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D Blozovski

Publications and source records attributed to D Blozovski.

At least 19 recordsLinked to original sources
PubMed1990

[Intrahippocampal injection of NGF accelerates spontaneous alteration ontogenesis and the maturation of septohippocampal cholinergic innervation in rats].

A single intrahippocampal injection of nerve growth factor (NGF), performed on postnatal (PND) 8 or 13, accelerated the development of spontaneous alternation in rats. This precocity was of approximately 5 days, appearing on the 4th day after the treatment and persisting through to the end of the development (PND 40). Combined microinjections of NGF and an antimuscarinic (atropine) or an antinicotinic (mecamylamine) substance have indicated that NGF probably acts through accelerating the development of the septo-hippocampal cholinergic fibers involved in this behavior.

Animals↗
PubMed1989

Hippocampal nicotinic cholinergic mechanisms mediate spontaneous alternation and fear during ontogenesis but not later in the rat.

Spontaneous alternation was examined in young rats following microinjections of antinicotinic agents into one of the 4 hippocampal sites: anterodorsal, or posteroventral dentate gyrus, hippocampal gyrus, or entorhinal cortex. In control and saline-injected animals, the alternation rate was shown to grow suddenly from 40 to 80% between days 15 and 17 (the adult level being 85-90%), to regress partly (to 55%) between days 20 and 30, and return to a near-adult level (75%) by day 40. Meanwhile fear responses to environment (defecation and vocalization) emerged between days 20 and 25, increased to a maximum until day 30, and returned to the typically low adult level by day 40. Injections of mecamylamine (5, 20 micrograms) or hexamethonium (5, 20 micrograms) into any of the 4 sites significantly reduced the rate of alternation from as early as day 10 on, but were no longer effective from day 30 on; on the other hand, they did not alter the level of defecation, but had a tendency to lower the level of vocalization on day 30 only. These results indicate that hippocampal nicotinic cholinergic mechanisms play a role in spontaneous alternation and appear to be involved in the control of one fear reaction (vocalization) until day 30.

Aging↗
PubMed1988

Passive avoidance memory consolidation and reinstatement in the young rat.

Young rats (16-30 days), trained on a one-trial passive avoidance task, were subsequently submitted to the amnesic agent hypothermia 0, 5, 10, 20 or 30 min later, and tested for retention 6 h after training. While hypothermia administered 10 min after training was no longer effective in 30-day rats, it still induced a significant retrograde amnesia in younger animals. In 16- and 18-day rats, administration of hypothermia 20 min after training could still produce a slight but statistically non-significant amnesia. Additionally, exposition to a reinstatement treatment was found to alleviate the amnesic effects of hypothermia in 20- and 30-day-old animals, while it seemed ineffective in 16- and 18-day rats. These findings suggest that the more immature the animal, the longer the consolidation period, the more vulnerable the mnemonic trace, and the less effective a reinstatement treatment for alleviation of retrograde amnesia.

Aging↗
PubMed1988

Enhancement of passive avoidance learning through small doses of intra-amygdaloid physostigmine in the young rat. Its relation to the development of acetylcholinesterase.

Passive avoidance learning was studied in young rats 7-20 days old, in control conditions and after bilateral injections of physostigmine into the lateral amygdaloid nucleus. Acquisition in controls was possible from postnatal Day 8 on, progressed markedly after Day 11, and nearly reached maturity by Day 20. Physostigmine differentially altered acquisition depending on the dose: facilitation with low doses, no effect with moderate doses, and impairment with high doses. Enhanced learning through small doses of physostigmine was observed at all ages from Day 8 on, and was greater with 0.2 microgram than with 0.1 microgram. Maturation of the cholinergic innervation of the amygdaloid region was also studied between Days 9-20 using acetylcholine-esterase histochemistry. The results suggest that passive avoidance learning is dependent on amygdaloid cholinergic mechanisms early in life. In addition, very immature cholinergic systems, which are known to be uninfluenced by anticholinergic agents, react to anticholinesterases.

Acetylcholinesterase↗
PubMed1987

Development of amygdaloid cholinergic mediation of passive avoidance learning in the rat. I. Muscarinic mechanisms.

Passive avoidance learning was studied in young rats 13-30 days of age following bilateral injections of saline or antimuscarinic and/or muscarinic agents into three amygdaloid nuclei--lateral (L), basolateral (BL), and cortical (CO). While acquisition was not influenced by saline injections into various other cerebral structures, it was significantly altered by similar injections into these amygdaloid nuclei, especially by those into the BL nucleus, suggesting that this nucleus is particularly involved in passive avoidance learning. Atropine induced significant deficits from as early as 13 days on. These deficits increased and were of similar strength after injections into any of the three studied nuclei until day 16; after that age, they diminished slightly following CO and L nuclei administration, while remaining substantial after BL nucleus injections at all ages, even at 30 days. No facilitatory effects could be elicited by arecoline injected alone, while arecoline could antagonize the disturbing effect of atropine, when given in combination, from day 13 on. These results suggest a muscarinic cholinergic mediation of passive avoidance learning through the synaptic elements located in the basal lateral part of the amygdala in the young rat.

