gamma-Hydroxybutyrate modulation of glutamate levels in the hippocampus: an in vivo and in vitro study.

The effect of gamma-hydroxybutyric acid on extracellular glutamate levels in the hippocampus was studied by microdialysis in freely moving rats and in isolated hippocampal synaptosomes. Intra-hippocampal (CA1) perfusion with gamma-hydroxybutyric acid (10 nM-1 mM) concentration-dependently influenced glutamate levels: gamma-hydroxybutyric acid (100 and 500 nM) increased glutamate levels; 100 and 300 microM concentrations were ineffective; whereas the highest 1 mM concentration reduced local glutamate levels. The stimulant effect of gamma-hydroxybutyric acid (100 nM) was suppressed by the locally co-perfused gamma-hydroxybutyric acid receptor antagonist NCS-382 (10 microM) but not by the GABA(B) receptor antagonist CGP-35348 (500 microM). Furthermore, the gamma-hydroxybutyric acid (1 mM)-induced reduction in CA1 glutamate levels was counteracted by NCS-382 (10 microM), and it was also reversed into an increase by CGP-35348. Given alone, neither NCS-382 nor CGP-35348 modified glutamate levels. In hippocampal synaptosomes, gamma-hydroxybutyric acid (50 and 100 nM) enhanced both the spontaneous and K(+)-evoked glutamate efflux, respectively, both effects being counteracted by NCS-382 (100 nM), but not by CGP-35348 (100 microM). These findings indicate that gamma-hydroxybutyric acid exerts a concentration-dependent regulation of hippocampal glutamate transmission via two opposing mechanisms, whereby a direct gamma-hydroxybutyric acid receptor mediated facilitation is observed at nanomolar gamma-hydroxybutyric acid concentrations, and an indirect GABA(B) receptor mediated inhibition predominates at millimolar concentrations.

Prenatal exposure to a low concentration of carbon monoxide disrupts hippocampal long-term potentiation in rat offspring.

The aim of the present study was to investigate whether functional changes at CA3-CA1 synapses in the hippocampus could underlie learning and memory deficits produced in rat offspring by a prenatal exposure model simulating the carbon monoxide (CO) exposure observed in human cigarette smokers. Electrophysiological endpoints, including long-term potentiation, were examined in 15- to 30-day-old male rats whose mothers were exposed, from day 0 to day 20 of gestation, to 150 ppm of CO resulting in blood levels of carboxyhemoglobin comparable to those found in human cigarette smokers. Evoked field excitatory postsynaptic potentials were measured in the stratum radiatum in hippocampal slices. Results show that before tetanus, input/output functions, presynaptic volley, and paired-pulse facilitation were not affected in CO-exposed offspring, indicating that basal synaptic excitability and terminal Ca(2+) influx were not influenced by prenatal exposure to this gas. Conversely, evoked field excitatory postsynaptic potentials potentiation in response to tetanization was reduced by about 23% and decayed rapidly to baseline values in slices from CO-exposed animals. No changes between and within groups were observed in paired-pulse facilitation after tetanus. The selective impairment of long-term potentiation expression exhibited by CO-exposed rats was paralleled by a significant decrease in heme-oxygenase 2 and neuronal nitric-oxide synthase in the hippocampus. No changes in either enzymatic activity were found in frontal cortex and cerebellum. These electrophysiological and biochemical alterations might account for cognitive deficits previously observed in rats exposed prenatally to CO. Our findings could have clinical implications for the offspring of mothers who smoke during pregnancy.

A role for Src kinase in spontaneous epileptiform activity in the CA3 region of the hippocampus.

Members of the Src family of nonreceptor protein tyrosine kinases (PTKs) have been implicated in the regulation of cellular excitability and synaptic plasticity. We have investigated the role of these PTKs in in vitro models of epileptiform activity. Spontaneous epileptiform discharges were induced in vitro in the CA3 region of rat hippocampal slices by superfusion with the potassium channel blocker 4-aminopyridine in Mg(2+)-free medium. In hippocampal slices treated in this fashion, Src kinase activity was increased and the frequency of epileptiform discharges could be greatly reduced by inhibitor of the Src family of PTKs, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), but not by the inactive structural analog 4-amino-7-phenylpyrazol[3,4-d]pyrimidine (PP3). 4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine also reduced epileptiform activity induced by either 4-aminopyridine or Mg(2+)-free medium alone. These observations demonstrate a role for Src family PTKs in the pathophysiology of epilepsy and suggest potential therapeutic targets for antiepileptic therapy.

