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Cholinergic Agents (cholinergic + agent)
Selected AbstractsElectrophysiological characterization of laminar synaptic inputs to the olfactory tubercle of the rat studied in vitro: modulation of glutamatergic transmission by cholinergic agents is pathway-specificEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2001G. S. Owen Abstract We have exploited the complementary arrangement of afferents in a coronal slice (300,400 µm) of the rat olfactory tubercle (OT) maintained in vitro to investigate transmission in two separate synaptic pathways. We recorded extracellular responses within the OT dense cell layer in slices and stimulated either the outermost layer to activate primary olfactory fibres or deeper to activate secondary input. Superficial stimulation produced a synaptic potential with superimposed population spike. This interpretation was based on blockade by calcium removal from the bathing medium and the use of the glutamate antagonist DNQX (10 µm); the spike was found to be selectively suppressed by tetrodotoxin applied near the cells. The spike, but not the synaptic wave, was depressed by 12 mm Ca2+ and enhanced by 1 mm Ba2+ in the bathing medium. Deep stimulation to activate association and intrinsic fibres elicited a nerve volley followed by a later response, also blocked by Ca2+ removal or 10 µm DNQX. It was unaffected by high Ca2+ or Ba2+, hence resulting from synaptic and not action current flow. Removal of Mg2+ from the bathing medium revealed an NMDA component of synaptic transmission at both loci that was selectively blocked by D-AP-5. The deep synaptic response, only, was depressed by carbachol IC50 7 µm or muscarine IC50 13 µm. This depression was also induced by AChE inhibitors eserine or tacrine and was antagonized by 1 µm atropine or 5,10 µm clozapine. These results characterize transmission in the OT and demonstrate a role for muscarinic modulation of deeper synapses in the OT that is influenced by psychotherapeutic drugs. [source] Soman-induced seizures: limbic activity, oxidative stress and neuroprotective proteins,,JOURNAL OF APPLIED TOXICOLOGY, Issue S1 2001T. L. Pazdernik Abstract Soman, a potent acetylcholinesterase inhibitor, induces status epilepticus in rats followed by conspicuous neuropathology, most prominent in piriform cortex and the CA3 region of the hippocampus. Cholinergic seizures originate in striatal,nigral pathways and with fast-acting agents (soman) rapidly spread to limbic related areas and finally culminate in a full-blown status epilepticus. This leads to neurochemical changes, some of which may be neuroprotective whereas others may cause brain damage. Pretreatment with lithium sensitizes the brain to cholinergic seizures. Likewise, other agents that increase limbic hyperactivity may sensitize the brain to cholinergic agents. The hyperactivity associated with the seizure state leads to an increase in intracellular calcium, cellular edema and metal delocalization producing an oxidative stress. These changes induce the synthesis of stress-related proteins such as heat shock proteins, metallothioneins and heme oxygenases. We show that soman-induced seizures cause a depletion in tissue glutathione and an increase in tissue ,catalytic' iron, metallothioneins and heme oxygenase-1. The oxidative stress induces the synthesis of stress-related proteins, which are indicators of ,stress' and possibly provide neuroprotection. These findings suggest that delocalization of iron may catalyze Fenton-like reactions, causing progressive cellular damage via free radical products. Copyright © 2001 John Wiley & Sons, Ltd. [source] Cholinergic modulation of synaptic physiology in deep layer entorhinal cortex of the ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2001Mi Young Cheong Abstract We have recently shown that cholinergic effects on synaptic transmission and plasticity in the superficial (II/III) layers of the rat medial entorhinal cortex (EC) are similar, but not identical, to those in the hippocampus (Yun et al. [2000] Neuroscience 97:671,676). Because the superficial and deep layers of the EC preferentially convey afferent and efferent hippocampal projections, respectively, it is of interest to compare cholinergic effects between the two regions. We therefore investigated the physiological effects of cholinergic agents in the layer V of medial EC slices under experimental conditions identical to those in the previous study. Bath application of carbachol (0.5 ,M) induced transient depression of field potential responses in all cases tested (30 of 30; 18.5% ± 2.3%) and rarely induced long-lasting potentiation (only 3 of 30; 20.4% ± 3.2% in successful cases). At 5 ,M, carbachol induced transient depression only (20 of 20, 48.9% ± 2.8%), which was blocked by atropine (10 ,M). Paired-pulse facilitation was enhanced during carbachol-induced depression, suggesting presynaptic action of carbachol. Long-term potentiation (LTP) could be induced in the presence of 10 ,M atropine by theta burst stimulation, but its magnitude was significantly lower (9.1% ± 4.7%, n = 15) compared to LTP in control slices (22.4% ± 3.9%, n = 20). These results, combined with our previous findings, demonstrate remarkably similar cholinergic modulation of synaptic transmission and plasticity across the superficial and deep layers of EC. J. Neurosci. Res. 66:117,121, 2001. © 2001 Wiley-Liss, Inc. [source] Incomplete emptying and urinary retention in multiple-system atrophy: When does it occur and how do we manage it?MOVEMENT DISORDERS, Issue 6 2006Takashi Ito MD Abstract Neurogenic urinary retention can be a major cause of morbidity in multiple-system atrophy (MSA). However, the timing of its appearance has not been entirely clear, and neither have the medical and surgical modalities for managing patients. We present the data obtained from our uroneurological assessment and therapeutic interventions at various stages of MSA. We recruited 245 patients with probable MSA. We measured postvoid residuals (PVR) and performed EMG cystometry in all patients. The grand average volume of PVR was 140 mL (range, 0,760) in our patients. The average PVR volume was 71 mL in the first year, increasing to 129 mL in the second year and 170 mL by the fifth year. The percentages of patients with complete urinary retention, acontractile detrusor, and detrusor,sphincter dyssynergia (DSD) also increased. The increase in PVR resulted in a decrease in functional bladder capacity, together with an increase in detrusor overactivity and neurogenic sphincter EMG. Clean intermittent self-catheterization (CISC) was introduced in most patients. Bladder-oriented therapy (cholinergic agents) had a limited value, whereas urethra-oriented therapy benefited patients with DSD (surgery) for up to 2 years, but syncope occurred in a subset of patients (,-blockers). MSA patients present with large PVR by the second year of illness, and that large PVR secondarily causes urinary frequency. CISC is the recommended treatment for most patients. Urethra-oriented medication and surgery benefit patients who would have difficulty performing CISC, although careful consideration of the short-term efficacy and potential adverse effects of these alternatives is mandatory. © 2006 Movement Disorder Society [source] | ||||||||||