with an increase in paired pulse ratio. These agonists reduced the frequency of miniature EPSCs without significantly affecting their amplitude distribution. These results suggest that glutamatergic excitatory transmission in the neocortex is under the control of presynaptic inhibition mediated by multiple neuromodulator receptors co expressed in single presynaptic terminals.

title: Title Glycine binding sites of presynaptic NMDA receptors may tonically regulate glutamate release in the rat visual cortex
abstract: In the central nervous system, activation of N methyl D aspartate receptor (NMDA R) glycine binding sites is a prerequisite for activation of postsynaptic NMDA Rs by the excitatory neurotransmitter glutamate. Here we provide electrophysiological evidence that the glycine binding sites of presynaptic NMDA Rs regulate glutamate release in layer II/III pyramidal neurons of the rat visual cortex. Specifically, our results reveal that the frequency of miniature excitatory postsynaptic currents (mEPSCs) is significantly reduced by 7 chloro kynurenic acid (7 Cl KYNA) a NMDA R glycine binding site antagonist, and glycine or D serine reverses this effect. Similar results are obtained when the open channel NMDA receptor blocker, MK 801, is included in the recording pipette. Our data indicate that the glycine binding site of postsynaptic NMDA Rs is not saturated. Moreover, they suggest that presynaptic NMDA Rs are located in layer II/III pyramidal neurons of the rat visual cortex, and that the glycine binding site of presynaptic NMDA Rs tonically regulates glutamate release.

title: Development of neurotransmitter parameters in lateral geniculate body, superior colliculus and visual cortex of the albino rat.
abstract: The postnatal development of some neurotransmitter parameters was measured in lateral geniculate body, superior colliculus and visual cortex of the rat. The following parameters were studied: (i) high affinity uptake of L glutamate or D aspartate as markers for glutamergic neurons; (ii) high affinity uptake of GABA, which reflects both glial and neuronal uptake of GABA; (iii) HA beta alanine uptake as a marker for accumulation of GABA in glial structures; (iv) activity of glutamic acid decarboxylase which reflects GABAergic neurons; and (v) activity of choline acetyltransferase as a cholinergic marker. Km and Vmax were determined for high affinity uptake of glutamate and GABA in newborn and adult animals. The possible glial influence on the uptake during development is discussed. In lateral geniculate body and visual cortex the HA glutamate uptake showed increasing activity from birth to adulthood, whereas in superior colliculus, the uptake was higher at birth, reaching a small significant peak after 12 days of age, and was then reduced to adult level. Km showed no such change between neonatal and adult animals. At birth, high affinity GABA uptake was similar to the adult level in superior colliculus and lateral geniculate body. In visual cortex, the uptake of GABA was 50% of adults. However, on day 15, the GABA uptake showed 2 to 3 fold higher activity in all regions when compared to adult level. Km for GABA uptake in neonatals and adults differed only in lateral geniculate body. High affinity uptake of beta alanine was 50 80% lower in adults than in newborn rats. Glutamate decarboxylase activity, however, increased continuously in all 3 regions examined. This was true also for choline acetyltransferase.

title: The release of endogenous amino acids from rat visual cortex by calcium ions in the presence of the calcium ionophores X537A and A23187
abstract: USING a cortical cup technique (MITCHELL, 1963) it has recently been shown that the application of salt solutions containing high concentrations of potassium ions, and of electrical stimulation to the surface of the visual cortex of the anaesthetized rat is accompanied by changes in the release of several physiologically active endogenous amino acids (CLARK COLLINS, 1975, 1976; COLLINS, 1975) One of the criteria by which it is possible to identify which of these compounds might be a neurotransmitter is whether such evoked release is dependent on the extracellular concentration of calcium ions. When such experiments were carried out (CLARK COLLINS, 1976) the evoked release of GABA, aspartate and glutamate but not that of taurine appeared to be calcium dependent. Nevertheless, it is difficult to lower calcium levels in uiuo as stores are continually being replenished from the circulation. In this study, an attempt has been made to overcome this difficulty by monitoring the effect of compounds X537A and A23187, two calcium ionophores, on the release of some endogenous amino acids from the visual cortex of the anaesthetized rat.