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The latencies of excitatory and inhibitory post‐synaptic potentials (e.p.s.p.s and i.p.s.p.s) evoked by electrical stimulation of afferents from the lateral geniculate nucleus were recorded in neurones of area 17 of the cat visual cortex. After application of an extrapolation procedure to compensate for the conduction time of the afferent axons, a histogram of latencies formed three distinct peaks. Potentials in each of these were interpreted as being mediated by mono‐, di‐ and trisynaptic pathways. Characteristic laminar differences in the extracellular field potentials evoked from the lateral geniculate nucleus (l.g.n.) and in the antidromic activation of neurones from the l.g.n. and superior colliculus were used to determine the laminar position of recorded neurones. It was found that within a given layer, all cells maintained similar connexions with relay cells in the l.g.n. Cells in layers 3, 4, upper 5 and 6 were monosynaptically excited by geniculate afferents, while cells in layers 2 and lower 5 received only indirect excitation via other cortical neurones. Layer 3 cells were unique in receiving a prominent disynaptic e.p.s.p. in addition to the direct excitation from the l.g.n. Late, trisynaptic e.p.s.p. components were seen in many layer 5 and 6 cells. The orderly laminar arrangement of the connexions had the consequence that identified cortico‐geniculate neurones were monosynaptically excited and cortico‐collicular neurones di‐ and trisynaptically excited by geniculate afferents. Cortico‐cortical neurones in layers 2 and 3 received di‐ or mono‐ plus disynaptic excitation, depending on laminar position. Post‐synaptic inhibitory potentials were evoked in all impaled cells, following stimulation of the geniculo‐cortical pathway. Except for a few layer 2 cells, this inhibition was mediated through disynaptic pathways of the feed‐forward type. There was a good positive correlation between conduction times for monosynaptic e.p.s.p.s and disynaptic i.p.s.p.s in the same cells, suggesting that cortical neurones receive excitation and inhibition from the same type of geniculate afferents. The stimulating electrodes activated not only geniculo‐cortical afferents, but antidromically activated cortical efferent neurones from their extracortical axons. These neurones possess intracortical collaterals, and care must be taken to distinguish the resulting potentials from those mediated by orthodromic activation of geniculate afferents. In doing so, evidence was obtained for excitatory connexions from layers 2 and 3 to layer 5, from layer 5 to layer 6, and from layer 6 to layer 4. Typical recurrent inhibition was not observed.(ABSTRACT TRUNCATED AT 400 WORDS)

Antidromic activation of layer 6 cortico‐geniculate cells from the lateral geniculate nucleus (l.g.n.) was used to study synaptic effects mediated by their intracortical axon collaterals. A specific stimulation procedure, earlier shown to suppress geniculo‐cortical synaptic effects and to enhance synaptic effects from layer 6 cell collaterals was employed to differentiate between inputs from the two pathways. Single cells in different cortical layers were recorded both extra‐ and intracellularly with glass micro‐electrodes. Antidromic activation of cortico‐geniculate cells at 10‐16 Hz induced massive, usually repetitive, spike discharges in almost all cells in layers 2‐5. The shortest latency for this synaptic activation (3.4‐7.5 ms) was found for simple cells in layer 4. Cells in layers 2, 3 and 5 responded with progressively longer latencies. Cortico‐geniculate cells in layer 6 were atypical in that hardly any responded with synaptic discharges to the stimulation. Intracellular recordings from layer 4 cells revealed, besides a monosynaptic excitatory post‐synaptic potential (e.p.s.p.) from geniculo‐cortical fibres, a late e.p.s.p. with a latency of 3.0‐4.2 ms. This e.p.s.p. could only be evoked from stimulation sites within the A laminae of the l.g.n. in retinotopic register with the recording site in the cortex. No corresponding potential was obtained by stimulation of the optic tract or the superior colliculus. The threshold intensity for the late e.p.s.p. in layer 4 cells was much higher than for the geniculo‐cortical e.p.s.p.s from the same stimulation sites, indicating that the effect was mediated by thin fibres. The late e.p.s.p.s increased dramatically in size with repetitive stimulation of the l.g.n. at frequencies above 7 Hz, while the geniculo‐cortical e.p.s.p.s remained unchanged. In all these properties, the late e.p.s.p.s resemble similar e.p.s.p.s evoked monosynaptically in principal cells of the l.g.n. by orthodromic activation of cortico‐geniculate fibres. Large e.p.s.p.s were evoked also in complex cells of layers 2, 3 and 5 and in simple cells of layer 6 upon antidromic stimulation of cortico‐geniculate fibres. The sample included many efferent neurones, identified as projection cells by antidromic activation from extracortical stimulation sites. The latency and behaviour of the e.p.s.p.s in these cells indicate that the effect was mediated indirectly via layer 4 cells. Presumably, the excitation travelled along an earlier identified chain of neurones, going from layer 4 to layers 2 and 3, from there to layer 5 and then to layer 6.(ABSTRACT TRUNCATED AT 400 WORDS)

