Electrical Stimulation Of Area Research Articles

Histamine suppresses non-NMDA excitatory synaptic currents in rat supraoptic nucleus neurons.

Whole cell patch-clamp recordings were obtained from supraoptic neurons to investigate the effects of histamine on excitatory postsynaptic currents evoked by electrical stimulation of areas around the posterior supraoptic nucleus. When cells were voltage-clamped at -70 mV, evoked excitatory postsynaptic currents had amplitudes of 88.4 +/- 9.6 pA and durations of 41.1 +/- 3.0 ms (mean +/- SE; n = 43). With twin stimulus pulses (20 Hz) used, paired-pulse facilitation ratios were 1.93 +/- 0.12. Bath application of 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX) abolished synaptic currents. Histamine at concentrations approximately 0.1-10 microM reversibly suppressed excitatory postsynaptic currents in all supraoptic neurons tested. Within 2 min after application of (10 microM) histamine, current amplitudes and durations decreased by 61. 5 and 31.0%, respectively, with little change in the paired-pulse facilitation ratio. Dimaprit or imetit (H(2) or H(3) receptor agonists) did not reduce synaptic currents, whereas pyrilamine (H(1) receptor antagonist) blocked histamine-induced suppression of synaptic currents. When patch electrodes containing guanosine 5'-O-(2-thiodiphosphate) (GDP-beta-S) were used to record cells, histamine still suppressed current amplitudes by 49.1% and durations by 41.9%. Similarly, intracellular diffusion of bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) and H(7) did not abolish histamine-induced suppression of synaptic currents, either. Bath perifusion of 8-bromo-quanosine 3',5'-cyclic monophosphate reduced current amplitudes by 32.3% and durations by 27.9%. After bath perfusion of slices with N(omega)-nitro-L-arginine methyl ester (L-NAME), histamine injection decreased current amplitudes only by 31.9%, much less than the inhibition rate in control (P < 0.01). In addition, histamine induced little change in current durations and paired-pulse facilitation ratios, representing a partial blockade of histamine effects on synaptic currents by L-NAME. In supraoptic neurons recorded using electrodes containing BAPTA and perifused with L-NAME, the effects of histamine on synaptic currents were completely abolished. Norepinephrine injection reversibly decreased current amplitudes by 39.1% and duration by 64.5%, with a drop in the paired-pulse facilitation ratio of 47.9%. Bath perifusion of L-NAME, as well as intracellular diffusion of GDP-beta-S, 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine, or BAPTA, failed to block norepinephrine-induced suppression of evoked synaptic currents. The present results suggest that histamine suppresses non-N-methyl-D-aspartate synaptic currents in supraoptic neurons through activation of H(1) receptors. It is possible that histamine first acts at supraoptic cells (perhaps both neuronal and nonneuronal) and induces the production of nitric oxide, which then diffuses to nearby neurons and modulates synaptic transmission by a postsynaptic mechanism.

Involvement of subdivisions of the medial prefrontal cortex in learned cardiac adjustments in rabbits.

Electrical stimulation of area 24 and area 32 of the medial prefrontal cortex (mPFC) in rabbits elicited increases in respiration rate and decreases in heart rate (HR) and blood pressure. However, stimulation in area 25 elicited pressor responses and a biphasic HR response consisting of an initial HR increase followed by an HR decrease. Administration of an alpha-adrenergic receptor antagonist eliminated the pressor response and bradycardiac response produced by area 25 stimulation but it had no effect on the bradycardia elicited by stimulation of area 24 or area 32. Lesions centered on area 32 of the mPFC greatly attenuated the conditioned bradycardiac response elicited by paired tone and paraorbital shock presentations. Lesions of area 24 produced a decrease in discrimination between a reinforced conditioned stimulus and a nonreinforced conditioned stimulus but had no effect on the magnitude of the conditioned response. Area 25 lesions had no effect on any aspect of conditioned responding.

Electrical stimulation of the paraventricular nucleus attenuates pyrogen fever in the rabbit

Arginine vasopressin (AVP) perfused within the ventral septal area (VSA) suppresses fever normally evoked by pyrogenic substances, including Salmonella abortus equi (SAE). Neurons containing AVP and located within the paraventricular nucleus (PVN) or the nearby bed nucleus of the stria terminalis (BnST) are believed to have projections to this septal region. A series of experiments was undertaken to determine whether electrical stimulation of these areas, which might be expected to cause the release of AVP within the VSA, would affect similarly the pathogenesis of fever. A stainless steel cannula was implanted surgically in each of 22 male New Zealand White rabbits and a monopolar electrode was lowered through this guide cannula to the PVN or BnST areas. Electrical stimulation (20 Hz, 10 s on, 10 s off, 2.6–3.2 V) was initiated 30 min prior to and was continued until 90 min after the intravenous (i.v.) adminisstration of 0.1–1.0 μg of SAE (1.0 ml carrier vehicle ). While afebrile body temperature remained unchanged, electrical stimulation of sites located in the rostral extension of the PVN effectively attenuated the pyrogen-induced fever. Stimulation of sites outside these areas did not affect either the absolute magnitude or the duration of the fever. Although the reduction in fever was most pronounced during the period of electrical stimulation, in some cases the fever remained suppressed beyond the application of the current. These experiments provide the first evidence that electrical stimulation of paraventricular areas with AVP-containing cell bodies is effective in suppressing a fever evoked by systemic administration of a pyrogen. Although untested, it is possible that a stimulus-induced release of AVP within the VSA is responsible for the attenuation of the fever.