Gamma-Hydroxybutyrate inhibits excitatory postsynaptic potentials in rat hippocampal slices.

Gamma-Hydroxybutyrate (GHB) has been shown to mimic different central actions of ethanol, to suppress alcohol withdrawal syndrome, and to reduce alcohol consumption both in rats and in humans. The aim of the present study was to determine if GHB shared with alcohol the ability to inhibit glutamate action at both NMDA and AMPA/kainate receptors. The NMDA or the AMPA/kainate receptors-mediated postsynaptic potentials were evoked in CA1 pyramidal neurons by stimulation of Schaffer-collateral commissural fibers in the presence of CGP 35348, bicuculline to block the GABA(B) and GABA(A) receptors, and 10 microM 6,7-dinitroquinoxaline-2,3-dione (DNQX) or 30 microM DL-2-amino-5-phosphonovalerate (d-APV) to block AMPA/kainate or NMDA receptors, respectively. GHB (600 microM) produced a depression of both NMDA and AMPA/kainate receptors-mediated excitatory postsynaptic potentials with recovery on washout. The GHB receptors antagonist, NCS-382, at the concentration of 500 microM had no effect per se on these responses but prevented the depressant effect of GHB (600 microM) on the NMDA and AMPA/kainate-mediated responses. In the paired-pulse experiments, GHB (600 microM) depressed the amplitude of the first and the second evoked AMPA/kainate excitatory postsynaptic potentials, and significantly increased the paired-pulse facilitation (PPF). These results suggest that GHB inhibits excitatory synaptic transmission at Schaffer-collateral commissural-pyramidal neurons synapses by decreasing the probability of release of glutamate.

Antagonistic action of pitrazepin on human and rat GABA(A) receptors.

Pitrazepin, 3-(piperazinyl-1)-9H-dibenz(c,f) triazolo(4,5-a)azepin is a piperazine antagonist of GABA in a variety of electrophysiological and in vitro binding studies involving GABA and glycine receptors. In the present study we have investigated the effects of pitrazepin, and the GABA(A) antagonist bicuculline, on membrane currents elicited by GABA in Xenopus oocytes injected with rat cerebral cortex mRNA or cDNAs encoding alpha1beta2 or alpha1beta2gamma2s human GABA(A) receptor subunits. The three types of GABA(A) receptors expressed were reversibly antagonized by bicuculline and pitrazepin in a concentration-dependent manner. GABA dose-current response curves for the three types of receptors were shifted to the right, in a parallel manner, by increasing concentrations of pitrazepin. Schild analyses gave pA2 values of 6.42+/-0.62, n = 4, 6.41+/-1.2, n = 5 and 6.21+/-1.24, n = 6, in oocytes expressing rat cerebral cortex, alpha1beta2 or alpha1beta2gamma2s human GABA(A) receptors respectively (values are given as means +/- s.e. mean), and the Hill coefficients were all close to unity. All this is consistent with the notion that pitrazepin acts as a competitive antagonist of these GABA(A) receptors; and that their antagonism by pitrazepin is not strongly dependent on the subunit composition of the receptors here studied. Since pitrazepin has been reported to act also at the benzodiazepine binding site, we studied the effect of the benzodiazepine antagonist Ro 15-1788 (flumazenil) on the inhibition of alpha1beta2gamma2s receptors by pitrazepin. Co-application of Ro 15-1788 did not alter the inhibiting effect of pitrazepin. Moreover, pitrazepin did not antagonize the potentiation of GABA-currents by flunitrazepam. All this suggests that pitrazepin does not affect the GABA receptor-chloride channel by interacting with the benzodiazepine receptor site.

Acamprosate enhances N-methyl-D-apartate receptor-mediated neurotransmission but inhibits presynaptic GABA(B) receptors in nucleus accumbens neurons.