Evoked potentials were recorded in the visual cortex of the cat after electrical stimulation of the lateral geniculate nucleus (l.g.n.). The primary response, mediated by geniculo‐cortical fibres, was depressed at stimulation frequencies above 7 Hz and replaced by a late potential, the incremental response, which gradually increased in amplitude with successive stimuli. The incremental response was a negative‐positive potential in the depth of the cortex with the negative component having maximal amplitude in layer 4. The response reversed polarity in layer 1 to become a positive‐negative potential at the surface. The latency of the negative component of the incremental response was about 3.5‐4 ms in layer 4, compared to about 1.5 and 2.5 ms for the mono‐ and disynaptic components of the primary response. The incremental response could only be evoked from the l.g.n. and the optic radiation, not from the optic tract, superior colliculus or other surrounding structures. Within the l.g.n., the effect was only evoked from stimulation sites in approximate retinotopic register with the recording site in the cortex. Low threshold points were found in the A laminae, completely overlapping with the low threshold points for the primary response. Thresholds increased steeply when the stimulation electrode was lowered into the C laminae. The incremental response could still be evoked ten days after the destruction of all cells in the l.g.n. complex by kainic acid. It is concluded that the described incremental response is identical to the augmenting response of Dempsey & Morison (1943) and is mediated by intracortical axon collaterals of antidromically activated cortico‐geniculate neurones.

Brain‐stem control of inhibitory circuits in the dorsal lateral geniculate nucleus (d.l.g.n.) of the cat was studied with extracellular recordings from functionally identified interneurones and with intracellular recordings from principal cells. Perigeniculate neurones, the recurrent inhibitory interneurones of the d.l.g.n., were inhibited by low‐threshold stimulation within a wide bilateral field of the brainstem reticular formation extending from the rostral mesencephalon to the caudal medulla oblongata. The inhibition had a latency of 10‐12 ms for stimulation sites in the mesencephalon and a duration of about 100 ms. The brain‐stem stimulation evoked large hyperpolarizing potentials in intracellularly recorded perigeniculate neurones, indicating that the effect was due to post‐synaptic inhibition. Intrageniculate interneurones, the feed‐forward inhibitory interneurones of the d.l.g.n., were inhibited with a similar time course from the same region of the brain stem. Both feed‐forward and recurrent inhibitory post‐synaptic potentials (i.p.s.p.s) in principal cells were depressed by a preceding stimulation of brain‐stem sites effective for the interneurones. The depression had about the same time course as the inhibition of the interneurones and it occurred without a concomitant change in the membrane potential of the recorded principal cells. A small depolarizing potential, with a latency of 10‐20 ms, was observed in some principal cells after brain‐stem stimulation. The potential reversed polarity when i.p.s.p.s were reversed by current injection into the recorded cell indicating that it was due to disinhibition of the principal cells. The possible neuronal pathway for the inhibition of the d.l.g.n. in interneurones is considered and it is proposed that the effect is mediated by a group of neurones located in the caudal mesencephalon and the rostral pons close to the fibres of the brachium conjunctivum.