Acetylcholine↗
PubMed1987

Development of amygdaloid cholinergic mediation of passive avoidance learning in the rat. II. Nicotinic mechanisms.

Young rats 10-30 days of age received bilateral injections of antinicotinic and/or nicotinic agents into the lateral (L), the basolateral (BL), or the cortical (CO) amygdaloid nucleus, and were trained to learn a cool-draft stimulus passive-avoidance task, 17 min later. Mecamylamine produced age- and dose-dependent acquisition deficits; these deficits appeared on day 11, increased similarly after injections into any of the three nuclei until day 16, and decreased thereafter, more rapidly after administration into CO nucleus than after injections into L and BL nuclei. In the latter nucleus, the deficits had nearly disappeared on day 30. Nicotine injected alone induced slight facilitatory effects, significant at 20 days but not reliable at earlier stages. However, nicotine could hinder the antagonistic effects of mecamylamine, when given in combination, as early as the 11th day of age on. The results suggest the existence of nicotinic synaptic elements in the basal lateral part of the rat amygdala; however, these seem to play an important role in passive avoidance learning only during the early stages of ontogenesis.

Acetylcholine↗
PubMed1987

Hippocampal muscarinic cholinergic mediation of spontaneous alternation and fear in the developing rat.

Spontaneous alternation was examined in young rats following microinjections of anticholinergic agents into 4 hippocampal sites: anterodorsal or posteroventral dentate gyrus, hippocampus or entorhinal complex. The rate of alternation remained around 40% at 5, 10, and 15 days, increased suddenly to 80% on day 17, did not vary until day 20, regressed partly and temporarily until day 30, and returned to a near-adult level on day 40. Concomitantly with the transient regression of alternation between days 20 and 40, fear responses to environment were seen to emerge (boluses and squeaks), to reach a maximum on day 30, and to return to a low level by day 40. Injections of atropine (4, 8 micrograms) or scopolamine (4, 10 micrograms) into any of the 4 sites significantly reduced the rate of alternation from day 17 on. Only the highest doses were active at 10 and 15 days. These results demonstrate that spontaneous alternation and hippocampal muscarinic cholinergic mechanisms develop simultaneously and progress suddenly on postnatal day 17. Atropine and scopolamine also affected fear responses, abolishing or potentiating them according to the site of injection, showing that hippocampal cholinergic mechanisms exert complex influences on fear-induced emotional reactions.

Acetylcholine↗
PubMed1986

Passive avoidance deficits following lesions of the posteroventral hippocampo-subiculo-entorhinal area in the developing rat.

Young rats, 13, 16, and 20 days of age, underwent discrete bilateral electrolytic lesions of the posteroventral hippocampo-subiculo-entorhinal area, and were trained on a cool-draft-stimulus passive avoidance task 20 min later. Significant deficits in passive avoidance learning were observed at all ages studied following either small or more extended damage as compared to performance of sham-lesioned animals. The impairment was dependent upon the size of the lesion. Extended bilateral lesions of the parietal cortex overlying hippocampus induced no deficit. These results confirm that this part of the hippocampal complex plays a role in passive avoidance learning in the rat. They also show that this control of behavior is already established by the second week of life, thus supporting our previous experiments that demonstrate a cholinergic nicotinic involvement of this region in acquisition of passive avoidance as early as the 11th day of age.

Age Factors↗
PubMed1985

Mediation of passive avoidance learning by nicotinic hippocampo-entorhinal components in young rats.

Young rats, 11, 16, and 20 days of age, received bilateral injections of three antinicotinic agents into the posteroventral hippocampo-subiculo-entorhinal area, and were trained to learn a cool-draft-stimulus, passive-avoidance task shortly after (17 min). Gallamine triethiodide had no action at low doses and provoked convulsions at higher concentrations. Pempidine tartrate produced age- and dose-dependent impairments of the passive avoidance, and was much more effective in younger groups (11 and 16 days) than at 20 days. alpha-bungarotoxin also induced dose-dependent deficits. These results, together with the mecamylamine-induced deficits already reported, suggest that nicotinic cholinergic synapses located in the posteroventral part of the hippocampal complex play a role in passive-avoidance learning in the young rat as soon as this type of conditioning is possible, but become relatively less important at older ages, when muscarinic mechanisms also become involved.

Age Factors↗
PubMed1984

Time-dependent effects of hippocampo-entorhinal atropine on passive avoidance learning in the young rat.