Acamprosate (calcium acetylhomotaurine) is used therapeutically in Europe to reduce relapse in weaned alcoholics. However, the mechanisms of acamprosate action in the central nervous system are still obscure, although early studies suggested an action on GABA receptors. The nucleus accumbens (NAcc) is a brain region thought to underlie ethanol reinforcement. Recent studies from our laboratory have demonstrated that ethanol inhibits both N-methyl-D-aspartate (NMDA) and non-NMDA types of glutamatergic synaptic transmission in the NAcc. In the present study, we used voltage- and current-clamp intracellular recording of NAcc core neurons in a slice preparation to examine acamprosate actions on resting membrane properties and pharmacologically isolated synaptic responses. We isolated NMDA and non-NMDA receptor-mediated excitatory postsynaptic potentials or currents (EPSP/Cs) with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonovalerate (d-APV), respectively. Bicuculline was also included to block GABA(A) receptors. Superfusion of acamprosate (5, 50, and 300 microM) did not alter the resting membrane properties of NAcc neurons. However, 300 microM acamprosate significantly increased the NMDA receptor-mediated components of EPSP/Cs (NMDA-EPSP/Cs) with recovery on washout. In contrast, 300 microM acamprosate had no significant effect on the non-NMDA receptor component of the EPSP/Cs (non-NMDA-EPSP/Cs). To test acamprosate actions on the GABA system, we superfused 60 microM d-APV and 20 microM CNQX to block glutamatergic transmission and evoked monosynaptic GABA(A) receptor-mediated synaptic responses within the NAcc. Acamprosate (300 microM) did not change these monosynaptic GABA(A)-IPSCs. We also used a paired-pulse paradigm to test whether acamprosate could act on presynaptic GABA(B) autoreceptors, in the presence of d-APV and CNQX to block glutamatergic transmission. Like 0.5 microM CGP 34358 (a GABA[B] receptor blocker), acamprosate significantly decreased the paired-pulse inhibition (PPI) of GABA(A)-IPSCs at short interstimulus intervals (ISIs). Thus, acamprosate may concomitantly enhance NMDA-EPSP/Cs while blocking presynaptic GABA(B) receptor-mediated inhibition of GABA release. These results suggest that acamprosate's clinical efficacy in preventing relapse in weaned alcoholics could derive from its interactions with both the glutamatergic and GABAergic systems in the NAcc.

Allosteric modulation by single enantiomers of a C3-chiral 1,4-benzodiazepine of the gamma aminobutyric acid type A receptor channel expressed in Xenopus oocytes.

Xenopus laevis oocytes injected with Poly(A)(+)-RNA isolated from neuronal tissue express membrane proteins peculiar to the origin of mRNA. The translation of gamma aminobutyric acid type A (GABAA) receptors has been shown by dose/ response behavior of GABA and the reversible blockade of the GABA-induced current by picrotoxin. This current was analyzed quantitatively under two electrode voltage-clamp conditions. This methodology has been applied for the first time to study the functional properties of the receptor as a function of the stereochemistry of the ligands. The (+)-S and (-)-R enantiomers of a water-soluble benzodiazepine derivative, 7-chloro-1,3-dihydro-3-hemisuccinyloxy-5-phenyl-1,4-benzodiazep in-2-one (OXHEM), obtained by preparative high performance liquid chromatographic (HPLC) resolution on chiral stationary phase, act as agonists in the in vitro modulation of the chloride channel. The (+)-S-OXHEM enantiomer was the more active.

Naloxone blocks long-term depression of excitatory transmission in rat CA1 hippocampus in vitro.

In rat hippocampal slices, high intensity tetanic stimulation (two 1 s trains of 100 Hz separated by 20 s, 3-5X intensity of the test stimulus) of the Schaffer collateral-commissural (SCC) fibers induced a long-term depression (LTD) of the negative field excitatory postsynaptic potentials (fEPSP) in stratum radiatum of the CA1 region. The initial slope of the fEPSP, evoked by a single test shock applied to the SCC fibers, was depressed for a period longer than 40 min following such high intensity tetanic stimulation to this fiber system. However, the same tetanic stimulation delivered at low (test) intensity induced long-term potentiation (LTP) of the fEPSPs. Thus, similar patterns of stimulation can induce either LTP or LTD, depending on whether low- or high-intensity tetanic stimuli are delivered. The LTD induced by high strength tetanic stimulation was clearly blocked by the opioid antagonist naloxone (1 microM); however, the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate (AP5; 50 microM) had no effect on the LTD. Our data suggest that the strong stimulation used for LTD induction may have activated other afferent fiber systems and/or local interneurons in addition to SCC fibers, such as the enkephalin-containing terminals of the perforant path (PP) projecting to the stratum lacunosum moleculare or opioid peptide-containing interneurons. Thus, the resulting release of endogenous opioid peptides could play a role in the cellular mechanisms involved in some forms of long-term synaptic depression.