1. Reflex effects of cold stimulation of the lower urinary tract were studied in cats anaesthetized with alpha‐chloralose. The bladder and the urethra were catheterized for separate fluid instillations and the bladder pressure was monitored together with the evoked efferent nerve responses in pelvic nerve filaments. 2. A bladder cooling reflex could be evoked from both the bladder and the urethra. The response was an efferent discharge in preganglionic pelvic motor fibres to the bladder. 3. Bladder mechanoreceptors that drive the normal micturition reflex were not directly involved in the cooling reflex. Their tension sensitivity was decreased by cooling and the efferent reflex response typically occurred before any activation of these receptors. The efferent activity of the cooling reflex also survived an intentional unloading of the mechanoreceptors, a manipulation that abolishes the normal micturition reflex. 4. The dynamic threshold temperature of the cooling reflex was about 30‐32 degrees C, which was at the thermal neutral point of the bladder in our experimental situation. 5. The bladder‐evoked component of the reflex was greatly reduced or abolished by an intravesical infusion of the local anaesthetic Xylocaine. It was also abolished by total bladder denervation. 6. The vesical component of the reflex was unchanged by bilateral transections of the hypogastric nerves but abolished by pelvic nerve transection. The cooling reflex from the distal urethra was abolished by transection of the pudendal nerves. 7. It was proposed that the cooling reflex originates from cold receptors in the bladder and urethral walls and that the responsible afferent fibres are unmyelinated C fibres. The function of the reflex may be to rid the body of a thermal ballast when under cooling stress.

1. Inhibitory connections of X‐ and Y‐type principal cells in the cat's dorsal lateral geniculate nucleus were studied with intracellular recording techniques in barbiturate‐anaesthetized animals. Cells were identified as principal cells by antidromic activation from the visual cortex and as X or Y types by their responses to visual stimulation. 2. Graded electrical stimulation was used to obtain selective activation of X and Y ganglion cell axons. The optic nerves were stimulated through ring electrodes behind the eye bulbs and the evoked nerve volley was monitored by an optic tract electrode. The nerve volley consisted of two well‐segregated components, an early, low‐threshold Y component and a late, high‐threshold X component. 3. All principal cells received monosynaptic excitation and disynaptic feed‐forward inhibition from optic nerve fibres. The excitatory and inhibitory postsynaptic potentials were evoked by Y axons in Y cells and by X axons in X cells. Thus, the feed‐forward inhibitory pathway to principal cells is type selective. 4. Recurrent inhibition was evoked in all cells by antidromic activation of principal cell axons in the visual cortex. The recurrent inhibitory potentials had significantly shorter latencies in Y than in X cells but with considerable overlap between the two samples. This overlap presumably reflects a similar overlap in antidromic conduction times for X and Y principal cell axons. 5. Recurrent inhibitory potentials evoked in the orthodromic direction by optic nerve stimulation originated from Y axons in Y principal cells and from X axons in X cells as would be expected for a type‐selective recurrent inhibitory pathway. 6. It is concluded that X and Y principal cells in the dorsal lateral geniculate nucleus have similar but functionally separate inhibitory circuits.

1. The recurrent facilitation of motoneurones is a disinhibition, i.e. a release of the motoneurones from a sustained hyperpolarization evoked by tonically active inhibitory interneurones. Only two groups of interneurones are known to receive recurrent inhibition from motor axon collaterals via Renshaw cells; the interneurones mediating the reciprocal Ia inhibition and the Renshaw cells themselves. The properties of these two groups of neurones were studied to determine if they could produce the tonic inhibition of motoneurones removed during recurrent facilitation.

1. The effects of impulses in recurrent motor axon collaterals on reflex transmission from different types of primary afferents to motoneurones were investigated in the cat by conditioning of PSPs evoked in motoneurones.

1. The pattern of depression of Ia IPSPs by volleys in recurrent motor axon collaterals was investigated in motoneurones supplying hind‐limb muscles in the cat. The test IPSPs were evoked by stimulation of dorsal roots and the conditioning antidromic volleys by stimulation of motor fibres in different peripheral muscle nerves.

1. Interneurones monosynaptically excited from large muscle spindle (Ia) afferents and inhibited from motor axon collaterals were searched for in the lumbar spinal cord of the cat.

1. Interneurones identified by physiological criteria (Hultborn, Jankowska & Lindström, 1971b) to mediate Ia reciprocal inhibition of motoneurones in the spinal cord of the cat were stained by intracellular injection of a fluorescent dye (Procion Yellow).