scholarly journals Does the inability of CA1 area to respond to ischemia with early rapid adenosine release contribute to hippocampal vulnerability?

2021 ◽  
Author(s):  
Natalia V. Gulyaeva
Keyword(s):  
Adenosine Release ◽  
Ca1 Area

Expression of autophagy and microtubule-associated protein 1 light chain 3 in hippocampus CA1 area of vascular dementia rats

2013 ◽  
Vol 33 (9) ◽  
pp. 940-945
Author(s):  
Bin LIU ◽  
Jing TANG ◽  
Min YUAN ◽  
Shi-ying LI
Keyword(s):  
Vascular Dementia ◽  
Light Chain ◽  
Ca1 Area

Forskolin and phosphodiesterase inhibitors release adenosine but inhibit morphine-evoked release of adenosine from spinal cord synaptosomes

1991 ◽  
Vol 69 (6) ◽  
pp. 877-885 ◽  
Author(s):  
D. Nicholson ◽  
T. D. White ◽  
J. Sawynok
Keyword(s):  
Spinal Cord ◽  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Phosphodiesterase Inhibitors ◽  
Dorsal Spinal Cord ◽  
Adenosine Release ◽  
Basal Release ◽  
Phosphodiesterase Isoenzymes ◽  
Dorsal Spinal ◽  
Ventral Spinal Cord

The effects of forskolin, Ro 20-1724, rolipram, and 3-isobutyl-1-methylxanthine (IBMX) on morphine-evoked release of adenosine from dorsal spinal cord synaptosomes were evaluated to examine the potential involvement of cyclic AMP in this action of morphine. Ro 20-1724 (1–100 μM), rolipram (1–100 μM), and forskolin (1–10 μM) increased basal release of adenosine, and at 1 μM inhibited morphine-evoked release of adenosine. Release of adenosine by Ro 20-1724, rolipram, and forskolin was reduced 42–77% in the presence of α, β-methylene ADP and GMP, which inhibits ecto-5′-nucleotidase activity by 81%, indicating that this adenosine originated predominantly as nucleotide(s). Significant amounts of adenosine also were released from the ventral spinal cord by these agents. Ro 20-1724 and rolipram did not significantly alter the uptake of adenosine into synaptosomes. Although Ro 20-1724 and rolipram had only limited effects on the extrasynaptosomal conversion of added cyclic AMP to adenosine, IBMX, a phosphodiesterase inhibitor with a broader spectrum of inhibitory activity for phosphodiesterase isoenzymes, significantly inhibited the conversion of cyclic AMP to adenosine and resulted in recovery of a substantial amount of cyclic AMP. As with the non-xanthine phosphodiesterase inhibitors, IBMX increased basal release of adenosine and reduced morphine-evoked release of adenosine. Adenosine released by IBMX was reduced 70% in the presence of α, β-methylene ADP and GMP, and release from the ventral spinal cord was 61% of that from the dorsal spinal cord. Collectively, these results indicate that forskolin and phosphodiesterase inhibitors release nucleotide(s) which is (are) converted extrasynaptosomally to adenosine. For forskolin, Ro 20-1724, and rolipram, the nucleotide released could be cyclic AMP. Morphine releases adenosine per se, and forskolin and phosphodiesterase inhibitors reduce this release. The lack of increase in the action of morphine with phosphodiesterase inhibitors in particular does not support a role for stimulation of cyclic AMP production by morphine in the release of adenosine. The reduction in morphine-evoked release of adenosine by forskolin and phosphodiesterase inhibitors suggests either (a) that a reduction in cyclic levels by morphine promotes adenosine release, or (b) that cyclic AMP interferes with the release process.Key words: forskolin, Ro 20-1724, 3-isobutyl-1-methylxanthine, cyclic AMP, morphine, adenosine release, spinal cord.