Low ethanol concentrations enhance GABAergic inhibitory postsynaptic potentials in hippocampal pyramidal neurons only after block of GABAB receptors.

Despite considerable evidence that ethanol can enhance chloride flux through the gamma-aminobutyric acid type A (GABA/A/) receptor-channel complex in several central neuron types, the effect of ethanol on hippocampal GABAergic systems is still controversial. Therefore, we have reevaluated this interaction in hippocampal pyramidal neurons subjected to local monosynaptic activation combined with pharmacological isolation of the various components of excitatory and inhibitory synaptic potentials, using intracellular current- and voltage-clamp recording methods in the hippocampal slice. In accord with our previous findings, we found that ethanol had little effect on compound inhibitory postsynaptic potentials/currents (IPSP/Cs) containing both GABA/A/ and GABA/B/ components. However, after selective pharmacological blockade of the GABA/B/ component of the IPSP (GABA/B/-IPSP/C) by CGP-35348, low concentrations of ethanol (22-66 mM) markedly enhanced the peak amplitude, and especially the area, of the GABA/A/ component (GABA/A/-IPSP/C) in most CA1 pyramidal neurons. Ethanol had no significant effect on the peak amplitude or area of the pharmacologically isolated GABA/B/-inhibitory postsynaptic current (IPSC). These results provide new data showing that activation of GABAB receptors can obscure ethanol enhancement of GABA/A/ receptor function in hippocampus and suggest that similar methods of pharmacological isolation might be applied to other brain regions showing negative or mixed ethanol-GABA interactions.

Modulation of electrically elicited blink reflex components by visual and acoustic prestimuli in man.

The effects of a prestimulus on the electrically elicited blink reflex components were investigated in 20 healthy subjects. In the first group of 10 subjects (warned group), electric shocks were delivered in isolation or preceded, at an interstimulus interval (ISI) of 0.1 s, 1 s, or 10 s, by a visual or acoustic warning stimulus. In the second group of 10 subjects (unwarned group), the electric shocks were delivered either in isolation or preceded, at the same ISI, by visual or acoustic stimuli having no warning value. The modulation of the three blink reflex components was then analysed. Compared to the baseline condition, the R1 oligosynaptic component was enhanced at 0.1 s and 1 s ISI, in the warned group with the visual prestimulus, but only at 0.1 s after a visual and acoustic prestimulus in the unwarned group. On the contrary, the polysynaptic responses showed a different course: R2 was significantly reduced at the 0.1 s interval in the warned group with both the prestimuli, and only with the visual prestimulus in the unwarned group. The R3 was inhibited at all three intervals with the visual prestimulus, and at the 0.1 s and 1 s with the acoustic one in the warned group, and only at 0.1 s in the unwarned group, both after visual and acoustic prestimuli. The decrement in R2 and R3 observed with the shortest interval was probably related to the prepulse inhibition of startle reflex. Furthermore, only R3 was still inhibited at longer intervals, when the sustained processes of attention may have influenced this component. Perhaps this combination of events represents, in the warned group, the best preparation for voluntary reflex reaction.

The beta-carboline derivative DMCM decreases gamma-aminobutyric acid responses and Ca(2+)-mediated K(+)-conductance in rat neocortical neurons in vitro.

Electrophysiological recordings from neurons of rat frontal neocortical slices have been used to investigate the action of the beta-carboline methyl-6,7-dimethoxy-4-ethyl-beta- carboline-3-carboxylate (DMCM), on responses to gamma-aminobutyric acid (GABA) and on the excitability of the neurons. Iontophoretic application of GABA close to the intracellularly recorded cells (resting membrane potential -74 +/- 0.9 mV) elicited a depolarization associated with a decrease of input resistance, mediated by GABAA receptors. Bath application of DMCM (0.1-1 microM) reduced these GABA responses decreasing the affinity of the receptors for GABA. This effect was blocked by the benzodiazepine receptor (BZR) antagonist ZK 93426 (1 microM). DMCM (0.1 microM) also decreased the hyperpolarization that followed a train of action potentials (AHP), mediated by Ca(2+)-dependent K+ conductance, and increased the duration of Ca(2+)-dependent action potentials recorded after blockade of Na+ and K+ conductances. Neither effect was blocked by BZR antagonists. These results indicate that DMCM increases the excitability of neurons not only by reducing the gain of the GABAA/BZR complex, but also by modulating intrinsic membrane mechanisms.

Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices.

Hippocampal slices from guinea-pigs were used to examine the long-term potentiation (LTP) of the N-methyl-d-aspartate (NMDA)-mediated excitatory postsynaptic potential (EPSP). Intracellular recordings were performed from CA1 pyramidal neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5 - 10 microM) and picrotoxin (50 microM). In these experimental conditions test stimuli applied at low frequency (0.1 Hz) to the Schaffer collateral - commissural pathway evoked a prolonged EPSP (150 - 200 ms). To obtain this CNQX-resistant EPSP, stimulus intensities had to be raised above the level required to evoke an EPSP of comparable amplitude in physiological solution. Tetanic stimulation (two trains of 100 Hz, 1 s every 20 s) led to a potentiation of the CNQX-resistant EPSP, and this potentiated response was abolished with d-(-)-2-amino-5-phosphonovaleric acid (50 microM). The potentiation of the NMDA receptor-mediated EPSP was more pronounced for strong than for weak test stimuli, and was suppressed when test EPSPs were evoked during membrane hyperpolarization. These results suggest that NMDA receptor-mediated responses can undergo LTP, and hence can contribute to the maintenance of LTP.

[Changes in the neuronal excitability of rat hippocampal slices isolated after destruction of the medial septal area]. / Izmenenie neironnoi vozbudimosti v srezakh gippokampa krysy, izolirovannykh posle razrusheniia medial'noi septal'noi oblasti.

To determine if electrophysiological properties of hippocampal pathways are altered after medial septal area (MSA) destruction, extracellular recordings were made from hippocampal slices of rats 30 days following lesion and compared with those from unoperated controls. The preparation of slices, data accumulation and data analyses were done under the same conditions. The electrophysiological parameters of interest were the population spike (PS) and the field EPSP, produced in the CA1 pyramidal layer by stimulation of the Schaffer collaterals. The principal finding of this study was that neuronal excitability in slices from MSA-lesioned rats was altered. The most striking abnormalities were an epileptiform activity, which consisted of multiple PSs, and multiple seizure-like after discharges with a delayed onset to low stimulation intensities. In the CA1 region of the slices collected from lesioned rats the input-output curve of field EPSP versus PS showed a leftward shift as compared with their counterparts in normal slices. These changes may be related to relative reduction of inhibitory processes in interneuronal circuits of CA1 region.

Effects of dopamine, D-1 and D-2 dopaminergic agonists on the excitability of hippocampal CA1 pyramidal cells in guinea pig.

In hippocampal pyramidal cells (HPCs), Dopamine (DA) application (1 microM) produced, in 50% of recorded cells, an hyperpolarization of the resting membrane potential (r.m.p.) and an increase of the afterhyperpolarization (AHP) amplitude and duration in 79% of recorded cells. DA-induced effects on both the r.m.p. and AHP were mimicked by bath application of a D-1 selective agonist, SKF 38393 (20 microM). In addition, we have observed that a D-1 selective antagonist such as SCH 23390 (1 microM) abolished the action of both DA and SKF 38393. In contrast, the activation of D-2 receptors through LY 171555 (10 microns) produced, in 50% of cells, a depolarization of the r.m.p. and a depression of the AHP in 67% of recorded cells. These results suggest that the effects observed in hippocampal pyramidal neurons after DA application of micromolar concentration are mediated by D-1 subtype of receptors.

Cholinergic mechanisms in the reticular control of transmission in the cat lateral geniculate nucleus.

