Lecture � Neurosciences II

@5 on Thursday, 11 May, 2000

 

PVC

posterior striate cortex of macaque monkey

lamination pattern based on density of nissel staining

relate input to PVC to the lamination pattern

 

LGN

radioactive tracer into layers of LGN

parvocellular = transported up to cortex along axons 4Cbeta (radioactivity visible in dark band)

magno 4alpha

 

koniocellular pathway

complicates interpretation of m and p pathways

may be implicated in colour vision

probably there, to an extent in the old world primates (more difficult to visualise)

because can get different antibodies to stain the LGN � identify this 3rd group of cells

interlaminar zones

effect on interpretation of lesions � must also be affecting the interlaminar cells

 

anatomy of resolution of m and p pathways

parvo

numerically signficant

injection of horseradish peroxidase into a parvo axons � receptive field like an LGN cell, some colour specificity � then slice up the cortex to establish where it terminates

= quite tightly-focused for an affluent axon into the cortex

 

magno

much more diffusely spread

 

cone mosaic

simple cell � capable of responding 1-2 cones wide (= quite a focused input, as you would expect from the anatomy)

 

why do the bars seem to get more spaced apart on narrowing spatial frequency grating?

aliasing:

spatial frequency = too high, too fine for the pixels on the retina � appearing as lumpy stuff

 

some binoc stuff in the LGN � all inhibitory, not very precisely focused

mysteriously, there are more synapses to the LGN from the cortex than from the retina

 

very significant area of cortex = devoted to vision (25-50%)

 

Hubel + Wiesel � very old physiological recordings from V1

does work with spots, not just lines

disc covering whole receptive field � no response

can map out discrete receptive fields of simple cells

 

orientation + direction-selective

copmlex cell � does not have discrete on/off zones � light + dark are both able to excite receptive field

many cells for identifying constrast sign

but cortex � many cells which don�t care about the sign of the contrast

usually the contrast sign = very important (e.g. difficulty of recognising negative photograph)

 

moved recording site at 20micron intervals (averaged a number of cells, rather than single units) along 2mm of the surface of the cortex to show smooth curve of preferred orientation

 

binocular cells actually = equally balanced input from the left + right eyes

is not actually co-ordinated binocular input

all these experiments in anaesthetised animals

eyes were paralysed with curare-like drug so that they don�t wobble, but unfortunately this causes the eyes wander off in different directions

 

inject tracer into one eye

transports up through the LGN and into the cortex

correlate the anatomical readings electrophysiologically by penetrating in an electrode too

 

very tightly focused (deep) vs very wide speading cells (50microns across most of an ocular dominance band)

but we don�t really understand how many types of cells there are in the cortex

there is a lot of mixing of signals at this stage

 

blobs

probably getting specific input from the interlaminar koniocellular cells

 

reverse correlation

the stimulus sequence is presented, e.g. bar flashing on coputer screen at random locations

then, each time an AP occurs, refer it back to the stimulus on screen which preceded it by a set time

build up a picture of the receptive field through time, dynamic map for single cell of cortex of on/off regions

basic temporal response = biphasic (like a pendulum)

 

you can have end-stopped complex + simple cells

 

predictability � defines simple cells as simple

 

structure in the cortex � hypercolumn:

= a set of orientation-selective detectors for that particular location in the field

also ones with different scales, spatial frequency selectivities

would obviously need many more small than large receptive fields

 

give a functional interpretation to cellular properties

pipette intracellularly into a cell in the PVC

spikes selective for particular orientation, leads to much stronger depolarisation, much stronger than the noise

much discussion about: whetherh the selectivity for orientation primarily excitatory or inhibitory

old H+W theory: a row of on centre LGN cells �/span> simple cells

initial input = excitatory, but not very focused

much of the orientation selectivity = inhibitory

 

both EPSPs and IPSPs respond to the same region

\ H+W's theory cannot be right, since there is both EPSPs and IPSPs on the same on/off region within a receptive field

as opposed to EPSPs from all regions (whether on or off), but of different flavours

�/span> amplified, push/pull, differentiated

can�t visualise these simultaneously at the same membrane potential

 

 

Questions

nissel(?) staining

doughnut shaped receptive fields