DOPAMINE RECEPTORS IN THE CA1 AREA OF THE HIPPOCAMPUS PLAY A ROLE IN SENSORIMOTOR GATING

1999 ◽  
Vol 10 (SUPPLEMENT 1) ◽  
pp. S30
Author(s):  
Bart A. Ellenbroek
Keyword(s):  
Dopamine Receptors ◽  
Sensorimotor Gating ◽  
Ca1 Area

Choline substitution for sodium triggers glutamate and adenosine release from rat hippocampal slices

1995 ◽  
Vol 197 (2) ◽  
pp. 97-100 ◽  
Author(s):  
J.C. Fowler
Keyword(s):  
Hippocampal Slices ◽  
Adenosine Release

Loss of sigma binding sites in the CA1 area of the anterior hippocampus in Alzheimer's disease correlates with CA1 pyramidal cell loss

1993 ◽  
Vol 623 (2) ◽  
pp. 299-302 ◽  
Author(s):  
K.L.R. Jansen ◽  
R.L.M. Faull ◽  
P. Storey ◽  
R.A. Leslie
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pyramidal Cell ◽  
Binding Sites ◽  
Cell Loss ◽  
Ca1 Area

Nonsynaptic epileptogenesis in the mammalian hippocampus in vitro. I. Development of seizurelike activity in low extracellular calcium

1986 ◽  
Vol 56 (2) ◽  
pp. 409-423 ◽  
Author(s):  
A. Konnerth ◽  
U. Heinemann ◽  
Y. Yaari
Keyword(s):  
Epileptiform Activity ◽  
Large Population ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Discharge Zone ◽  
Critical Threshold ◽  
Mean Velocity ◽  
Stratum Pyramidale ◽  
Ca1 Area

Epileptiform activity induced in rat hippocampal slices by lowering extracellular Ca2+ concentration ([Ca2+]o) was studied with extracellular and intracellular recordings. Perfusing the slices with low Ca2+ (less than or equal to 0.2 mM) or EGTA-containing solutions blocked the synaptic responses of hippocampal pyramidal cells (HPCs). Despite the block, spontaneous paroxysms, termed seizurelike events (SLEs), appeared in the CA1 area and then recurred regularly at a stable frequency. Transient hypoxia accelerated their development and increased their frequency. When [Ca2+]o was raised in a stepwise manner, the SLEs disappeared at 0.3 mM. With extracellular recording from the CA1 stratum pyramidale, a SLE was characterized by a large negative shift in the field potential, which lasted for several seconds. During this period a large population of CA1 neurons discharged intensely and often in synchrony, as concluded from the frequent appearance of population spikes. Synchronization, however, was not a necessary precursor for the development of paroxysmal activity, but seemed to be the end result of massive neuronal excitation. The cellular counterpart of a SLE, as revealed by intracellular recording from HPCs in the discharge zone of the paroxysms, was a long-lasting depolarization shift (LDS) of up to 20 mV. This was accompanied by accelerated firing of the neuron. A prolonged after-hyperpolarization succeeded each LDS and arrested cell firing. Brief (approximately 50 ms) bursts were commonly observed before LDS onset. Single electrical stimuli applied focally to the stratum pyramidale or alveus evoked paroxysms identical to the spontaneous SLEs, provided they surpassed a critical threshold intensity. Subthreshold stimuli elicited only small local responses, whereas stimuli of varied suprathreshold intensities evoked the same maximal SLEs. Thus the buildup of a SLE is an all or nothing or a regenerative process, which mobilizes the majority, if not all, of the local neuronal population. Each SLE was followed by absolute and relative refractory periods during which focal stimulation was, respectively, ineffective and less effective in evoking a maximal SLE. In most slices the spontaneous SLEs commenced at a "focus" located in the CA1a subarea (near the subiculum). SLEs evoked by focal stimulation arose near the stimulating electrode. From their site of origin the paroxysmal discharges spread transversely through the entire CA1 area at a mean velocity of 1.74 mm/s. Consequently, the discharge zone of a SLE could encompass for several seconds the entire CA1 area.(ABSTRACT TRUNCATED AT 400 WORDS)

Relationship between coronary flow and adenosine release in reactive hyperemia

Life Sciences ◽  
1985 ◽  
Vol 36 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Michael O. Onwochei ◽  
S. Jamal Mustafa
Keyword(s):  
Coronary Flow ◽  
Reactive Hyperemia ◽  
Adenosine Release

The effects of galanin on long-term synaptic plasticity in the CA1 area of rodent hippocampus

Neuroscience ◽  
2002 ◽  
Vol 112 (1) ◽  
pp. 173-182 ◽  
Author(s):  
U. Coumis ◽  
C.H. Davies
Keyword(s):  
Synaptic Plasticity ◽  
Ca1 Area
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