1. We examined the hypothesis that the ascending reticular arousal system influences thalamic transmission through a cholinergic mechanism. Extra- and intracellular recordings were obtained from neurons of the dorsal lateral geniculate nucleus (LGNd) and the perigeniculate nucleus (PGN) of cats anesthetized either with N2O and pentobarbital or with N2O and halothane. We compared the effects that electrical stimulation of the mesencephalic reticular formation (MRF) and ionophoretically applied acetylcholine (ACh) have on spontaneous and evoked activity of individual neurons and tested whether these effects could be antagonized by ionophoretic administration of the muscarinic receptor blocker scopolamine. The effects of ionophoretically applied glutamate (GLU), N-methyl-D-aspartate, and bicuculline were examined in addition. 2. The prominent effects in LGNd relay cells of both ACh application and of MRF stimulation were an enhancement of the resting discharge, a facilitation of the excitatory responses to light, a reduction of the amplitude and duration of evoked inhibitory episodes, and a blockade of postinhibitory rebound burst. These latter effects resembled those induced with bicuculline. Under barbiturate anesthesia neither ACh application nor MRF stimulation elicited discharges when the excitatory input from the retina was blocked. Ionophoretic application of hte muscarinic antagonist scopolamine abolished the effects of ACh ionophoresis in all relay cells tested (n = 20), and in 10 cells it also antagonized completely the effects of MRF stimulation. In the remaining cells scopolamine reduced the effects of MRF stimulation. 3. Increasing the depth of anesthesia reduced or abolished the effects of ACh application and MRF stimulation on the cells' resting activity but did not interfere with the facilitation of evoked responses. 4. The effects of the excitatory amino acids GLU and NMDA differed from those of MRF stimulation and ACh application, since the former always enhanced both spontaneous and evoked discharges but neither shortened phases of evoked inhibition nor abolished postinhibitory rebound bursts. 5. There was a high correlation between the effectiveness of MRF stimulation and ACh application in individual neurons. On the average, the facilitation of evoked responses was more pronounced in X- than in Y-cells, and the fraction of cells responding with an increase of resting activity to both procedures was considerably higher among X- than among Y-cells.(ABSTRACT TRUNCATED AT 400 WORDS)

The pigeon pattern electroretinogram is not affected by massive loss of cell bodies in the ganglion layer induced by chronic section of the optic nerve.

In pigeons, electroretinographic responses to contrast reversal of sinusoidal gratings (pattern ERGs) were recorded before and after section of the left optic nerve. Ninety and 270 days following optic nerve section the ganglion cell layer of the side that underwent the surgical procedure showed an 80% reduction in the number of cell bodies as compared with the intact side. At these times the pattern ERGs showed comparable amplitudes in both eyes. There is a possibility that the inner nuclear layer of the pigeon retina plays a major role in the generation of the pattern ERG.

Retinal and tectal responses to alternating gratings are unaffected by monocular deprivation in pigeons.

Retinal and tectal potentials to alternating gratings were recorded in pigeons raised monocularly deprived. Deprived eyes showed consistent myopia and anterior-posterior axis elongation. In addition, vitreal opacities were observed in 70% of the deprived eyes. In pigeons with vitreal opacities, a reduction of retinal and tectal response amplitude was consistently found in the high spatial frequency range. Pigeons with clear media of the deprived eyes showed normal retinal and tectal responses.

An automated apparatus for the study of visual discriminations in pigeons.

A fully automated apparatus for the study of visual discriminations in pigeons is described. The apparatus allows the presentation of a single stimulus for successive discriminations and of two or more stimuli at the same time for simultaneous discriminations. It has proven advantageous for comparing successive and simultaneous discriminations in tests of interocular transfer.

Mapping of functional activity in the falcon visual system with [14C] 2-deoxyglucose.

[14C] 2-Deoxyglucose uptake was mapped in the brain of one awake falcon which had one eye covered during the experiment, with the aim of providing tentative data on the identification of this bird's visual centers. Most of the structures with increased [14C] 2-Deoxyglucose uptake receive information from the exposed eye. Labeling was rather symmetrical in the hyperstriatum which receives bilateral projections from the visual thalamic centers. The results are largely consistent with what is known about the visual pathways in pigeons and owls. The falcon's visual Wulst as detected by the [14C] 2-Deoxyglucose labeling, is proportionally larger than that found in the pigeon. This result is consistent with the marked representation of the binocular visual field in the falcon's Wulst.

Pigeon pattern electroretinogram: a response unaffected by chronic section of the optic nerve.

Retinal evoked responses to sinusoidal gratings modulated in counterphase (pattern ERG) have been recorded from the pigeon eye. The pattern ERG amplitude depends upon the temporal frequency of the modulation, the contrast, the spatial frequency and the area of the stimulus. In 8 pigeons the pattern ERG has been recorded at different times after the unilateral section of the optic nerve. It has been found that the pattern ERG has a comparable amplitude in the two eyes as a function of the spatial frequency, 3 and 9 months after the section of the left optic nerve. At these times, histological evidence shows a drastic reduction in the density of the retinal ganglion cells on the operated side in comparison to the control one. These findings suggest that retinal sources other than the ganglion cells are responsible for te generation of the pigeon pattern ERG.