Daily Electrical Stimulation Of Amygdala Research Articles

Changes in neuromodulatory effect of adenosine A 1 receptors on piriform cortex field potentials in amygdala kindled rats

Adenosine exerts its anticonvulsants effect through different brain regions including piriform cortex. In this study, the effect of amygdala kindled seizures on adenosine A 1 receptor-mediated neuromodulation in piriform cortex pyramidal neurons was tested at 24 h and 1 month after kindling. Animals were kindled by daily electrical stimulation of amygdala. Field potentials were recorded from layer II of piriform cortex pyramidal cells following stimulation of the lateral olfactory tract. Obtained results showed that N 6-cyclohexyladenosine (CHA), a selective adenosine A 1 receptor agonist (1, 10 and 100 μM; i.c.v.), reduced A1 slope and B1 amplitude of field potentials in both kindled and non-kindled (control) rats. However, its effects on kindled animals were more potent at 24 h, but not 1 month post-kindling. 8 cyclopenthyl-1,3-dimethylxanthine (CPT), a selective adenosine A 1 receptor antagonist (50 μM, i.c.v.), had no significant effect on the field potential parameters. However, CPT (50 μM, i.c.v.) pretreatment eliminated effects of CHA (10 μM; i.c.v.) on the field potentials. These results indicate that activation of adenosine A 1 receptors has an inhibitory effect on the field potentials of piriform cortex pyramidal neurons and the efficiency of adenosine A 1 receptor neuromodulation in piriform cortex is increased at short-term (24 h) but return to normal at long-term (1 month) after kindling implementation.

The role of adenosine A 1 receptors in the interaction between amygdala and entorhinal cortex of kindled rats

In this study the effect of adenosine A 1 receptors of the entorhinal cortex (EC) and amygdala on kindled seizures was investigated. Animals were kindled by daily electrical stimulation of amygdala (group 1) or EC (group 2). In the fully kindled animals, N 6-cyclohexyladenosine (CHA), a selective A 1 receptor agonist, and 1,3-dimethyl-8-cyclopenthylxanthine (CPT), a selective A 1 receptor antagonist, were microinjected bilaterally into the EC (group 1) or amygdala (group 2). The seizure parameters were measured at 5, 15, 60 and 120 min post injection. Obtained data showed that in group 1, intra-EC microinjection of CHA at concentration of 10 μM reduced amygdala- and, EC-afterdischarge duration and stage 5 seizure duration at 5, 15, 60 and 120 min post drug injection. It also increased the latency to stage 4 seizure but no alteration was observed in seizure stage. At concentrations of 0.1 and 1 μM, CHA reduced only EC-afterdischarge duration at 5 and 15 min post drug infusion. Bilateral microinjection CPT at concentrations of 5 and 10 μM into the EC did not alter seizure parameters. Intra-EC microinjection of CPT (5 μM), 5 min before CHA (10 μM), blocked the anticonvulsant effects of CHA. On the other hand, in group 2 animals, intra-amygdala CHA (10, 50 and 100 μM) or CPT (5 and 10 μM) had no significant effect on seizure parameters of EC-kindled rats. These results suggest that adenosine A 1 receptors activation of the EC may have an inhibitory effect on amygdala-kindled seizures. But, despite of reciprocal interconnections between these two regions, activation of the A 1 receptors of the amygdala has no effect on EC-kindled seizures.

Intraventricular injection of antiserum to nerve growth factor delays the development of amygdaloid kindling

To investigate the possibility that nerve growth factor (NGF) may play some role in the development of kindling, rabbit anti-NGF serum was injected into the third ventricle on the first 3 days of daily electrical stimulation of the basolateral amygdala. The number of stimulations required to reach full amygdaloid kindling increased significantly in the rat injected with anti-NGF serum compared to that in the rat injected with normal rabbit serum. It was confirmed that anti-NGF serum did not act as an anticonvulsant. The results demonstrate that NGF may be important for the long-lasting neuronal changes induced by daily electrical stimulation of the amygdala.

The generalized convulsive seizure state induced by daily electrical stimulation of the amygdala in split brain cats.

Daily unilateral electrical stimulation of amygdala in forebrain bisected cats provoked the development of the final stage of the kindled convulsion with remarkable rapidity regardless of presence or absence of anterior commissure. The chronological and spatial pattern of propagation of afterdischarge, interictal spike discharge, and clinical manifestations strongly suggest the significant role played by the midbrain reticular formation and possibly other brainstem structures in the progressive electroclinical seizure development. This assumption was supported by the results of a lesion study in which placement of a destructive lesion in the ipsilateral midbrain reticular formation markedly increased the generalized seizure triggering threshold, lateralized the afterdischarge to the stimulated hemisphere when induced with increased intensity stimulation, fragmented clinical seizure manifestations, and failed to produce progression of clinical and electrographic events with prolonged daily stimulation. This is in contrast to the insignificant effect produced by a peduncular lesion. Our findings suggest that vertical (limbic-brainstem), but not horizontal (transhemispheric interlimbic) connection is critically involved in the amygdaloid seizure development while the forebrain commissures may play a role in the development of bisynchronous and bisymmetrical ictal and interictal electrographic and clinical manifestations. Finally, possible differential effect of forebrain bisection depending on developing in contrast with a established (cerebral) hemispheric epileptogenic process is postulated to explain the "facilitatory" effect observed in our series in contrast to the beneficial effects reported on some intractable seizure patients.