Biomedical subjects

Jorge A Bergado

Publications and source records attributed to Jorge A Bergado.

6 recordsLinked to original sources

PubMed2006

Stimulation of the basolateral amygdala improves the acquisition of a motor skill.

PURPOSE: We have previously shown that the stimulation of limbic structures related to affective life such as the amygdale can improve and reinforce neural plastic processes related to hippocampus-dependent forms of explicit memory, as spatial memory and LTP. We now assessed whether this effect is restricted to the mentioned structure and memory type, or represents a more general form of modulatory influence. METHODS: Young, male Sprague Dawley rats were implanted stereotactically with one electrode in the basolateral amygdala (BLA) and trained to acquire a motor skill using their right anterior limb. A group of animals received 3 trains of 15 impulses at the BLA 15 minutes after each daily training session. A second group of implanted animals was handled in the same way, but not stimulated, while a third group was not implanted. After reaching the training criterion the left motor cortex was mapped by the observation of the movements induced by stimuli applied in discrete points of the cortex. RESULTS: Cortical representation of the anterior limb was increased in all trained animals, showing that the motor cortex is involved in the acquisition of the new skill. Animals receiving stimulation of the BLA showed similar cortical changes, but learned faster than non-stimulated controls. CONCLUSIONS: Reinforcement of neural plasticity by the activation of the amygdala is not restricted to hippocampus-dependent explicit memory, but it might represent a universal mechanism to modulate plasticity.

Amygdala↗

PubMed2005

Long-term potentiation in the dentate gyrus in freely moving rats is reinforced by intraventricular application of norepinephrine, but not oxotremorine.

Growing evidence suggests that processes of synaptic plasticity, such as long-term potentiation (LTP) occurring in one synaptic population, can be modulated by consolidating afferents from other brain structures. We have previously shown that an early-LTP lasting less than 4 h (E-LTP) in the dentate gyrus can be prolonged by stimulating the basolateral amygdala, the septum or the locus coeruleus within a specific time window. Pharmacological experiments have suggested that noradregeneric (NE) and/or cholinergic systems might be involved in these effects. We have therefore investigated whether the direct intraventricular application of agonists for NE- or muscarinic receptors is able to modulate synaptic plasticity. E-LTP was induced at the dentate gyrus of freely moving rats using a mild tetanization protocol that induces only an E-LTP. NE or oxotremorine (OXO) were applied icv 10 min after the tetanus. Results show that low doses of NE (1.5 and 5 nM) effectively prolong LTP. A higher dose (50 nM) was not effective. None of the OXO doses employed (5, 25, and 50 nM) showed similar effects. These results stress the importance of transmitter-specific modulatory influences on the time course of synaptic plasticity, in particular NE whose application mimics the reinforcing effect of directly stimulating limbic structures on LTP.

Analysis of Variance↗

PubMed2005

Post-training stimulation of the basolateral amygdala improves spatial learning in rats with lesion of the fimbria-fornix.

PURPOSE: To evaluate the capacity of amygdala stimulation to improve neural plasticity in animals bearing lesions of the fimbria-fornix (FF) system. METHODS: The animals were lesioned under narcosis (chloral hydrate, 420 mg/kg ip.) using a bilateral transection of the FF procedure. During the same surgery some animals were implanted with an electrode in the right basolateral amygdala (BLA) to allow the electrical stimulation of this structure. Training was carried out one week after surgery using a Morris water maze. Animals were trained in four consecutive days (8 trials/day) in the non-visible platform condition except in the fourth day in which only 4 trials were performed followed by a probe trial in which the escape platform was removed. On day 5 of training 8 trials with visible platform were performed. After each of the first 3 training days one group of animals received trains of electrical stimulation to the BLA, while control groups were not stimulated. A group of non-lesioned animals served as control. The location of the electrode was confirmed histologically after the end of the experiments. RESULTS: The learning capacity of the lesioned animals was improved by the electrical stimulation of the amygdala. The latency to find the submerged platform within this group approaches that of the non lesioned animals in the course of training (2-way ANOVA with repeated measures), while other lesioned animals continued to show severely impaired learning abilities. CONCLUSIONS: This is the first evidence that stimulating the BLA can positively influence the learning abilities of lesioned animals. Further experiments should contribute to improve the stimulation paradigms to make it more effective, if possible.

Amygdala↗

PubMed2003

Behavioral reinforcement of long-term potentiation in rat dentate gyrus in vivo is protein synthesis-dependent.

A transient, protein synthesis-independent long-term potentiation (early-LTP, <4 h) can be reinforced into a maintained protein synthesis-dependent late-LTP (>4 h) by specific electrical stimulation of limbic structures (J. Neurosci. 21 (2001) 3697). Similarly, LTP-modulation can be obtained by behavioral stimuli with strong motivational content. However, the requirement of protein synthesis during behavioral reinforcement has not been shown so far. Thus, we have studied here this specific question using a behavioral reinforcement protocol, i.e. allowing water-deprived animals to drink 15 min after induction of early-LTP. This procedure transformed early-LTP into late-LTP. Anisomycin, a reversible protein synthesis inhibitor, abolished behavioral LTP-reinforcement. These results demonstrate that behavioral reinforcement depends on protein synthesis.

Action Potentials↗

PubMed2002

Aging and synaptic plasticity: a review.

Aging affects all systems, but the brain seems to be particularly vulnerable to the action of negative, age-dependent factors. A gradual loss of memory functions is one of the earliest and most widespread consequences of brain aging. The causes for such impairment are still unclear. Long-term potentiation (LTP) is one form of neural plasticity, which has been proposed as the cellular correlate for memory. LTP is affected by aging, and such alteration might be causally related to memory dysfunction. In the present paper, we review the evidence sustaining the existence of a causal link between cognitive and LTP impairments, as well as the possible mechanisms involved. New results indicate a possible involvement of a deficient reinforcement of LTP by affective influences.

Aging↗

PubMedDate not supplied

Aging impairs amygdala-hippocampus interactions involved in hippocampal LTP.

Aging impairs amygdala-hippocampus interactions involved in hippocampal LTP. NEUROBIOL. AGING. We have recently shown that the stimulation of the basolateral nucleus of the amygdala (BLA) is able to prolong early-LTP (<4h) into late-LTP (>4h) in the dentate gyrus. To study whether aging affects this interaction, aged (24-27 months) rats were used, classified as cognitively impaired (I), or non-impaired (N) by means of their results in the Morris water maze. Paired pulses (30-90 ms interval) showed no differences among age groups. Among young controls, the early-LTP induced in the dentate gyrus by stimulation of the perforant path (PP) was prolonged in a late-LTP when the BLA was stimulated 15 min later. In aged-impaired rats the stimulation of the PP induced a reduced LTP, decaying to baseline in less than 2 h. BLA stimulation was without effect. Aged non-impaired rats showed an early-LTP identical to that of young animals; however, stimulation of the BLA showed no effect. These results suggest that deficient synaptic plasticity and memory functions in aged animals might be caused, in part by impaired mechanisms of heterosynaptic reinforcement.

Aging↗