Comparative characteristics of activity in grafted and intact neocortex in slice preparations

Background single unit activity and mixed single and multiunit responses to electrical stimulation of rat's embryonic cortex grafted into the somatosensory cortex of adult rats were investigated in a slice preparation. The relative number of neurons exhibiting background activity in the grafts was higher than in slices of intact cortex (23 and 6%, respectively), however, the portion of neurons responding to electrical stimulation of areas of neighboring neocortex in the recipient was lower than in intact cortex. The latent periods of population responses in the grafts were consistently longer than in those in intact neocortex (19.4±5 and 5.8±1.1 msec, respectively), although the extreme values coincided. The duration of population responses in the grafts was approximately an order of magnitude longer. The data presented suggests the existence of local connections between the graft and the brain of the recipient and shows weakness of inhibitory processes in the grafts. A functional integration of graft and brain in recipients with craniocerebral trauma was demonstrated.

Cardiovascular and phrenic nerve responses to stimulation of the amygdala central nucleus in the anaesthetized rabbit.

1. The cardiovascular responses to electrical stimulation of the central nucleus of the amygdala (c.n.) have been studied in chloralose-anaesthetized rabbits. A pattern of response involving bradycardia, hypotension and hind-limb vasodilatation, accompanied by an increase in the rate of phrenic nerve discharge, was evoked only in response to stimulation within the medial portion of the c.n. 2. The cardiovascular responses were not secondary to the changes in respiratory activity since they were unaffected by altering central respiratory drive by either hypo- or hyperventilation of the animal. 3. The bradycardia was attenuated by the administration of atropine sulphate and abolished by the subsequent administration of propranolol, which when given alone attenuated the bradycardia. Atropine or propranolol given alone also attenuated the hypotension evoked by medial c.n. stimulation but the concurrent hind-limb vasodilatation was unaffected. 4. Atenolol, which unlike propranolol does not cross the blood-brain barrier, had little effect on the bradycardia in response to medial c.n. stimulation, but the subsequent administration of atropine abolished it. The hypotension in response to medial c.n. stimulation was also unaffected by atenolol. 5. The vasodilatation in response to medial c.n. stimulation was abolished by administration of guanethidine even after restoration of hind-limb perfusion pressure to control values by the infusion of angiotensin II into the hind-limb perfusion circuit. 6. Electrical stimulation of areas within 0.5 mm of the medial c.n. also resulted in bradycardia but then it was accompanied by hypertension and hind-limb vasoconstriction. Stimulation of areas 1.0 mm distant to the medial c.n. resulted in small and inconsistent cardiovascular responses. 7. These results show that hind-limb vasodilatation, mediated by withdrawal of sympathetic tone, occurs in response to stimulation within the medial c.n. of the rabbit and is in part responsible for the observed hypotension. It has also been confirmed that the bradycardia in response to medial c.n. stimulation is mediated by the vagus nerves.

Organization of afferent inputs of the parietal association (area 7) and Clare-Bishop areas of the cat neocortex

Unit activity was recorded from two parietal areas of the cat neocortex in semichronic experiments. Cell responses to presentation of adequate stimuli of different modalities and to direct electrical stimulation of various cortical zones were studied. About 4% of neurons of the Clare-Bishop area did not respond to visual stimulation. Cells responding to stimuli of different modalities were found in the Clare-Bishop area. A high percentage of cells in this area responded to direct electrical stimulation of area 17. In the association area (area 7) 27% of neurons tested responded to visual stimuli, but only a very small relative number of cells (compared with responding neurons of the Clare-Bishop area) responded to stimulation of the primary sensory areas. Electrical stimulation of area 7 inhibited evoked and spontaneous unit activity in the Clare-Bishop area. The hypothesis that these areas are the association representation of two different sections of the visual system — retino-geniculocortical and retino-tecto-thalamocortical — is discussed.

Catecholamines and Depression: A Physiological Theory of Depression

MS. KICEY is a graduate of the Lancaster General Hospital School of Nursing, Lancaster, Pa., and received her B.A. in psychology from Franklin and Marshall College, Lancaster. Her special interest is in physiological psychology. She is an instructor and supervisor of practical nursing students in Lancaster vocational technical schools and is working on her master's in psychology at Villanova University. NE in the brain. This theory of depression had its origin in the Olds and Milner discovery that electrical stimulation of areas in the brain of animals and man can serve as sources of reward(1). Stein has proposed an explanation of how the reward centers and

The effect of antiparkinson drugs on the linguomandibular reflex in cats

The linguomandibular reflex (LMR) is a polysynaptic reflex involving interneurons within the brain stem. Electrical stimulation of areas in the basal ganglia have been shown to influence this reflex. The effect of known antiparkinson drugs on the linguomandibular reflex in cats investigated. 1-Dopa and apomorphine poduced dose-related inhibition of the LMR whereas amantadine and benztropine were ineffective. Apomorphine-induced inhibition of the LMR was antagonized surmountably by haloperidol, a relatively specific dopamine antagonist but not by phenoxybenzamine, an α-adrenergic blocking agent. 1-Dopa-induced inhibition of the LMR was not antagonized by either haloperidol or phenoxybenzamine. Known metabolites of 1-dopa, dopamine and norepinephrine were tested for their effects on the LMR and none was more potent than 1-dopa. These results suggest that 1-dopa might inhibit the LMR via a direct effect of its own.

Thumping behavior in the rabbit

Abstract Electrical stimulation of areas in the diencephalon and central grey of the conscious rabbit produces a response of thumping the ground with the hindfeet. The response is not elicitable from the neocortex, striatum or internal capsule. Thumping movements occur mainly after offset of the eliciting stimulus and the likelihood of a response decreases regularly with time, suggesting the decay of a central excitatory state. Central stimulation which produces thumping behavior tends to be aversive in tests for self-stimulation. Further, the behavior can be elicited by peripheral electric shock. Therefore, thumping behavior may be a sign of fear in the rabbit.