Young rats 20 and 16 days of age received bilateral micro-injections of saline or atropine (115 micrograms/kg) into the posteroventral hippocampo-subiculo-entorhinal area, and were trained on a cool-draft-stimulus passive avoidance task thereafter. The delay between injection and training was variable: 17 min, 4 h and 6 h at 20 days; 17 min, 6 h and 12 h at 16 days. Atropine-induced learning deficits were observed after the short and intermediate intervals, but not after the longer ones, indicating that the action of atropine injected intracerebrally lasted for several hours (at least 4 h at 20 days, and 6 h at 16 days) and was over after 6 h and 12 h respectively.

Animals↗
PubMed1984

Implication of amygdaloid muscarinic cholinergic mechanisms in passive avoidance learning in the developing rat.

Young rats, 12-20 days of age, received bilateral microinjections of atropine sulfate (1, 5 and 20 micrograms) into the basolateral part of the amygdala, and were trained to learn a cool-draft-stimulus passive avoidance task 17 min later. Twelve-day rats did not perform differently from their controls. In contrast, rats 13-20 days of age exhibited significant age- and dose-related acquisition deficits. Sensitivity to atropine was high until day 17, and decreased progressively thereafter. These results demonstrate that muscarinic cholinergic synaptic elements located in the basolateral part of the amygdala are involved in passive avoidance learning in the young rat and begin to function on postnatal day 13. They also suggest that the number of functioning muscarinic receptor sites increase reliably after day 17.

Amygdala↗
PubMed1983

Deficits in passive avoidance learning in young rats following mecamylamine injections in the hippocampo-entorhinal area.

Young rats 11, 13, 16, and 20 days old were injected bilaterally with the nicotinic antagonist mecamylamine hydrochloride (5, 50, and 100 micrograms on each side) into the posteroventral hippocampo-entorhinal (VHE) area and trained on a "cool-draft-stimulus" passive avoidance task. The data showed impaired acquisition and reduced resistance to extinction. The deficits observed were age- and dose-dependent, rats being highly sensitive to the drug when 11 and 13 days old and decreasingly responsive up to day 20. The results may indicate that nicotinic cholinergic sites in the VHE area mediate passive avoidance learning in the young rat as soon as acquisition emerges. Muscarinic cholinergic mechanisms only develop later in this region, becoming progressively more important for passive avoidance behavior.

Animals↗
PubMed1982

Effects of antimuscarinic cholinergic drugs injected systemically or into the hippocampo-entorhinal area upon passive avoidance learning in young rats.

Passive avoidance learning was significantly impaired by atropine (5 mg/kg, IP) or scopolamine (0.5 mg/kg), but not by methyl-atropine (5 mg/kg) or methyl-scopolamine (0.5 mg/kg), from postnatal day 15 on. In contrast, an improvement was observed, not significant at 11 days and significant at 13 days, probably due to nonspecific effects. Retention of the response increased from 6 h at 13 days, to 24 h at 17 days. In treated rats, retention was abolished at 13 and 15 days, and impaired at 17 and 20 days. Acquisition of the response was also significantly impaired by bilateral injections of atropine (1, 5, and 20 micrograms) into the posteroventral hippocampo-entorhinal (VHE) area, from day 15 on. Concomitantly, extinction was accelerated. At 14 days, atropine had no influence. At 13 days, a facilitatory action was observed, with better acquisition and greater resistance to extinction, possibly linked to affective changes. The results confirm that central muscarinic cholinergic mechanisms are involved in passive avoidance learning from postnatal day 15 on, and demonstrate that some pathways of this system are located in the VHE area, become efficient at 15 days, and improve markedly between 17 and 18 days.

Age Factors↗
PubMed1980

Passive avoidence learning in the young rat.

A step-through locomotor passive avoidance task is described requiring the suppression of a spontaneous escape reaction from a cool toward a warm compartment in order to avoid an electric shock delivered in the warm side. We observed no lerning of this task at 9 days of age, a very low but significant level of acquisition at 11 days, a slow but progressive improvement of avoidance from the 13th until the 17th day when the adult capacity was achieved, and a marked increase in the rate between 17-20 days.

Aging↗
PubMed1980

Acquisition and retention of classical conditioning in the newborn rat.

The development of memory of a conditioned response was examined in London black rats between 0 and 4 days of age. For the conditioning, a vibrotactile stimulus paired with an electric shock was presented to the animal 80 times with an interval of 2000 msec between stimuli. The animals were retested at retention intervals of 3 min or 24 hr. The results showed that 0-, 2-, 3-, and 4-day-old rats possess a retention capacity of at least 24 hr and suggest that the emergence of memory may be task-specific.

Animals↗
PubMed1979

PA-learning in young rats with dorsal hippocampal- and hippocampo-entorhinal atropine.

Twenty-one-day-old rats injected with atropine into dorsal hippocampus and trained on a white-black step-through passive avoidance task, did not perform differently from their controls in acquisition or extinction. In contrast, when atropine was administered into the ventral hippocampo-entorhinal area, the animals displayed a passive avoidance deficit. The results support the finding that the posteroventral but not the anterodorsal part of the hippocampal complex is implicated in passive avoidance learning and suggest a cholinergic mediation of this effect.

Animals↗